PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
21437243-0	2011	FGF19 regulates cell proliferation, glucose and bile acid metabolism via FGFR4-dependent and independent pathways.	Glucose	36-43	fibroblast growth factor 15	Mus musculus	0-5
21616061-4	2011	FGFR4-ECD inhibited FGF19-induced activation of FGFR4 signaling and reduced steatosis of HepG2 induced by palmitic acid in vitro.	Palmitic Acid	106-119	fibroblast growth factor 15	Mus musculus	20-25
21437243-1	2011	Fibroblast growth factor 19 (FGF19) is a hormone-like protein that regulates carbohydrate, lipid and bile acid metabolism.	Carbohydrates	77-89	fibroblast growth factor 15	Mus musculus	0-27
21437243-1	2011	Fibroblast growth factor 19 (FGF19) is a hormone-like protein that regulates carbohydrate, lipid and bile acid metabolism.	Carbohydrates	77-89	fibroblast growth factor 15	Mus musculus	29-34
21437243-0	2011	FGF19 regulates cell proliferation, glucose and bile acid metabolism via FGFR4-dependent and independent pathways.	Bile Acids and Salts	48-57	fibroblast growth factor 15	Mus musculus	0-5
21437243-1	2011	Fibroblast growth factor 19 (FGF19) is a hormone-like protein that regulates carbohydrate, lipid and bile acid metabolism.	Bile Acids and Salts	101-110	fibroblast growth factor 15	Mus musculus	0-27
21437243-1	2011	Fibroblast growth factor 19 (FGF19) is a hormone-like protein that regulates carbohydrate, lipid and bile acid metabolism.	Bile Acids and Salts	101-110	fibroblast growth factor 15	Mus musculus	29-34
20018895-1	2010	FGF19 and FGF21, unique members of the fibroblast growth factor (FGF) family, are hormones that regulate glucose, lipid, and energy homeostasis.	Glucose	105-112	fibroblast growth factor 15	Mus musculus	0-5
21437243-5	2011	Our results demonstrate that FGFR4 activation mediates the induction of hepatocyte proliferation and the suppression of bile acid biosynthesis by FGF19, but is not essential for FGF19 to improve glucose and lipid metabolism in high fat diet fed mice as well as in leptin-deficient ob/ob mice.	Bile Acids and Salts	120-129	fibroblast growth factor 15	Mus musculus	146-151
22130247-1	2011	Human fibroblast growth factor 19 (FGF19) is an enterohepatic hormone that is involved in the regulation of hepatic metabolism of bile acids, lipids, and glucose.	Bile Acids and Salts	130-140	fibroblast growth factor 15	Mus musculus	6-33
22130247-1	2011	Human fibroblast growth factor 19 (FGF19) is an enterohepatic hormone that is involved in the regulation of hepatic metabolism of bile acids, lipids, and glucose.	Bile Acids and Salts	130-140	fibroblast growth factor 15	Mus musculus	35-40
22130247-1	2011	Human fibroblast growth factor 19 (FGF19) is an enterohepatic hormone that is involved in the regulation of hepatic metabolism of bile acids, lipids, and glucose.	Glucose	154-161	fibroblast growth factor 15	Mus musculus	6-33
22130247-1	2011	Human fibroblast growth factor 19 (FGF19) is an enterohepatic hormone that is involved in the regulation of hepatic metabolism of bile acids, lipids, and glucose.	Glucose	154-161	fibroblast growth factor 15	Mus musculus	35-40
22130247-4	2011	Recombinant FGF19 treatment (400 microg/kg/d) for 3 d prevented the accumulation of lipid droplets and decreased serum alanine aminotransferase activity and hepatic lipid levels, including those of triglycerides and free fatty acids.	Triglycerides	198-211	fibroblast growth factor 15	Mus musculus	12-17
22130247-4	2011	Recombinant FGF19 treatment (400 microg/kg/d) for 3 d prevented the accumulation of lipid droplets and decreased serum alanine aminotransferase activity and hepatic lipid levels, including those of triglycerides and free fatty acids.	Fatty Acids, Nonesterified	216-232	fibroblast growth factor 15	Mus musculus	12-17
22130247-6	2011	FGF19 treatment (4 microg/kg/d) for 3 d also decreased the hepatic free fatty acid levels and mRNA levels of Acc1, Cd36, and Srebp-1c.	Fatty Acids, Nonesterified	67-82	fibroblast growth factor 15	Mus musculus	0-5
21266813-0	2011	FGF19 protects colonic epithelial cells against hydrogen peroxide.	Hydrogen Peroxide	48-65	fibroblast growth factor 15	Mus musculus	0-5
21266813-3	2011	In the present study, we investigate the anti-apoptosis effect of FGF19 in colonic epithelial cells treated with H2O2.	Hydrogen Peroxide	113-117	fibroblast growth factor 15	Mus musculus	66-71
21266813-7	2011	RESULTS: We demonstrated that pretreatment of FGF19 (50 ng/ml) significantly protects YAMC cells treated with H2O2 assessed by WST-8.	Hydrogen Peroxide	110-114	fibroblast growth factor 15	Mus musculus	46-51
21266813-8	2011	We also demonstrated Hoechst staining of YAMC cells and that H2O2-induced apoptosis is significantly reduced by FGF19 treatment via inhibition of the caspase-3 pathway.	Hydrogen Peroxide	61-65	fibroblast growth factor 15	Mus musculus	112-117
21266813-9	2011	CONCLUSION: These results indicate FGF19 protects YAMC cells against H2O2 and might be related to the pathogenesis of IBD.	Hydrogen Peroxide	69-73	fibroblast growth factor 15	Mus musculus	35-40
21436455-0	2011	FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis.	Glycogen	78-86	fibroblast growth factor 15	Mus musculus	0-5
21436455-1	2011	Fibroblast growth factor (FGF) 19 is an enterokine synthesized and released when bile acids are taken up into the ileum.	Bile Acids and Salts	81-91	fibroblast growth factor 15	Mus musculus	0-33
21436455-2	2011	We show that FGF19 stimulates hepatic protein and glycogen synthesis but does not induce lipogenesis.	Glycogen	50-58	fibroblast growth factor 15	Mus musculus	13-18
21436455-4	2011	Mice lacking FGF15 (the mouse FGF19 ortholog) fail to properly maintain blood concentrations of glucose and normal postprandial amounts of liver glycogen.	Glucose	96-103	fibroblast growth factor 15	Mus musculus	13-18
21436455-4	2011	Mice lacking FGF15 (the mouse FGF19 ortholog) fail to properly maintain blood concentrations of glucose and normal postprandial amounts of liver glycogen.	Glycogen	145-153	fibroblast growth factor 15	Mus musculus	13-18
21436455-4	2011	Mice lacking FGF15 (the mouse FGF19 ortholog) fail to properly maintain blood concentrations of glucose and normal postprandial amounts of liver glycogen.	Glycogen	145-153	fibroblast growth factor 15	Mus musculus	30-35
21436455-5	2011	FGF19 treatment restored the loss of glycogen in diabetic animals lacking insulin.	Glycogen	37-45	fibroblast growth factor 15	Mus musculus	0-5
21436455-6	2011	Thus, FGF19 activates a physiologically important, insulin-independent endocrine pathway that regulates hepatic protein and glycogen metabolism.	Glycogen	124-132	fibroblast growth factor 15	Mus musculus	6-11
21691100-3	2011	We hypothesized that the altered bile acid homeostasis resulted from ileal trapping of bile acids that act via the farnesoid X receptor (FXR) to induce overexpression of FGF15.	Bile Acids and Salts	33-42	fibroblast growth factor 15	Mus musculus	170-175
21691100-3	2011	We hypothesized that the altered bile acid homeostasis resulted from ileal trapping of bile acids that act via the farnesoid X receptor (FXR) to induce overexpression of FGF15.	Bile Acids and Salts	87-97	fibroblast growth factor 15	Mus musculus	170-175
21655243-2	2011	Fgf15 is highly expressed in the ileum and functions as an endocrine signal to regulate liver function, including bile acid synthesis, hepatocyte proliferation and insulin sensitivity.	Bile Acids and Salts	114-123	fibroblast growth factor 15	Mus musculus	0-5
20531290-0	2010	Intestinal FXR-mediated FGF15 production contributes to diurnal control of hepatic bile acid synthesis in mice.	Bile Acids and Salts	83-92	fibroblast growth factor 15	Mus musculus	24-29
20531290-1	2010	Hepatic bile acid synthesis is subject to complex modes of transcriptional control, in which the bile acid-activated nuclear receptor farnesoid X receptor (FXR) in liver and intestine-derived, FXR-controlled fibroblast growth factor 15 (Fgf15) are involved.	Bile Acids and Salts	8-17	fibroblast growth factor 15	Mus musculus	208-235
20531290-1	2010	Hepatic bile acid synthesis is subject to complex modes of transcriptional control, in which the bile acid-activated nuclear receptor farnesoid X receptor (FXR) in liver and intestine-derived, FXR-controlled fibroblast growth factor 15 (Fgf15) are involved.	Bile Acids and Salts	8-17	fibroblast growth factor 15	Mus musculus	237-242
20531290-1	2010	Hepatic bile acid synthesis is subject to complex modes of transcriptional control, in which the bile acid-activated nuclear receptor farnesoid X receptor (FXR) in liver and intestine-derived, FXR-controlled fibroblast growth factor 15 (Fgf15) are involved.	Bile Acids and Salts	97-106	fibroblast growth factor 15	Mus musculus	208-235
20531290-1	2010	Hepatic bile acid synthesis is subject to complex modes of transcriptional control, in which the bile acid-activated nuclear receptor farnesoid X receptor (FXR) in liver and intestine-derived, FXR-controlled fibroblast growth factor 15 (Fgf15) are involved.	Bile Acids and Salts	97-106	fibroblast growth factor 15	Mus musculus	237-242
20531290-2	2010	The Fgf15 pathway is assumed to contribute significantly to control of hepatic bile acid synthesis.	Bile Acids and Salts	79-88	fibroblast growth factor 15	Mus musculus	4-9
20531290-9	2010	In conclusion, this study is the first to demonstrate the physiological relevance of the contribution of the intestinal FXR-Fgf15 signalling pathway in control of hepatic bile acid synthesis.	Bile Acids and Salts	171-180	fibroblast growth factor 15	Mus musculus	124-129
20531290-10	2010	Fgf15 contributes to the regulation of hepatic bile acid synthesis in mice mainly during the dark phase.	Bile Acids and Salts	47-56	fibroblast growth factor 15	Mus musculus	0-5
20531290-11	2010	Expansion of the circulating bile acid pool as well as bile acid sequestration diminishes the contribution of intestinal FXR-Fgf15 signalling in control of hepatic bile acid synthesis and bile formation.	Bile Acids and Salts	29-38	fibroblast growth factor 15	Mus musculus	125-130
20660733-5	2010	We also have generated FGF19 variants that have lost the ability to induce hepatocyte proliferation but that still are effective in lowering plasma glucose levels and improving insulin sensitivity in mice.	Glucose	148-155	fibroblast growth factor 15	Mus musculus	23-28
20018895-1	2010	FGF19 and FGF21, unique members of the fibroblast growth factor (FGF) family, are hormones that regulate glucose, lipid, and energy homeostasis.	Glucose	105-112	fibroblast growth factor 15	Mus musculus	0-3
20080590-3	2010	Analyses of functional interactions between alpha- and beta-Kl and FGF19 factors in wild-type, alpha-kl(-/-), and beta-kl(-/-) mice revealed a comprehensive regulatory scheme of mineral homeostasis involving the mutually regulated positive/negative feedback actions of alpha-Kl, FGF23, and 1,25(OH)(2)D and an analogous regulatory network composed of beta-Kl, FGF15/humanFGF19, and bile acids that regulate bile acid/cholesterol metabolism.	Bile Acids and Salts	382-392	fibroblast growth factor 15	Mus musculus	67-72
20080590-3	2010	Analyses of functional interactions between alpha- and beta-Kl and FGF19 factors in wild-type, alpha-kl(-/-), and beta-kl(-/-) mice revealed a comprehensive regulatory scheme of mineral homeostasis involving the mutually regulated positive/negative feedback actions of alpha-Kl, FGF23, and 1,25(OH)(2)D and an analogous regulatory network composed of beta-Kl, FGF15/humanFGF19, and bile acids that regulate bile acid/cholesterol metabolism.	Bile Acids and Salts	382-391	fibroblast growth factor 15	Mus musculus	67-72
20080590-3	2010	Analyses of functional interactions between alpha- and beta-Kl and FGF19 factors in wild-type, alpha-kl(-/-), and beta-kl(-/-) mice revealed a comprehensive regulatory scheme of mineral homeostasis involving the mutually regulated positive/negative feedback actions of alpha-Kl, FGF23, and 1,25(OH)(2)D and an analogous regulatory network composed of beta-Kl, FGF15/humanFGF19, and bile acids that regulate bile acid/cholesterol metabolism.	Cholesterol	417-428	fibroblast growth factor 15	Mus musculus	67-72
19706524-1	2009	FGF19 is a hormone that regulates bile acid and glucose homeostasis.	Bile Acids and Salts	34-43	fibroblast growth factor 15	Mus musculus	0-5
19767447-0	2009	Administration of ampicillin elevates hepatic primary bile acid synthesis through suppression of ileal fibroblast growth factor 15 expression.	Ampicillin	18-28	fibroblast growth factor 15	Mus musculus	103-130
19767447-10	2009	These results suggest that ABPC administration elevates hepatic primary bile acid synthesis, at least in part, through suppression of ileal FGF15 expression.	Ampicillin	27-31	fibroblast growth factor 15	Mus musculus	140-145
19706524-5	2009	We show that betaKlotho was essential for FGF19 interaction with FGFRs 1c, 2c, and 3c, but FGF19 was able to interact directly with FGFR4 in the absence of betaKlotho in a heparin-dependent manner.	Heparin	172-179	fibroblast growth factor 15	Mus musculus	91-96
19706524-11	2009	These results suggest that FGF19-regulated liver bile acid metabolism could be independent of its glucose-lowering effect, and direct FGFR activation in adipose tissue may play an important role in the regulation of glucose homeostasis.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	27-32
18772362-3	2008	FGF-15 secretion by the intestine regulates hepatic bile acid biosynthesis.	Bile Acids and Salts	52-61	fibroblast growth factor 15	Mus musculus	0-6
19390091-4	2009	Here, we report surprising findings that SHP is a rapidly degraded protein via the ubiquitin-proteasomal pathway and that bile acids or bile acid-induced intestinal fibroblast growth factor 19 (FGF19) increases stability of hepatic SHP by inhibiting proteasomal degradation in an extracellular signal-regulated kinase (ERK)-dependent manner.	Bile Acids and Salts	122-132	fibroblast growth factor 15	Mus musculus	165-192
19390091-4	2009	Here, we report surprising findings that SHP is a rapidly degraded protein via the ubiquitin-proteasomal pathway and that bile acids or bile acid-induced intestinal fibroblast growth factor 19 (FGF19) increases stability of hepatic SHP by inhibiting proteasomal degradation in an extracellular signal-regulated kinase (ERK)-dependent manner.	Bile Acids and Salts	122-132	fibroblast growth factor 15	Mus musculus	194-199
19390091-4	2009	Here, we report surprising findings that SHP is a rapidly degraded protein via the ubiquitin-proteasomal pathway and that bile acids or bile acid-induced intestinal fibroblast growth factor 19 (FGF19) increases stability of hepatic SHP by inhibiting proteasomal degradation in an extracellular signal-regulated kinase (ERK)-dependent manner.	Bile Acids and Salts	122-131	fibroblast growth factor 15	Mus musculus	194-199
18772362-9	2008	FGF-15 secretion into cell culture media by CT-26 cells was diminished after siFGF-15 or sibeta-Klotho treatment and enhanced by chenodeoxycholic acid.	sibeta-klotho	89-102	fibroblast growth factor 15	Mus musculus	0-6
19608735-8	2009	However, ileal mRNA expression of Fgf15 (inhibitor of bile salt synthesis) was significantly reduced, in agreement with absent inhibition of the hepatic bile salt synthesis.	Bile Acids and Salts	54-63	fibroblast growth factor 15	Mus musculus	34-39
19608735-11	2009	In conclusion, our data indicate that EFA deficiency is associated with interrupted negative feedback of bile salt synthesis, possibly because of reduced ileal Fgf15 expression.	Fatty Acids, Essential	38-41	fibroblast growth factor 15	Mus musculus	160-165
19085950-1	2009	UNLABELLED: Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid-induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7alpha-hydroxylase gene (C YP7A1) transcription in mouse liver.	Bile Acids and Salts	107-116	fibroblast growth factor 15	Mus musculus	18-45
19085950-1	2009	UNLABELLED: Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid-induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7alpha-hydroxylase gene (C YP7A1) transcription in mouse liver.	Bile Acids and Salts	107-116	fibroblast growth factor 15	Mus musculus	47-52
19085950-1	2009	UNLABELLED: Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid-induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7alpha-hydroxylase gene (C YP7A1) transcription in mouse liver.	Bile Acids and Salts	157-166	fibroblast growth factor 15	Mus musculus	18-45
19085950-1	2009	UNLABELLED: Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid-induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7alpha-hydroxylase gene (C YP7A1) transcription in mouse liver.	Bile Acids and Salts	157-166	fibroblast growth factor 15	Mus musculus	47-52
19085950-2	2009	The mechanism underlying FGF15/FGF19 inhibition of bile acid synthesis in hepatocytes remains unclear.	Bile Acids and Salts	51-60	fibroblast growth factor 15	Mus musculus	25-30
18772362-9	2008	FGF-15 secretion into cell culture media by CT-26 cells was diminished after siFGF-15 or sibeta-Klotho treatment and enhanced by chenodeoxycholic acid.	Chenodeoxycholic Acid	129-150	fibroblast growth factor 15	Mus musculus	0-6
18660672-7	2008	SUMMARY: Recent mouse genetic studies have broadened our understanding of molecular pathways involved in mineral and bile acid homeostasis regulated by FGF23 and FGF19, respectively.	Bile Acids and Salts	117-126	fibroblast growth factor 15	Mus musculus	162-167
18660672-9	2008	Further investigations on endocrine axes mediated by the Klotho family and FGF19 subfamily members are expected to provide new insights into the molecular mechanisms by which the endocrine fibroblast growth factors regulate bile acid, energy, and phosphate/vitamin D metabolism.	Bile Acids and Salts	224-233	fibroblast growth factor 15	Mus musculus	75-80
18660672-9	2008	Further investigations on endocrine axes mediated by the Klotho family and FGF19 subfamily members are expected to provide new insights into the molecular mechanisms by which the endocrine fibroblast growth factors regulate bile acid, energy, and phosphate/vitamin D metabolism.	Phosphates	247-256	fibroblast growth factor 15	Mus musculus	75-80
18660672-9	2008	Further investigations on endocrine axes mediated by the Klotho family and FGF19 subfamily members are expected to provide new insights into the molecular mechanisms by which the endocrine fibroblast growth factors regulate bile acid, energy, and phosphate/vitamin D metabolism.	Vitamin D	257-266	fibroblast growth factor 15	Mus musculus	75-80
18179175-3	2008	The FGF19 subfamily has reduced heparin binding resulting from a disrupted beta-trefoil domain.	Heparin	32-39	fibroblast growth factor 15	Mus musculus	4-9
18179175-6	2008	FGF19 expression is regulated by the farnesoid X receptor, a nuclear hormone receptor that is a key regulator of bile acid biosynthesis and transport.	Bile Acids and Salts	113-122	fibroblast growth factor 15	Mus musculus	0-5
18179175-7	2008	In line with its regulation by a bile acid receptor, FGF19 is involved in the regulation of bile acid biosynthesis and gallbladder filling.	Bile Acids and Salts	33-42	fibroblast growth factor 15	Mus musculus	53-58
17627937-2	2007	FGF19 regulates bile acid homeostasis and gall bladder filling; FGF19 binds only to FGF receptor 4 (FGFR4), but its liver-specific activity cannot be explained solely by the distribution of this receptor.	Bile Acids and Salts	16-25	fibroblast growth factor 15	Mus musculus	0-5
17823457-0	2007	FXR agonists and FGF15 reduce fecal bile acid excretion in a mouse model of bile acid malabsorption.	Bile Acids and Salts	36-45	fibroblast growth factor 15	Mus musculus	17-22
17823457-0	2007	FXR agonists and FGF15 reduce fecal bile acid excretion in a mouse model of bile acid malabsorption.	Bile Acids and Salts	76-85	fibroblast growth factor 15	Mus musculus	17-22
17823457-2	2007	Feedback regulation of bile acid synthesis is under the control of an endocrine pathway wherein activation of the nuclear bile acid receptor, farnesoid X receptor (FXR), induces enteric expression of the hormone, fibroblast growth factor 15 (FGF15).	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	213-240
17823457-2	2007	Feedback regulation of bile acid synthesis is under the control of an endocrine pathway wherein activation of the nuclear bile acid receptor, farnesoid X receptor (FXR), induces enteric expression of the hormone, fibroblast growth factor 15 (FGF15).	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	242-247
17823457-3	2007	In liver, FGF15 acts together with FXR-mediated expression of small heterodimer partner to repress bile acid synthesis.	Bile Acids and Salts	99-108	fibroblast growth factor 15	Mus musculus	10-15
17823457-4	2007	Here, we show that the FXR-FGF15 pathway is disrupted in mice lacking apical ileal bile acid transporter, a model of bile acid malabsorption.	Bile Acids and Salts	83-92	fibroblast growth factor 15	Mus musculus	27-32
17823457-4	2007	Here, we show that the FXR-FGF15 pathway is disrupted in mice lacking apical ileal bile acid transporter, a model of bile acid malabsorption.	Bile Acids and Salts	117-126	fibroblast growth factor 15	Mus musculus	27-32
17823457-5	2007	Treatment of Asbt-/- mice with either a synthetic FXR agonist or FGF15 downregulates hepatic cholesterol 7alpha-hydroxylase mRNA levels, decreases bile acid pool size, and reduces fecal bile acid excretion.	Bile Acids and Salts	147-156	fibroblast growth factor 15	Mus musculus	65-70
17823457-5	2007	Treatment of Asbt-/- mice with either a synthetic FXR agonist or FGF15 downregulates hepatic cholesterol 7alpha-hydroxylase mRNA levels, decreases bile acid pool size, and reduces fecal bile acid excretion.	Bile Acids and Salts	186-195	fibroblast growth factor 15	Mus musculus	65-70
17823457-6	2007	These findings suggest that FXR agonists or FGF15 could be used therapeutically to interrupt the cycle of excessive bile acid production in patients with bile acid malabsorption.	Bile Acids and Salts	116-125	fibroblast growth factor 15	Mus musculus	44-49
17823457-6	2007	These findings suggest that FXR agonists or FGF15 could be used therapeutically to interrupt the cycle of excessive bile acid production in patients with bile acid malabsorption.	Bile Acids and Salts	154-163	fibroblast growth factor 15	Mus musculus	44-49
14976145-9	2004	Thus, FGF19 is able to increase metabolic rate concurrently with an increase in fatty acid oxidation.	Fatty Acids	80-90	fibroblast growth factor 15	Mus musculus	6-11
16284190-6	2006	In all of the mice studied, dietary taurocholate increased ileal expression of FGF15, a FXR-inducible murine homologue of human FGF19.	Taurocholic Acid	36-48	fibroblast growth factor 15	Mus musculus	79-84
16284190-7	2006	CONCLUSIONS: Hepatic PON1 and CYP7A1 mRNA expression is repressed by bile acids via FXR-mediated induction of FGF15.	Bile Acids and Salts	69-79	fibroblast growth factor 15	Mus musculus	110-115
16213224-0	2005	Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis.	Bile Acids and Salts	77-86	fibroblast growth factor 15	Mus musculus	0-27
16213224-2	2005	Here, we demonstrate that fibroblast growth factor 15 (FGF15) signals from intestine to liver to repress the gene encoding cholesterol 7alpha-hydroxylase (CYP7A1), which catalyzes the first and rate-limiting step in the classical bile acid synthetic pathway.	Bile Acids and Salts	230-239	fibroblast growth factor 15	Mus musculus	26-53
16213224-2	2005	Here, we demonstrate that fibroblast growth factor 15 (FGF15) signals from intestine to liver to repress the gene encoding cholesterol 7alpha-hydroxylase (CYP7A1), which catalyzes the first and rate-limiting step in the classical bile acid synthetic pathway.	Bile Acids and Salts	230-239	fibroblast growth factor 15	Mus musculus	55-60
16213224-4	2005	Mice lacking FGF15 have increased hepatic CYP7A1 mRNA and protein levels and corresponding increases in CYP7A1 enzyme activity and fecal bile acid excretion.	Bile Acids and Salts	137-146	fibroblast growth factor 15	Mus musculus	13-18
17456796-7	2007	Cafestol did not affect genes known to be up-regulated by FXR in the liver of wild-type mice, but did increase expression of the positive FXR-target genes intestinal bile acid-binding protein and fibroblast growth factor 15 (FGF15) in the intestine.	cafestol	0-8	fibroblast growth factor 15	Mus musculus	196-223
17456796-7	2007	Cafestol did not affect genes known to be up-regulated by FXR in the liver of wild-type mice, but did increase expression of the positive FXR-target genes intestinal bile acid-binding protein and fibroblast growth factor 15 (FGF15) in the intestine.	cafestol	0-8	fibroblast growth factor 15	Mus musculus	225-230
17456796-8	2007	Because FGF15 has recently been shown to function in an enterohepatic regulatory pathway to repress liver expression of bile acid homeostatic genes, its direct induction in the gut may account for indirect effects of cafestol on liver gene expression.	Bile Acids and Salts	120-129	fibroblast growth factor 15	Mus musculus	8-13
17456796-8	2007	Because FGF15 has recently been shown to function in an enterohepatic regulatory pathway to repress liver expression of bile acid homeostatic genes, its direct induction in the gut may account for indirect effects of cafestol on liver gene expression.	cafestol	217-225	fibroblast growth factor 15	Mus musculus	8-13
17456796-10	2007	Using a double FXR/PXR knockout mouse model, we found that both receptors contribute to the cafestol-dependent induction of intestinal FGF15 gene expression.	cafestol	92-100	fibroblast growth factor 15	Mus musculus	135-140
16213224-5	2005	These studies define FGF15 and FGFR4 as components of a gut-liver signaling pathway that synergizes with SHP to regulate bile acid synthesis.	Bile Acids and Salts	121-130	fibroblast growth factor 15	Mus musculus	21-26
33235221-2	2020	Fibroblast Growth Factor-15/19 (mouse FGF15, human FGF19) are bile acid-induced late fed-state gut hormones that decrease hepatic lipid levels by unclear mechanisms.	Bile Acids and Salts	62-71	fibroblast growth factor 15	Mus musculus	0-30
12057932-4	2002	Increased proliferation of pericentral hepatocytes was demonstrated by 5-bromo-2"-deoxyuridine incorporation in the FGF19 transgenic mice before tumor formation and in nontransgenic mice injected with recombinant FGF19 protein.	Bromodeoxyuridine	71-94	fibroblast growth factor 15	Mus musculus	116-121
33235221-2	2020	Fibroblast Growth Factor-15/19 (mouse FGF15, human FGF19) are bile acid-induced late fed-state gut hormones that decrease hepatic lipid levels by unclear mechanisms.	Bile Acids and Salts	62-71	fibroblast growth factor 15	Mus musculus	38-43
34906775-6	2022	In vitro, the results suggested that FGF19 ameliorated the PA-induced decline in osteoblast proliferation, increased cell death and impaired cell morphology.	Palmitic Acid	59-61	fibroblast growth factor 15	Mus musculus	37-42
33235319-9	2020	FGF401 synergistically acted with the microtubule-depolymerizing drug vinorelbine to further suppress tumor growth, promote apoptosis, and prolong the OS of mice bearing high FGF19 tumors, with no evidence of increased toxicity.	Vinorelbine	70-81	fibroblast growth factor 15	Mus musculus	175-180
34906775-7	2022	Additionally, FGF19 protected against the decline in activation of alkaline phosphatase (ALP) and protein expression of Collagen-1, Runx-2, and osteopontin (OPN) induced by PA.	Palmitic Acid	173-175	fibroblast growth factor 15	Mus musculus	14-19
34906775-8	2022	Furthermore, FGF19 might enhance osteogenic differentiation via the Wnt/beta-catenin pathway and inhibit osteoclastogenesis by regulating the osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) axis, thus attenuating the negative effect of PA in osteoblasts.	Palmitic Acid	257-259	fibroblast growth factor 15	Mus musculus	13-18
34965924-1	2022	Fibroblast growth factor 15/19 (FGF15/19) are endocrine growth factors that play an important role in bile acid homeostasis.	Bile Acids and Salts	102-111	fibroblast growth factor 15	Mus musculus	0-30
34387888-10	2022	Intestinal inflammation and ileal mRNAs (Nr1h4, Fgf15 and Ostalpha) were not different among groups, supporting a liver specific effect of GW4064 in this model CONCLUSION: GW4064 prevents PNAC in mice through restoration of hepatic FXR signaling resulting in increased expression of canalicular bile, sterol and phospholipid transporters, and suppression of macrophage recruitment and activation.	GW 4064	172-178	fibroblast growth factor 15	Mus musculus	48-53
34965924-1	2022	Fibroblast growth factor 15/19 (FGF15/19) are endocrine growth factors that play an important role in bile acid homeostasis.	Bile Acids and Salts	102-111	fibroblast growth factor 15	Mus musculus	32-40
34973477-0	2022	LKB1 in intestinal epithelial cells regulates bile acid metabolism by modulating FGF15/19 production.	Bile Acids and Salts	46-55	fibroblast growth factor 15	Mus musculus	81-89
33783283-3	2021	We performed qPCR, western blot and ELISA assays in different tissue samples to evaluate FXR-FGF15/19 signaling.Results: Abx treatment induced skeletal muscle atrophy in mice.	CHEMBL369125	121-124	fibroblast growth factor 15	Mus musculus	93-101
34973477-7	2022	A significant reduction of the farnesoid X receptor (FXR) target genes, including fibroblast growth factor 15/19 (FGF15/19), known to inhibit BA synthesis, was found in the small intestine (SI) ileum of LKB1DeltaIEC mice.	Bile Acids and Salts	142-144	fibroblast growth factor 15	Mus musculus	114-122
34973477-13	2022	CONCLUSIONS: LKB1 in IECs manages BA homeostasis by controlling FGF15/19 production.	Bile Acids and Salts	34-36	fibroblast growth factor 15	Mus musculus	64-72
33783283-5	2021	Ileal farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) signaling was inhibited in response to microbial BA disturbance.	Bile Acids and Salts	118-120	fibroblast growth factor 15	Mus musculus	33-60
33783283-5	2021	Ileal farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) signaling was inhibited in response to microbial BA disturbance.	Bile Acids and Salts	118-120	fibroblast growth factor 15	Mus musculus	62-67
33783283-7	2021	Treating Abx mice with FGF19 (human FGF15 ortholog) partly reversed skeletal muscle loss.Conclusions: These findings indicate that the BA-FXR-FGF15/19 axis acts as a regulator of gut microbiota to mediate host skeletal muscle.	CHEMBL369125	9-12	fibroblast growth factor 15	Mus musculus	23-28
34736501-14	2021	Notably, SWT efficiently improved the imbalance of BA homeostasis in livers caused by CCl4 via activating farnesoid X receptor (FXR)-fibroblast growth factor 15 enterohepatic and FXR-small heterodimer partner hepatic pathways.	Carbon Tetrachloride	86-90	fibroblast growth factor 15	Mus musculus	133-160
34585527-11	2021	Increase in expression of FGF15 in intestine (P < 0.01) suggested the activation of FXR signalling pathway which might contribute to the regulation of BA synthesis enzymes, transporters, and metabolic enzymes.	Bile Acids and Salts	151-153	fibroblast growth factor 15	Mus musculus	26-31
34492674-0	2021	Enterobacter aerogenes ZDY01 inhibits choline-induced atherosclerosis through CDCA-FXR-FGF15 axis.	Choline	38-45	fibroblast growth factor 15	Mus musculus	87-92
34858337-9	2021	Together, these results support the hypothesis that FGF19 increases glutamate release from AP and NTS neurons that project to the DMV in hyperglycemic mice.	Glutamic Acid	68-77	fibroblast growth factor 15	Mus musculus	52-57
34858337-9	2021	Together, these results support the hypothesis that FGF19 increases glutamate release from AP and NTS neurons that project to the DMV in hyperglycemic mice.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	130-133	fibroblast growth factor 15	Mus musculus	52-57
34778346-8	2021	In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group.	sco-pl	196-202	fibroblast growth factor 15	Mus musculus	79-106
34778346-8	2021	In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group.	sco-pl	196-202	fibroblast growth factor 15	Mus musculus	108-113
34778346-8	2021	In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group.	Triglycerides	222-224	fibroblast growth factor 15	Mus musculus	79-106
34778346-8	2021	In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group.	Triglycerides	222-224	fibroblast growth factor 15	Mus musculus	108-113
34778346-9	2021	From these results, the increase in the liver CYP7A1 expression by dietary SCO-PL was in part through the reduction of the ileum Fxr/Fgf15 regulatory pathway.	sco-pl	75-81	fibroblast growth factor 15	Mus musculus	133-138
34858337-5	2021	Glutamate photoactivation experiments confirmed that FGF19 increases synaptic glutamate release from AP and NTS neurons that connect to the DMV in hyperglycemic, but not normoglycemic mice.	Glutamic Acid	0-9	fibroblast growth factor 15	Mus musculus	53-58
34858337-5	2021	Glutamate photoactivation experiments confirmed that FGF19 increases synaptic glutamate release from AP and NTS neurons that connect to the DMV in hyperglycemic, but not normoglycemic mice.	Glutamic Acid	78-87	fibroblast growth factor 15	Mus musculus	53-58
34858337-5	2021	Glutamate photoactivation experiments confirmed that FGF19 increases synaptic glutamate release from AP and NTS neurons that connect to the DMV in hyperglycemic, but not normoglycemic mice.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	140-143	fibroblast growth factor 15	Mus musculus	53-58
34858337-6	2021	Contrary to expectations, FGF19 produced a mixed effect on intrinsic membrane properties in the NTS with a trend towards inhibition, suggesting that another mechanism was responsible for the observed effects on glutamate release in the DMV.	Glutamic Acid	211-220	fibroblast growth factor 15	Mus musculus	26-31
34858337-6	2021	Contrary to expectations, FGF19 produced a mixed effect on intrinsic membrane properties in the NTS with a trend towards inhibition, suggesting that another mechanism was responsible for the observed effects on glutamate release in the DMV.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	236-239	fibroblast growth factor 15	Mus musculus	26-31
34858337-7	2021	Consistent with the hypothesis, FGF19 increased action potential-dependent glutamate release in the NTS in hyperglycemic mice only.	Glutamic Acid	75-84	fibroblast growth factor 15	Mus musculus	32-37
34858337-8	2021	Finally, glutamate photoactivation experiments confirmed that FGF19 increases the activity of glutamatergic AP neurons that project to the NTS in hyperglycemic mice.	Glutamic Acid	9-18	fibroblast growth factor 15	Mus musculus	62-67
34164827-1	2021	BACKGROUND & AIM: Cholestasis is characterized by increased total bile acid (TBA) levels, which are regulated by farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15).	Bile Acids and Salts	66-75	fibroblast growth factor 15	Mus musculus	140-167
34164827-1	2021	BACKGROUND & AIM: Cholestasis is characterized by increased total bile acid (TBA) levels, which are regulated by farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15).	Bile Acids and Salts	66-75	fibroblast growth factor 15	Mus musculus	169-174
34164827-1	2021	BACKGROUND & AIM: Cholestasis is characterized by increased total bile acid (TBA) levels, which are regulated by farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15).	tba	77-80	fibroblast growth factor 15	Mus musculus	140-167
34164827-1	2021	BACKGROUND & AIM: Cholestasis is characterized by increased total bile acid (TBA) levels, which are regulated by farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15).	tba	77-80	fibroblast growth factor 15	Mus musculus	169-174
34164827-15	2021	CONCLUSION: Our studies demonstrate the novel findings that MC-FXR plays a key role in liver damage and DR, including TBA regulation through alteration of intestinal and biliary FXR/FGF15 signaling.	tba	118-121	fibroblast growth factor 15	Mus musculus	182-187
34492674-0	2021	Enterobacter aerogenes ZDY01 inhibits choline-induced atherosclerosis through CDCA-FXR-FGF15 axis.	Chenodeoxycholic Acid	78-82	fibroblast growth factor 15	Mus musculus	87-92
34492674-4	2021	Here, we demonstrated that E. aerogenes ZDY01 inhibited choline-induced atherosclerosis in ApoE-/- mice fed with 1.3% choline by reducing cecal TMA and modulating CDCA-FXR/FGF15 axis.	Choline	56-63	fibroblast growth factor 15	Mus musculus	172-177
34492674-4	2021	Here, we demonstrated that E. aerogenes ZDY01 inhibited choline-induced atherosclerosis in ApoE-/- mice fed with 1.3% choline by reducing cecal TMA and modulating CDCA-FXR/FGF15 axis.	Choline	118-125	fibroblast growth factor 15	Mus musculus	172-177
34596761-9	2021	Taurine intake reduced the ileal expression of FXR target genes fibroblast growth factor 15 (Fgf15) and small heterodimer partner (Shp).	Taurine	0-7	fibroblast growth factor 15	Mus musculus	64-91
34639207-5	2021	In the present study, we found that 28-week FLA treatment notably alleviated NASH development in NAFL model mice fed with an HFD, and the beneficial effects may be attributed to the regulation of and improvement in the gut flora- and microbiota-related BAs, which then activate the intestinal FXR-FGF15 and TGR5-NF-kappaB pathways.	fla	44-47	fibroblast growth factor 15	Mus musculus	297-302
34596761-9	2021	Taurine intake reduced the ileal expression of FXR target genes fibroblast growth factor 15 (Fgf15) and small heterodimer partner (Shp).	Taurine	0-7	fibroblast growth factor 15	Mus musculus	93-98
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Fatty Acids, Nonesterified	138-154	fibroblast growth factor 15	Mus musculus	59-64
34333737-6	2021	RESULTS: HCC PDX models expressing high levels of FGF19/FGFR4 or FGFR2/3 showed favorable initial treatment response to FGF401 and infigratinib, respectively.	infigratinib	131-143	fibroblast growth factor 15	Mus musculus	50-55
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Barium	0-2	fibroblast growth factor 15	Mus musculus	217-244
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Barium	0-2	fibroblast growth factor 15	Mus musculus	246-251
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Barium	0-2	fibroblast growth factor 15	Mus musculus	286-291
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Berberine	27-36	fibroblast growth factor 15	Mus musculus	217-244
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Berberine	27-36	fibroblast growth factor 15	Mus musculus	246-251
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Berberine	27-36	fibroblast growth factor 15	Mus musculus	286-291
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Berberine	175-184	fibroblast growth factor 15	Mus musculus	217-244
34603061-8	2021	BA species that respond to berberine treatment are known FXR agonists, thus we performed quantitative Real Time-PCR and western blot to examine the FXR pathway, and find that berberine up-regulates intestinal FXR and fibroblast growth factor 15 (FGF15) expression, and the secretion of FGF15 further inhibits lipogenesis and nuclear factor-kappaB activation in the liver.	Berberine	175-184	fibroblast growth factor 15	Mus musculus	246-251
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Glucose	101-108	fibroblast growth factor 15	Mus musculus	24-29
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Glucose	101-108	fibroblast growth factor 15	Mus musculus	59-64
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Triglycerides	119-132	fibroblast growth factor 15	Mus musculus	24-29
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Triglycerides	119-132	fibroblast growth factor 15	Mus musculus	59-64
34329971-6	2021	RESULTS: Overexpressing FGF15 or exogenously administering FGF19 reduced the levels of fasting blood glucose, HOMA-IR, triglycerides, and free fatty acids in pregnant high-fat diet mice compared to control mice (P < 0.05).	Fatty Acids, Nonesterified	138-154	fibroblast growth factor 15	Mus musculus	24-29
34329971-9	2021	Consistent with the results of the animal experiments, FGF19 increased the expression of p-IRS1 and GLUT4 in trophoblast cells cultured in high-glucose medium (P < 0.05).	Glucose	144-151	fibroblast growth factor 15	Mus musculus	55-60
34329971-10	2021	DISCUSSION: Overexpressing FGF15 or administering FGF19 to pregnant high-fat diet mice can improve glycolipid metabolism and alleviate systemic and local insulin resistance.	Glycolipids	99-109	fibroblast growth factor 15	Mus musculus	27-32
34329971-10	2021	DISCUSSION: Overexpressing FGF15 or administering FGF19 to pregnant high-fat diet mice can improve glycolipid metabolism and alleviate systemic and local insulin resistance.	Glycolipids	99-109	fibroblast growth factor 15	Mus musculus	50-55
34085773-6	2021	The supplementation with A. muciniphila is sufficient to protect mice against high sucrose-induced impairment of glucose intolerance by decreasing betaCDCA and increasing insulin secretion and FGF15/19.	Sucrose	83-90	fibroblast growth factor 15	Mus musculus	193-201
34225483-6	2021	Treatment with IBATi ameliorated the decreased hepatic cholesterol 7-a-monooxygenase (Cyp7a1) and increased ileal fibroblast growth factor 15 (Fgf15) mRNA expression in HFD mice.	ibati	15-20	fibroblast growth factor 15	Mus musculus	114-141
34225483-6	2021	Treatment with IBATi ameliorated the decreased hepatic cholesterol 7-a-monooxygenase (Cyp7a1) and increased ileal fibroblast growth factor 15 (Fgf15) mRNA expression in HFD mice.	ibati	15-20	fibroblast growth factor 15	Mus musculus	143-148
34362888-8	2021	These data point to an important role after VSG for intestinal FGF15 to protect the organism from deleterious effects of VSG potentially by limiting the increase in circulating bile acids.	Bile Acids and Salts	177-187	fibroblast growth factor 15	Mus musculus	63-68
34085773-7	2021	Furthermore, betaCDCA inhibits insulin secretion and FGF15/19 expression.	betacdca	13-21	fibroblast growth factor 15	Mus musculus	53-61
35133032-0	2022	TCF7L2 transcriptionally regulates Fgf15 to maintain bile acid and lipid homeostasis through gut-liver crosstalk.	Bile Acids and Salts	53-62	fibroblast growth factor 15	Mus musculus	35-40
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Taurine	141-148	fibroblast growth factor 15	Mus musculus	66-93
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Taurine	141-148	fibroblast growth factor 15	Mus musculus	95-100
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Bile Acids and Salts	291-293	fibroblast growth factor 15	Mus musculus	66-93
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Bile Acids and Salts	291-293	fibroblast growth factor 15	Mus musculus	95-100
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Cholesterol	339-350	fibroblast growth factor 15	Mus musculus	66-93
35500802-12	2022	The protein and mRNA expression of farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) were decreased in intestine, increased taurine-conjugated BAs inhibited the intestinal signaling pathway, which was associated with increased genes expression of enzymes in the alternative BA synthesis pathway that reduced the levels of cholesterol.	Cholesterol	339-350	fibroblast growth factor 15	Mus musculus	95-100
35367668-5	2022	We describe a novel effect of FGF19, namely the stimulation of water intake.	Water	63-68	fibroblast growth factor 15	Mus musculus	30-35
35462858-8	2022	Increased expression levels of ileal Fgf15, and decreased Asbt expression in Ostbeta -/- mice indicate the accumulation of bile acids in the enterocyte.	Bile Acids and Salts	123-133	fibroblast growth factor 15	Mus musculus	37-42
34076007-5	2021	These results suggested that VLE regulates both the NPY-mediated pathway and the bile acid-FGF15 pathway to control energy metabolism and body weight gain.	Bile Acids and Salts	81-90	fibroblast growth factor 15	Mus musculus	91-96
34276384-12	2021	APS relieved the LD-induced activation of the intestinal farnesoid X receptor and decreased ileal expression of fibroblast growth factor 15.	aps	0-3	fibroblast growth factor 15	Mus musculus	112-139
35133032-1	2022	FGF19/FGF15 is an endocrine regulator of hepatic bile salt and lipid metabolism, which has shown promising effects in the treatment of NASH in clinical trials.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	0-5
35133032-1	2022	FGF19/FGF15 is an endocrine regulator of hepatic bile salt and lipid metabolism, which has shown promising effects in the treatment of NASH in clinical trials.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	6-11
35133032-12	2022	These studies identify the critical role of TCF4 as an upstream regulator of the FGF15-mediated gut-liver crosstalk that maintains bile and liver triglyceride homeostasis.	Triglycerides	146-158	fibroblast growth factor 15	Mus musculus	81-86
33885179-5	2021	Alcohol feeding is associated with intestinal bile acid accumulation but paradoxically impaired ileal farnesoid x receptor (FXR) function, and repressed hepatic cholesterol 7alpha-hydrolase (CYP7A1) expression despite decreased hepatic small heterodimer partner (SHP) and ileal fibroblast growth factor 15 (FGF15) expression.	Alcohols	0-7	fibroblast growth factor 15	Mus musculus	278-305
35257010-0	2022	Chlorogenic Acid Inhibits Lipid Deposition by Regulating the Enterohepatic FXR-FGF15 Pathway.	Chlorogenic Acid	0-16	fibroblast growth factor 15	Mus musculus	79-84
35257010-8	2022	Conclusions: CGA increases the metabolic elimination of cholesterol by inhibiting the enterohepatic FXR/FGF15 pathway.	Cholesterol	56-67	fibroblast growth factor 15	Mus musculus	104-109
33895309-10	2021	Contrary, in mice with impaired enterohepatic circulation of BAs (Asbt-/-, Ostalpha-/-), administration of UDCA was still able to induce ileal Fgf15 and repress hepatic BA-synthesis, arguing that UDCA is only effective in the presence of endogenous FXR ligands.	Ursodeoxycholic Acid	107-111	fibroblast growth factor 15	Mus musculus	143-148
33890787-4	2021	Oral naringin mainly existed in the intestine due to the high water solubility of 7-O-nohesperidoside and alleviated atherosclerosis mainly by enhancing bile acid synthesis in the gut microbiota-FXR/FGF15-CYP7A1 pathway.	naringin	5-13	fibroblast growth factor 15	Mus musculus	199-204
35105957-8	2022	Reabsorbed BA affected liver BA synthetic enzymes by regulating Fgf15 expression.	Bile Acids and Salts	11-13	fibroblast growth factor 15	Mus musculus	64-69
35105957-8	2022	Reabsorbed BA affected liver BA synthetic enzymes by regulating Fgf15 expression.	Bile Acids and Salts	29-31	fibroblast growth factor 15	Mus musculus	64-69
33965587-7	2021	Mechanistically, the synergistic actions of GSK672 and FGF15 on inhibiting gut bile acid re-uptake and hepatic bile acid synthesis achieve greater magnitude of bile acid pool reduction that not only decreases bile acid burden in NASH livers but also limits intestinal lipid absorption, which, together with FGF15 signaling activation, produces weight loss, reduction of adipose inflammation, and attenuated hepatocellular organelle stress.	Bile Acids and Salts	79-88	fibroblast growth factor 15	Mus musculus	55-60
33965587-7	2021	Mechanistically, the synergistic actions of GSK672 and FGF15 on inhibiting gut bile acid re-uptake and hepatic bile acid synthesis achieve greater magnitude of bile acid pool reduction that not only decreases bile acid burden in NASH livers but also limits intestinal lipid absorption, which, together with FGF15 signaling activation, produces weight loss, reduction of adipose inflammation, and attenuated hepatocellular organelle stress.	Bile Acids and Salts	111-120	fibroblast growth factor 15	Mus musculus	55-60
33965587-7	2021	Mechanistically, the synergistic actions of GSK672 and FGF15 on inhibiting gut bile acid re-uptake and hepatic bile acid synthesis achieve greater magnitude of bile acid pool reduction that not only decreases bile acid burden in NASH livers but also limits intestinal lipid absorption, which, together with FGF15 signaling activation, produces weight loss, reduction of adipose inflammation, and attenuated hepatocellular organelle stress.	Bile Acids and Salts	111-120	fibroblast growth factor 15	Mus musculus	55-60
33965587-7	2021	Mechanistically, the synergistic actions of GSK672 and FGF15 on inhibiting gut bile acid re-uptake and hepatic bile acid synthesis achieve greater magnitude of bile acid pool reduction that not only decreases bile acid burden in NASH livers but also limits intestinal lipid absorption, which, together with FGF15 signaling activation, produces weight loss, reduction of adipose inflammation, and attenuated hepatocellular organelle stress.	Bile Acids and Salts	111-120	fibroblast growth factor 15	Mus musculus	55-60
33965587-8	2021	Furthermore, the combined treatment attenuates increased fecal bile acid excretion and repressed bile acid synthesis, which underlie diarrhea and hypercholesterolemia associated with ASBT inhibition and FGF19 analogue, respectively, in clinical settings.	Bile Acids and Salts	97-106	fibroblast growth factor 15	Mus musculus	203-208
33885179-5	2021	Alcohol feeding is associated with intestinal bile acid accumulation but paradoxically impaired ileal farnesoid x receptor (FXR) function, and repressed hepatic cholesterol 7alpha-hydrolase (CYP7A1) expression despite decreased hepatic small heterodimer partner (SHP) and ileal fibroblast growth factor 15 (FGF15) expression.	Alcohols	0-7	fibroblast growth factor 15	Mus musculus	307-312
33691750-7	2021	Mechanistically, high-dose melatonin facilitates the upregulation of FGF19 expression through activating endoplasmic stress (ER)-associated protein kinase RNA-like endoplasmic reticulum kinase (PERK)-Eukaryotic initiation factor 2 alpha (eIF2alpha)-activating transcription factor 4 (ATF4) pathway, which in turn promotes FGFR4-Vimentin invasive signaling and attenuates the role of melatonin in repressing metastasis.	Melatonin	383-392	fibroblast growth factor 15	Mus musculus	69-74
33534906-2	2021	However, no studies have examined how FGF19 affects hindbrain neurons that participate directly in autonomic control of systemic glucose regulation.	Glucose	129-136	fibroblast growth factor 15	Mus musculus	38-43
33534906-4	2021	This study tested the hypothesis that FGF19 acts in the hindbrain to alter DMV neuron excitability and lower blood glucose concentration.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	75-78	fibroblast growth factor 15	Mus musculus	38-43
33534906-5	2021	Fourth ventricle administration of FGF19 produced no effect on blood glucose concentration in control mice, but induced a significant, peripheral muscarinic receptor-dependent decrease in systemic hyperglycemia for up to 12 hours in streptozotocin (STZ)-treated mice, a model of type 1 diabetes.	Streptozocin	233-247	fibroblast growth factor 15	Mus musculus	35-40
33534906-5	2021	Fourth ventricle administration of FGF19 produced no effect on blood glucose concentration in control mice, but induced a significant, peripheral muscarinic receptor-dependent decrease in systemic hyperglycemia for up to 12 hours in streptozotocin (STZ)-treated mice, a model of type 1 diabetes.	Streptozocin	249-252	fibroblast growth factor 15	Mus musculus	35-40
33691750-0	2021	FGF19/FGFR4 signaling axis confines and switches the role of melatonin in head and neck cancer metastasis.	Melatonin	61-70	fibroblast growth factor 15	Mus musculus	0-5
33691750-5	2021	The therapeutic efficacy of FGF19/FGFR4 inhibition in melatonin-mediated tumor growth and metastasis was evaluated in orthotopic tongue tumor mice.	Melatonin	54-63	fibroblast growth factor 15	Mus musculus	28-33
33994911-9	2021	Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol-feeding and reduced CYP7A1 (cholesterol 7alpha-hydroxylase) expression and total bile acid levels in the liver tissue.	fucoidan	0-8	fibroblast growth factor 15	Mus musculus	86-113
33994911-9	2021	Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol-feeding and reduced CYP7A1 (cholesterol 7alpha-hydroxylase) expression and total bile acid levels in the liver tissue.	fucoidan	0-8	fibroblast growth factor 15	Mus musculus	115-120
33994911-9	2021	Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol-feeding and reduced CYP7A1 (cholesterol 7alpha-hydroxylase) expression and total bile acid levels in the liver tissue.	Alcohols	140-147	fibroblast growth factor 15	Mus musculus	86-113
33994911-9	2021	Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol-feeding and reduced CYP7A1 (cholesterol 7alpha-hydroxylase) expression and total bile acid levels in the liver tissue.	Alcohols	140-147	fibroblast growth factor 15	Mus musculus	115-120
33751819-6	2021	Increases in muscle atrophy markers (FOXO-3, Atrogin-1, MuRF-1) were abrogated by FGF19 in palmitic acid (PA)-treated C2C12 myotubes and in the skeletal muscle of HFD-fed mice.	Palmitic Acid	91-104	fibroblast growth factor 15	Mus musculus	82-87
33751819-6	2021	Increases in muscle atrophy markers (FOXO-3, Atrogin-1, MuRF-1) were abrogated by FGF19 in palmitic acid (PA)-treated C2C12 myotubes and in the skeletal muscle of HFD-fed mice.	Palmitic Acid	106-108	fibroblast growth factor 15	Mus musculus	82-87
33751819-8	2021	FGF19 treatment restored PA- and HFD-induced hyperglycaemia, impaired glucose tolerance and insulin resistance (IRS-1, GLUT-4) and mitigated the PA- and HFD-induced decrease in FNDC-5/irisin expression.	Palmitic Acid	25-27	fibroblast growth factor 15	Mus musculus	0-5
33751819-8	2021	FGF19 treatment restored PA- and HFD-induced hyperglycaemia, impaired glucose tolerance and insulin resistance (IRS-1, GLUT-4) and mitigated the PA- and HFD-induced decrease in FNDC-5/irisin expression.	Palmitic Acid	145-147	fibroblast growth factor 15	Mus musculus	0-5
33691750-7	2021	Mechanistically, high-dose melatonin facilitates the upregulation of FGF19 expression through activating endoplasmic stress (ER)-associated protein kinase RNA-like endoplasmic reticulum kinase (PERK)-Eukaryotic initiation factor 2 alpha (eIF2alpha)-activating transcription factor 4 (ATF4) pathway, which in turn promotes FGFR4-Vimentin invasive signaling and attenuates the role of melatonin in repressing metastasis.	Melatonin	27-36	fibroblast growth factor 15	Mus musculus	69-74
33691750-8	2021	Intriguingly, following long-term exposure to high-dose melatonin, epithelial HNSCC cells revert the process towards mesenchymal transition and turn more aggressive, which is enabled by FGF19/FGFR4 upregulation and alleviated by genetic depletion of the FGF19 and FGFR4 genes or the treatment of FGFR4 inhibitor H3B-6527.	Melatonin	56-65	fibroblast growth factor 15	Mus musculus	186-191
33691750-8	2021	Intriguingly, following long-term exposure to high-dose melatonin, epithelial HNSCC cells revert the process towards mesenchymal transition and turn more aggressive, which is enabled by FGF19/FGFR4 upregulation and alleviated by genetic depletion of the FGF19 and FGFR4 genes or the treatment of FGFR4 inhibitor H3B-6527.	Melatonin	56-65	fibroblast growth factor 15	Mus musculus	254-259
33691750-9	2021	CONCLUSIONS: Our study gains novel mechanistic insights into melatonin-mediated modulation of FGF19/FGFR4 signaling in HNSCC, demonstrating that activating this molecular node confines the role of melatonin in suppressing metastasis and even triggers the switch of its function from anti-metastasis to metastasis promotion.	Melatonin	61-70	fibroblast growth factor 15	Mus musculus	94-99
33691750-9	2021	CONCLUSIONS: Our study gains novel mechanistic insights into melatonin-mediated modulation of FGF19/FGFR4 signaling in HNSCC, demonstrating that activating this molecular node confines the role of melatonin in suppressing metastasis and even triggers the switch of its function from anti-metastasis to metastasis promotion.	Melatonin	197-206	fibroblast growth factor 15	Mus musculus	94-99
33691750-10	2021	The blockade of FGF19/FGFR4 signaling would have great potential in improving the efficacy of melatonin supplements in cancer treatment.	Melatonin	94-103	fibroblast growth factor 15	Mus musculus	16-21
33484478-2	2021	Monomeric FGF19 and dimeric Fgf15 are both necessary for liver regeneration and proper bile acid (BA) metabolism.	Bile Acids and Salts	87-96	fibroblast growth factor 15	Mus musculus	10-15
33631374-9	2021	This was also associated with increased intestinal FXR/Fgf15 signaling, which inhibits hepatic synthesis of bile acids.	Bile Acids and Salts	108-118	fibroblast growth factor 15	Mus musculus	55-60
32198567-10	2021	DCA-induced dysbiosis decreased the deconjugation of bile acids, and this regulation was associated with the repressed expression of target genes in the enterohepatic farnesoid X receptor-fibroblast growth factor (FXR-FGF15) axis, leading to upregulation of hepatic de novo bile acid synthesis.	Deoxycholic Acid	0-3	fibroblast growth factor 15	Mus musculus	218-223
32198567-10	2021	DCA-induced dysbiosis decreased the deconjugation of bile acids, and this regulation was associated with the repressed expression of target genes in the enterohepatic farnesoid X receptor-fibroblast growth factor (FXR-FGF15) axis, leading to upregulation of hepatic de novo bile acid synthesis.	Bile Acids and Salts	53-63	fibroblast growth factor 15	Mus musculus	218-223
32198567-10	2021	DCA-induced dysbiosis decreased the deconjugation of bile acids, and this regulation was associated with the repressed expression of target genes in the enterohepatic farnesoid X receptor-fibroblast growth factor (FXR-FGF15) axis, leading to upregulation of hepatic de novo bile acid synthesis.	Bile Acids and Salts	53-62	fibroblast growth factor 15	Mus musculus	218-223
32198567-11	2021	CONCLUSIONS: These results suggest that DCA-induced gut dysbiosis may act as a key etiologic factor in intestinal inflammation, associated with bile acid metabolic disturbance and downregulation of the FXR-FGF15 axis.	Deoxycholic Acid	40-43	fibroblast growth factor 15	Mus musculus	206-211
33484478-2	2021	Monomeric FGF19 and dimeric Fgf15 are both necessary for liver regeneration and proper bile acid (BA) metabolism.	Bile Acids and Salts	87-96	fibroblast growth factor 15	Mus musculus	28-33
33484478-2	2021	Monomeric FGF19 and dimeric Fgf15 are both necessary for liver regeneration and proper bile acid (BA) metabolism.	Bile Acids and Salts	98-100	fibroblast growth factor 15	Mus musculus	10-15
33484478-2	2021	Monomeric FGF19 and dimeric Fgf15 are both necessary for liver regeneration and proper bile acid (BA) metabolism.	Bile Acids and Salts	98-100	fibroblast growth factor 15	Mus musculus	28-33
33484478-3	2021	FGF19 elicits stronger effects than Fgf15 on glucose and fatty acid metabolism and only FGF19 induces hepatocellular carcinoma (HCC).	Glucose	45-52	fibroblast growth factor 15	Mus musculus	0-5
33484478-3	2021	FGF19 elicits stronger effects than Fgf15 on glucose and fatty acid metabolism and only FGF19 induces hepatocellular carcinoma (HCC).	Fatty Acids	57-67	fibroblast growth factor 15	Mus musculus	0-5
33107729-8	2020	Naringin modulated the abundances of bile salt hydrolase- and 7alpha-dehydroxylase-producing bacteria, promoting bile acid synthesis from cholesterol by upregulating CYP7A1 via suppression of the FXR/FGF15 pathway.	Bile Acids and Salts	37-46	fibroblast growth factor 15	Mus musculus	200-205
33417675-9	2021	Administration of fexaramine mitigated DCA-induced intestinal injury, restored intestinal FXR activity, activated fibroblast growth factor 15, and normalized bile acid metabolism.	fexaramine	18-28	fibroblast growth factor 15	Mus musculus	114-141
33127558-10	2021	The composition of GM is significantly changed with an increase in BA-metabolizing bacteria, leading to an increased expression of ileal FGF15 driven by FXR that has a higher affinity to unconjugated BAs.	Bile Acids and Salts	67-69	fibroblast growth factor 15	Mus musculus	137-142
33127558-11	2021	Notably, ABX or cholestyramine treatment decreased FGF15 expression and exacerbated liver injury.	CHEMBL369125	9-12	fibroblast growth factor 15	Mus musculus	51-56
33127558-11	2021	Notably, ABX or cholestyramine treatment decreased FGF15 expression and exacerbated liver injury.	Cholestyramine Resin	16-30	fibroblast growth factor 15	Mus musculus	51-56
33154041-9	2021	Circulating FGF15 activates hepatic FXR and together with hepatic Shp blocks Cyp7a1 and Cyp7b1 gene expression, key enzymes in bile acid metabolism.	Bile Acids and Salts	127-136	fibroblast growth factor 15	Mus musculus	12-17
33107729-8	2020	Naringin modulated the abundances of bile salt hydrolase- and 7alpha-dehydroxylase-producing bacteria, promoting bile acid synthesis from cholesterol by upregulating CYP7A1 via suppression of the FXR/FGF15 pathway.	naringin	0-8	fibroblast growth factor 15	Mus musculus	200-205
33144503-1	2020	As a physiological regulator of bile acid homeostasis, FGF19 is also a potent insulin sensitizer capable of normalizing plasma glucose concentration, improving lipid profile, ameliorating fatty liver disease, and causing weight loss in both diabetic and diet-induced obesity mice.	Bile Acids and Salts	32-41	fibroblast growth factor 15	Mus musculus	55-60
33144503-1	2020	As a physiological regulator of bile acid homeostasis, FGF19 is also a potent insulin sensitizer capable of normalizing plasma glucose concentration, improving lipid profile, ameliorating fatty liver disease, and causing weight loss in both diabetic and diet-induced obesity mice.	Glucose	127-134	fibroblast growth factor 15	Mus musculus	55-60
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Glucose	79-86	fibroblast growth factor 15	Mus musculus	32-37
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Glucose	79-86	fibroblast growth factor 15	Mus musculus	138-143
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Glucose	79-86	fibroblast growth factor 15	Mus musculus	145-152
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Glucose	79-86	fibroblast growth factor 15	Mus musculus	138-143
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Bile Acids and Salts	100-109	fibroblast growth factor 15	Mus musculus	32-37
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Bile Acids and Salts	100-109	fibroblast growth factor 15	Mus musculus	138-143
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Bile Acids and Salts	100-109	fibroblast growth factor 15	Mus musculus	145-152
33144503-4	2020	Here, we show that nonmitogenic FGF19 variants that retain the full beneficial glucose-lowering and bile acid regulatory activities of WT FGF19 (FGF19WT) can be engineered by diminishing FGF19"s ability to induce dimerization of its cognate FGF receptors (FGFR).	Bile Acids and Salts	100-109	fibroblast growth factor 15	Mus musculus	138-143
32259714-2	2020	The gut-liver axis is the main site for the regulation of BA synthesis and BA pool size via the combined action of the nuclear Farnesoid X Receptor (FXR) and the enterokine Fibroblast Growth Factor 19 (FGF19).	Bile Acids and Salts	58-60	fibroblast growth factor 15	Mus musculus	173-200
32404932-3	2020	Intestinal FXR is critical in suppressing hepatic bile acid (BA) synthesis by inducing fibroblast growth factor 15 (FGF15) in mice and FGF19 in humans.	Bile Acids and Salts	61-63	fibroblast growth factor 15	Mus musculus	87-114
32404932-3	2020	Intestinal FXR is critical in suppressing hepatic bile acid (BA) synthesis by inducing fibroblast growth factor 15 (FGF15) in mice and FGF19 in humans.	Bile Acids and Salts	61-63	fibroblast growth factor 15	Mus musculus	116-121
32404932-3	2020	Intestinal FXR is critical in suppressing hepatic bile acid (BA) synthesis by inducing fibroblast growth factor 15 (FGF15) in mice and FGF19 in humans.	Bile Acids and Salts	61-63	fibroblast growth factor 15	Mus musculus	135-140
32639145-0	2020	Teneligliptin promotes bile acid synthesis and attenuates Lipid Accumulation in Obese Mice by targeting the KLF15-Fgf15 pathway.	3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine	0-13	fibroblast growth factor 15	Mus musculus	114-119
32639145-7	2020	Importantly, teneligliptin suppressed the expression of the BA synthesis inhibitory factor Fgf15, which was mediated through phosphatidylinositol 3-kinase (PI3K)/AKT/Kruppel-like factor 15 (KLF15) signaling.	3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine	13-26	fibroblast growth factor 15	Mus musculus	91-96
32639145-7	2020	Importantly, teneligliptin suppressed the expression of the BA synthesis inhibitory factor Fgf15, which was mediated through phosphatidylinositol 3-kinase (PI3K)/AKT/Kruppel-like factor 15 (KLF15) signaling.	Bile Acids and Salts	60-62	fibroblast growth factor 15	Mus musculus	91-96
32681035-5	2020	Furthermore, we find that cholesterol-induced lysosomal stress feed-forward activates TFEB via promoting TFEB nuclear translocation, while bile acid-induced fibroblast growth factor 19 (FGF19), acting via mTOR/ERK signaling and TFEB phosphorylation, feedback inhibits TFEB nuclear translocation in hepatocytes.	Cholesterol	26-37	fibroblast growth factor 15	Mus musculus	186-191
32681035-5	2020	Furthermore, we find that cholesterol-induced lysosomal stress feed-forward activates TFEB via promoting TFEB nuclear translocation, while bile acid-induced fibroblast growth factor 19 (FGF19), acting via mTOR/ERK signaling and TFEB phosphorylation, feedback inhibits TFEB nuclear translocation in hepatocytes.	Bile Acids and Salts	139-148	fibroblast growth factor 15	Mus musculus	157-184
32681035-5	2020	Furthermore, we find that cholesterol-induced lysosomal stress feed-forward activates TFEB via promoting TFEB nuclear translocation, while bile acid-induced fibroblast growth factor 19 (FGF19), acting via mTOR/ERK signaling and TFEB phosphorylation, feedback inhibits TFEB nuclear translocation in hepatocytes.	Bile Acids and Salts	139-148	fibroblast growth factor 15	Mus musculus	186-191
32681035-6	2020	Consistently, blocking intestinal bile acid uptake by an apical sodium-bile acid transporter (ASBT) inhibitor decreases ileal FGF15, enhances hepatic TFEB nuclear localization and improves cholesterol homeostasis in Western diet-fed mice.	Bile Acids and Salts	34-43	fibroblast growth factor 15	Mus musculus	126-131
32967428-3	2020	Fibroblast growth factor 19 (FGF19) in human and its murine orthologue Fgf15 plays a pivotal role in this bile acid driven enterohepatic signaling.	Bile Acids and Salts	106-115	fibroblast growth factor 15	Mus musculus	71-76
32967428-10	2020	Post VSG both WT and KO mice had similarly altered bile acid enterohepatic flux, however Fgf15 deficient mice post VSG had increased hepatic accumulation of free and esterified cholesterol leading to lipotoxicity related ER stress, inflammasome activation, and increased Fgf21 expression.	Cholesterol	177-188	fibroblast growth factor 15	Mus musculus	89-94
32967428-11	2020	Intact Fgf15 mediated enterohepatic bile acid signaling, but not changes in bile acid flux, appear to be important for the metabolic improvements post-murine bariatric surgery.	Bile Acids and Salts	36-45	fibroblast growth factor 15	Mus musculus	7-12
32681035-0	2020	An FGF15/19-TFEB regulatory loop controls hepatic cholesterol and bile acid homeostasis.	Cholesterol	50-61	fibroblast growth factor 15	Mus musculus	3-11
32681035-0	2020	An FGF15/19-TFEB regulatory loop controls hepatic cholesterol and bile acid homeostasis.	Bile Acids and Salts	66-75	fibroblast growth factor 15	Mus musculus	3-11
32305136-5	2020	Therefore, we investigated the effect of FGF19 on palmitic acid (PA)-induced mitochondrial dysfunction and oxidative stress in C2C12 cells.	Palmitic Acid	50-63	fibroblast growth factor 15	Mus musculus	41-46
32305136-6	2020	In this study, we found that FGF19 can increase the mRNA and protein expression levels of mitochondrial biogenesis regulators (PGC-1alpha, Nrf-1, and TFAM) and antioxidant response regulators (Nrf-2 and HO-1), alleviating PA-induced mitochondrial dysfunction and oxidative stress.	Palmitic Acid	222-224	fibroblast growth factor 15	Mus musculus	29-34
32305136-8	2020	Taken together, these findings indicate that FGF19 might promote mitochondrial biogenesis and antioxidant response via the AMPK/PGC-1alpha pathway, attenuating the effect of PA on mitochondrial dysfunction and oxidative stress; therefore, FGF19 might be a potential therapeutic target for the effects of obesity on skeletal muscle.	Palmitic Acid	174-176	fibroblast growth factor 15	Mus musculus	45-50
32344084-0	2020	FGF19 alleviates palmitate-induced atrophy in C2C12 cells by inhibiting mitochondrial overload and insulin resistance.	Palmitates	17-26	fibroblast growth factor 15	Mus musculus	0-5
32344084-4	2020	In this study, the protective effects of FGF19 on palmitate-induced damages in differentiated mouse myoblast cells (C2C12) were studied, including myotube morphology, mitochondrial function and the regulation of pathways and genes.	Palmitates	50-59	fibroblast growth factor 15	Mus musculus	41-46
32344084-7	2020	FGF19 addition during the differentiation of C2C12 cells, returned the palmitate-induced mitochondrial respiration and apoptosis to the control levels and improved the insulin sensitivity.	Palmitates	71-80	fibroblast growth factor 15	Mus musculus	0-5
32344084-8	2020	The palmitate-induced upregulation of genes involved in beta-oxidation (PPARbeta/delta, PPARgamma, UCP-1, MCAD) and the downregulation of genes related to myotube atrophy (PPARalpha, PGC-1alpha and PGC-1beta) were also alleviated by FGF19.	Palmitates	4-13	fibroblast growth factor 15	Mus musculus	233-238
32344084-9	2020	In summary, FGF19 prevented excessive palmitate-induced dysfunction of C2C12 cells by protecting mitochondrial overload and apoptosis and maintaining normal insulin signaling.	Palmitates	38-47	fibroblast growth factor 15	Mus musculus	12-17
32259714-2	2020	The gut-liver axis is the main site for the regulation of BA synthesis and BA pool size via the combined action of the nuclear Farnesoid X Receptor (FXR) and the enterokine Fibroblast Growth Factor 19 (FGF19).	Bile Acids and Salts	58-60	fibroblast growth factor 15	Mus musculus	202-207
32259714-2	2020	The gut-liver axis is the main site for the regulation of BA synthesis and BA pool size via the combined action of the nuclear Farnesoid X Receptor (FXR) and the enterokine Fibroblast Growth Factor 19 (FGF19).	Bile Acids and Salts	75-77	fibroblast growth factor 15	Mus musculus	202-207
32259714-7	2020	FINDINGS: FGF19-M52 reduced BA synthesis and pool size, modulated its composition and protected mice from intestinal inflammation.	Bile Acids and Salts	28-30	fibroblast growth factor 15	Mus musculus	10-15
32259714-11	2020	INTERPRETATION: Reactivation of the FXR-FGF19 axis in a murine model of intestinal inflammation could bona fide provide positive changes in BA metabolism with consequent reduction of intestinal inflammation and modulation of microbiota.	Bile Acids and Salts	140-142	fibroblast growth factor 15	Mus musculus	40-45
32259714-12	2020	These results point to the therapeutic potential of FGF19 in the treatment of intestinal inflammation with concomitant derangement of BA homeostasis.	Bile Acids and Salts	134-136	fibroblast growth factor 15	Mus musculus	52-57
31920680-1	2019	Endocrine fibroblast growth factor (FGF) 19 has been shown to be capable of maintaining bile acid (BA) homeostasis and thus hold promise to be a potential therapeutic agent for cholestasis liver disease.	Bile Acids and Salts	99-101	fibroblast growth factor 15	Mus musculus	10-43
31645370-10	2020	It was suggested that the cytokine/c-Jun N-terminal kinase signaling pathway and the pregnane X receptor-mediated pathway are the predominant mechanisms, preferred over the FXR/small heterodimer partner and FXR/fibroblast growth factor 15 pathways, for controlling BA synthesis under hydrophobic BA composition.	Bile Acids and Salts	265-267	fibroblast growth factor 15	Mus musculus	211-238
32116693-9	2020	TPE-CA maintained the homeostasis of bile acids via modulation of the liver-gut axis related farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15) pathway and FXR-targeted protein.	Bile Acids and Salts	37-47	fibroblast growth factor 15	Mus musculus	120-147
32116693-9	2020	TPE-CA maintained the homeostasis of bile acids via modulation of the liver-gut axis related farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF15) pathway and FXR-targeted protein.	Bile Acids and Salts	37-47	fibroblast growth factor 15	Mus musculus	149-154
31206730-1	2020	Farnesoid X receptor (FXR) induces fibroblast growth factor 15 (FGF15; human ortholog FGF19) in the gut to potently inhibit bile acid (BA) synthesis in the liver.	Bile Acids and Salts	124-133	fibroblast growth factor 15	Mus musculus	64-69
31206730-1	2020	Farnesoid X receptor (FXR) induces fibroblast growth factor 15 (FGF15; human ortholog FGF19) in the gut to potently inhibit bile acid (BA) synthesis in the liver.	Bile Acids and Salts	135-137	fibroblast growth factor 15	Mus musculus	64-69
31206730-7	2020	CCl4 induced fibrosis with similar severity in all genotypes; however, cholestyramine increased fibrosis severity only in Fgf15-/- mice.	Cholestyramine Resin	71-85	fibroblast growth factor 15	Mus musculus	122-127
31767164-1	2019	OBJECTIVE: Fibroblast growth factor 19 (FGF19) is a postprandial hormone which plays diverse roles in the regulation of bile acid, glucose, and lipid metabolism.	Bile Acids and Salts	120-129	fibroblast growth factor 15	Mus musculus	11-38
31767164-1	2019	OBJECTIVE: Fibroblast growth factor 19 (FGF19) is a postprandial hormone which plays diverse roles in the regulation of bile acid, glucose, and lipid metabolism.	Bile Acids and Salts	120-129	fibroblast growth factor 15	Mus musculus	40-45
31767164-1	2019	OBJECTIVE: Fibroblast growth factor 19 (FGF19) is a postprandial hormone which plays diverse roles in the regulation of bile acid, glucose, and lipid metabolism.	Glucose	131-138	fibroblast growth factor 15	Mus musculus	11-38
31767164-1	2019	OBJECTIVE: Fibroblast growth factor 19 (FGF19) is a postprandial hormone which plays diverse roles in the regulation of bile acid, glucose, and lipid metabolism.	Glucose	131-138	fibroblast growth factor 15	Mus musculus	40-45
31767164-3	2019	The primary target organ of FGF19 is the liver, where it regulates bile acid homeostasis in response to nutrient absorption.	Bile Acids and Salts	67-76	fibroblast growth factor 15	Mus musculus	28-33
31539192-6	2019	CAP-induced suppression of enterohepatic FXR-fibroblast growth factor 15 (FGF15) signaling contributed to the increased BA pool size, followed by increases in the expression of cholesterol 7alpha-hydroxylase (CYP7A1) and hepatic BA synthesis.	Capsaicin	0-3	fibroblast growth factor 15	Mus musculus	41-72
31767164-10	2019	In mice treated with FGF19, there was a significant reduction in the mRNA expression of genes associated with hepatic bile acid synthesis enzymes, lowered levels of hepatic bile acid species, and a significant increase in fecal energy content, all indicative of reduced lipid absorption in animals treated with FGF19.	Bile Acids and Salts	118-127	fibroblast growth factor 15	Mus musculus	21-26
31767164-10	2019	In mice treated with FGF19, there was a significant reduction in the mRNA expression of genes associated with hepatic bile acid synthesis enzymes, lowered levels of hepatic bile acid species, and a significant increase in fecal energy content, all indicative of reduced lipid absorption in animals treated with FGF19.	Bile Acids and Salts	173-182	fibroblast growth factor 15	Mus musculus	21-26
31539192-6	2019	CAP-induced suppression of enterohepatic FXR-fibroblast growth factor 15 (FGF15) signaling contributed to the increased BA pool size, followed by increases in the expression of cholesterol 7alpha-hydroxylase (CYP7A1) and hepatic BA synthesis.	Capsaicin	0-3	fibroblast growth factor 15	Mus musculus	74-79
31539192-6	2019	CAP-induced suppression of enterohepatic FXR-fibroblast growth factor 15 (FGF15) signaling contributed to the increased BA pool size, followed by increases in the expression of cholesterol 7alpha-hydroxylase (CYP7A1) and hepatic BA synthesis.	Barium	120-122	fibroblast growth factor 15	Mus musculus	41-72
31767164-12	2019	Our data suggest that the primary way in which exogenous FGF19 lowers body weight in mice may be through the inhibition of bile acid synthesis and subsequently a reduction of dietary lipid absorption.	Bile Acids and Salts	123-132	fibroblast growth factor 15	Mus musculus	57-62
31539192-6	2019	CAP-induced suppression of enterohepatic FXR-fibroblast growth factor 15 (FGF15) signaling contributed to the increased BA pool size, followed by increases in the expression of cholesterol 7alpha-hydroxylase (CYP7A1) and hepatic BA synthesis.	Barium	120-122	fibroblast growth factor 15	Mus musculus	74-79
30996006-10	2019	Furthermore, FGF19 treatment increased occupancy of FXR at Abcg5/8 and Scarb1, expression of these genes, and cholesterol efflux from hepatocytes.	Cholesterol	110-121	fibroblast growth factor 15	Mus musculus	13-18
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	fibroblast growth factor 15	Mus musculus	116-121
31254596-12	2019	In accordance with its murine homolog FGF15, FGF19 might trigger relaxation and filling of the gallbladder which, in combination with increased cholesterol saturation and BA hydrophobicity, would enhance the risk of gallstone development.	Cholesterol	144-155	fibroblast growth factor 15	Mus musculus	45-50
31254596-12	2019	In accordance with its murine homolog FGF15, FGF19 might trigger relaxation and filling of the gallbladder which, in combination with increased cholesterol saturation and BA hydrophobicity, would enhance the risk of gallstone development.	Bile Acids and Salts	171-173	fibroblast growth factor 15	Mus musculus	45-50
31199929-0	2019	Downregulation of microRNA-302b-3p relieves oxygen-glucose deprivation/re-oxygenation induced injury in murine hippocampal neurons through up-regulating Nrf2 signaling by targeting fibroblast growth factor 15/19.	oxygen-glucose	44-58	fibroblast growth factor 15	Mus musculus	181-208
32694803-1	2019	Fibroblast growth factor (FGF) 15 in mice and its human orthologue FGF19 (together denoted FGF15/19) are gut hormones that control homeostasis of bile acids and glucose during the transition from the fed to the fasted state.	Bile Acids and Salts	146-156	fibroblast growth factor 15	Mus musculus	0-33
32694803-1	2019	Fibroblast growth factor (FGF) 15 in mice and its human orthologue FGF19 (together denoted FGF15/19) are gut hormones that control homeostasis of bile acids and glucose during the transition from the fed to the fasted state.	Glucose	161-168	fibroblast growth factor 15	Mus musculus	0-33
30996006-0	2019	Phosphorylation of hepatic farnesoid X receptor by FGF19 signaling-activated Src maintains cholesterol levels and protects from atherosclerosis.	Cholesterol	91-102	fibroblast growth factor 15	Mus musculus	51-56
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	4-13	fibroblast growth factor 15	Mus musculus	182-209
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	4-13	fibroblast growth factor 15	Mus musculus	211-216
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	4-13	fibroblast growth factor 15	Mus musculus	218-223
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	15-17	fibroblast growth factor 15	Mus musculus	182-209
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	15-17	fibroblast growth factor 15	Mus musculus	211-216
30996006-1	2019	The bile acid (BA) nuclear receptor, farnesoid X receptor (FXR/NR1H4), maintains metabolic homeostasis by transcriptional control of numerous genes, including an intestinal hormone, fibroblast growth factor-19 (FGF19; FGF15 in mice).	Bile Acids and Salts	15-17	fibroblast growth factor 15	Mus musculus	218-223
30996006-3	2019	Recently, phosphorylation at Tyr-67 by the FGF15/19 signaling-activated nonreceptor tyrosine kinase Src was shown to be important for FXR function in BA homeostasis.	Tyrosine	29-32	fibroblast growth factor 15	Mus musculus	43-51
30996006-3	2019	Recently, phosphorylation at Tyr-67 by the FGF15/19 signaling-activated nonreceptor tyrosine kinase Src was shown to be important for FXR function in BA homeostasis.	Bile Acids and Salts	150-152	fibroblast growth factor 15	Mus musculus	43-51
30996006-12	2019	We conclude that phosphorylation of hepatic FXR by FGF15/19-induced Src maintains cholesterol homeostasis and protects against atherosclerosis.	Cholesterol	82-93	fibroblast growth factor 15	Mus musculus	51-59
30653340-16	2019	In cystic fibrosis mice, treatment with the osmotic laxative polyethylene glycol is associated with decreased fecal bile acid loss and restoration of FXR-FGF15 signaling.	Polyethylene Glycols	61-80	fibroblast growth factor 15	Mus musculus	154-159
31117231-6	2019	Additionally, BAR502 increased the intestinal expression of Fgf15 and Glp1 and energy expenditure by white adipose tissues.	BAR502	14-20	fibroblast growth factor 15	Mus musculus	60-65
30803859-8	2019	The mRNA levels of hepatic Cyp7a1 and Shp, as well as intestinal Fgf15, were decreased in WT mice with ethanol feeding, which were further reduced in FXR-/- mice.	Ethanol	103-110	fibroblast growth factor 15	Mus musculus	65-70
30653340-0	2019	Defective FXR-FGF15 signaling and bile acid homeostasis in cystic fibrosis mice can be restored by the laxative polyethylene glycol.	Polyethylene Glycols	112-131	fibroblast growth factor 15	Mus musculus	14-19
30944079-3	2019	First, we conducted a histological analysis of FGF19-overexpressing Hep3B2.1-7 xenograft tumors collected from mice treated with lenvatinib.	lenvatinib	129-139	fibroblast growth factor 15	Mus musculus	47-52
30768114-6	2019	This regulation was associated with the alterations in the expression of target genes in the enterohepatic farnesoid X receptor-fibroblast growth factor (FXR-FGF15) axis and could be reversed using an FXR agonist, GW4064.	GW 4064	214-220	fibroblast growth factor 15	Mus musculus	158-163
30653340-10	2019	After PEG withdrawal, gene expression levels of intestinal FXR target genes Fgf15 and Shp were decreased in CF mice but unaffected in WT littermates.	Polyethylene Glycols	6-9	fibroblast growth factor 15	Mus musculus	76-81
30679232-0	2019	Therapeutic FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis.	Cholesterol	59-70	fibroblast growth factor 15	Mus musculus	12-17
30653340-12	2019	PEG treatment ameliorates intestinal BA malabsorption in CF mice and restores intestinal FXR-FGF15 signaling, independent from Asbt gene expression.	Polyethylene Glycols	0-3	fibroblast growth factor 15	Mus musculus	93-98
30521806-3	2019	We studied the functions of SHP and FGF19 in the intestines of mice, including their regulation of expression of the cholesterol transporter NPC1L1 )NPC1-like intracellular cholesterol transporter 1) and cholesterol absorption.	Cholesterol	117-128	fibroblast growth factor 15	Mus musculus	36-41
30521806-12	2019	FGF19 injection reduced expression of NPC1L1, decreased cholesterol absorption, and increased levels of hydrophilic BAs, including tauro-alpha- and -beta-muricholic acids; these changes were not observed in SHP-knockout mice.	Cholesterol	56-67	fibroblast growth factor 15	Mus musculus	0-5
30521806-12	2019	FGF19 injection reduced expression of NPC1L1, decreased cholesterol absorption, and increased levels of hydrophilic BAs, including tauro-alpha- and -beta-muricholic acids; these changes were not observed in SHP-knockout mice.	tauro-alpha- and -beta-muricholic acids	131-170	fibroblast growth factor 15	Mus musculus	0-5
30521806-15	2019	CONCLUSIONS: Postprandial FGF19 and SHP inhibit SREBF2, which leads to repression of intestinal NPC1L1 expression and cholesterol absorption.	Cholesterol	118-129	fibroblast growth factor 15	Mus musculus	26-31
30679232-1	2019	Fibroblast growth factor (FGF)19, an endocrine hormone produced in the gut, acts in the liver to control bile acid synthesis.	Bile Acids and Salts	105-114	fibroblast growth factor 15	Mus musculus	0-32
30679232-4	2019	Here, we report that FGF19 and NGM282 promote HDL biogenesis and cholesterol efflux from the liver by selectively modulating LXR signaling while ameliorating hepatic steatosis.	Cholesterol	65-76	fibroblast growth factor 15	Mus musculus	21-26
30679232-5	2019	We further identify ABCA1 and FGF receptor 4 as mediators of this effect, and that administration of a HMG-CoA reductase inhibitor or a blocking antibody against proprotein convertase subtilisin/kexin type 9 abolished FGF19-associated elevations in total cholesterol, HDL cholesterol (HDL-C), and LDL cholesterol in db/db mice.	Cholesterol	255-266	fibroblast growth factor 15	Mus musculus	218-223
30679232-5	2019	We further identify ABCA1 and FGF receptor 4 as mediators of this effect, and that administration of a HMG-CoA reductase inhibitor or a blocking antibody against proprotein convertase subtilisin/kexin type 9 abolished FGF19-associated elevations in total cholesterol, HDL cholesterol (HDL-C), and LDL cholesterol in db/db mice.	Cholesterol	272-283	fibroblast growth factor 15	Mus musculus	218-223
30679232-5	2019	We further identify ABCA1 and FGF receptor 4 as mediators of this effect, and that administration of a HMG-CoA reductase inhibitor or a blocking antibody against proprotein convertase subtilisin/kexin type 9 abolished FGF19-associated elevations in total cholesterol, HDL cholesterol (HDL-C), and LDL cholesterol in db/db mice.	Cholesterol	272-283	fibroblast growth factor 15	Mus musculus	218-223
30679232-6	2019	Moreover, we show that a constitutively active MEK1, but not a constitutively active STAT3, mimics the effect of FGF19 and NGM282 on cholesterol change.	Cholesterol	133-144	fibroblast growth factor 15	Mus musculus	113-118
30679232-9	2019	These findings outline a previously unrecognized role for FGF19 in the homeostatic control of cholesterol and may have direct impact on the clinical development of FGF19 analogs.	Cholesterol	94-105	fibroblast growth factor 15	Mus musculus	58-63
31201556-2	2019	FXR and its hepatic and intestinal target genes, small heterodimer partner (SHP, NR0B2) and fibroblast growth factor 15/19 (Fgf15 in mice, FGF19 in humans), transcriptionally regulate BA synthesis, detoxification, secretion, and absorption in the enterohepatic circulation.	Bile Acids and Salts	184-186	fibroblast growth factor 15	Mus musculus	92-119
30387017-6	2019	Using dual 1H/19F MRI of the gallbladders of live mice fed 19F-labeled bile acid analogues, we were able to differentiate wild-type mice from strains deficient in intestinal expression of a key bile acid transporter, the apical sodium-dependent bile acid transporter (ASBT), or FGF15, the mouse homologue of FGF19.	Bile Acids and Salts	71-80	fibroblast growth factor 15	Mus musculus	278-283
30387017-6	2019	Using dual 1H/19F MRI of the gallbladders of live mice fed 19F-labeled bile acid analogues, we were able to differentiate wild-type mice from strains deficient in intestinal expression of a key bile acid transporter, the apical sodium-dependent bile acid transporter (ASBT), or FGF15, the mouse homologue of FGF19.	Bile Acids and Salts	71-80	fibroblast growth factor 15	Mus musculus	308-313
31201556-2	2019	FXR and its hepatic and intestinal target genes, small heterodimer partner (SHP, NR0B2) and fibroblast growth factor 15/19 (Fgf15 in mice, FGF19 in humans), transcriptionally regulate BA synthesis, detoxification, secretion, and absorption in the enterohepatic circulation.	Bile Acids and Salts	184-186	fibroblast growth factor 15	Mus musculus	124-129
31201556-2	2019	FXR and its hepatic and intestinal target genes, small heterodimer partner (SHP, NR0B2) and fibroblast growth factor 15/19 (Fgf15 in mice, FGF19 in humans), transcriptionally regulate BA synthesis, detoxification, secretion, and absorption in the enterohepatic circulation.	Bile Acids and Salts	184-186	fibroblast growth factor 15	Mus musculus	139-144
30247920-0	2018	Attenuated Accumulation of Novel Fluorine (19F)-Labeled Bile Acid Analogues in Gallbladders of Fibroblast Growth Factor-15 (FGF15)-Deficient Mice.	Fluorine	33-41	fibroblast growth factor 15	Mus musculus	95-122
30464200-0	2018	Suppression of Hepatic Bile Acid Synthesis by a non-tumorigenic FGF19 analogue Protects Mice from Fibrosis and Hepatocarcinogenesis.	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	64-69
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	233-260
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	262-267
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	34-36	fibroblast growth factor 15	Mus musculus	233-260
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	34-36	fibroblast growth factor 15	Mus musculus	262-267
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	308-310	fibroblast growth factor 15	Mus musculus	233-260
30464200-1	2018	Critical regulation of bile acid (BA) pool size and composition occurs via an intensive molecular crosstalk between the liver and gut, orchestrated by the combined actions of the nuclear Farnesoid X receptor (FXR) and the enterokine fibroblast growth factor 19 (FGF19) with the final aim of reducing hepatic BA synthesis in a negative feedback fashion.	Bile Acids and Salts	308-310	fibroblast growth factor 15	Mus musculus	262-267
30464200-6	2018	Expression of the BA synthesis rate-limiting enzyme Cyp7a1 is reduced in FGF19-M52-treated mice compared to the GFP-treated control group with consequent reduction of BA pool and hepatic concentration.	Bile Acids and Salts	18-20	fibroblast growth factor 15	Mus musculus	73-78
30464200-6	2018	Expression of the BA synthesis rate-limiting enzyme Cyp7a1 is reduced in FGF19-M52-treated mice compared to the GFP-treated control group with consequent reduction of BA pool and hepatic concentration.	Bile Acids and Salts	167-169	fibroblast growth factor 15	Mus musculus	73-78
30464200-8	2018	Our data bona fide suggest the therapeutic potential of targeting the FXR-FGF19 axis to reduce hepatic BA synthesis in the control of BA-associated risk of fibrosis and hepatocarcinoma development.	Bile Acids and Salts	103-105	fibroblast growth factor 15	Mus musculus	74-79
30464200-8	2018	Our data bona fide suggest the therapeutic potential of targeting the FXR-FGF19 axis to reduce hepatic BA synthesis in the control of BA-associated risk of fibrosis and hepatocarcinoma development.	Bile Acids and Salts	134-136	fibroblast growth factor 15	Mus musculus	74-79
30124818-3	2018	At adulthood, FGF15/19 is mainly produced by the ileum, acting on the liver to repress hepatic bile acid synthesis and promote postprandial nutrient partitioning.	Bile Acids and Salts	95-104	fibroblast growth factor 15	Mus musculus	14-22
30247920-0	2018	Attenuated Accumulation of Novel Fluorine (19F)-Labeled Bile Acid Analogues in Gallbladders of Fibroblast Growth Factor-15 (FGF15)-Deficient Mice.	Fluorine	33-41	fibroblast growth factor 15	Mus musculus	124-129
30247920-0	2018	Attenuated Accumulation of Novel Fluorine (19F)-Labeled Bile Acid Analogues in Gallbladders of Fibroblast Growth Factor-15 (FGF15)-Deficient Mice.	Bile Acids and Salts	56-65	fibroblast growth factor 15	Mus musculus	95-122
30247920-0	2018	Attenuated Accumulation of Novel Fluorine (19F)-Labeled Bile Acid Analogues in Gallbladders of Fibroblast Growth Factor-15 (FGF15)-Deficient Mice.	Bile Acids and Salts	56-65	fibroblast growth factor 15	Mus musculus	124-129
30247920-2	2018	In the current study, we explored the ability of this approach to differentiate fibroblast growth factor-15 (FGF15)-deficient from wild-type (WT) mice, a potential diagnostic test for bile acid diarrhea, a commonly misdiagnosed disorder.	Bile Acids and Salts	184-193	fibroblast growth factor 15	Mus musculus	80-107
30247920-2	2018	In the current study, we explored the ability of this approach to differentiate fibroblast growth factor-15 (FGF15)-deficient from wild-type (WT) mice, a potential diagnostic test for bile acid diarrhea, a commonly misdiagnosed disorder.	Bile Acids and Salts	184-193	fibroblast growth factor 15	Mus musculus	109-114
30247920-6	2018	Both 19F bile acid analogues concentrated in the gallbladders of FGF15-deficient and WT mice, attaining peak concentrations at approximately 8.5 h after oral dosing.	Bile Acids and Salts	9-18	fibroblast growth factor 15	Mus musculus	65-70
30247920-9	2018	Our finding that 19F MRI differentiates FGF15-deficient from WT mice provides additional proof-of-concept for the development of 19F bile acid analogues and 19F MRI as a clinical test to diagnose bile acid diarrhea due to FGF19 deficiency and other disorders.	Bile Acids and Salts	133-142	fibroblast growth factor 15	Mus musculus	40-45
30247920-9	2018	Our finding that 19F MRI differentiates FGF15-deficient from WT mice provides additional proof-of-concept for the development of 19F bile acid analogues and 19F MRI as a clinical test to diagnose bile acid diarrhea due to FGF19 deficiency and other disorders.	Bile Acids and Salts	196-205	fibroblast growth factor 15	Mus musculus	40-45
29672888-3	2018	The mechanisms by which Fgf15 promotes liver regeneration are unclear, but Fgf15 may do so indirectly by reducing BA levels and/or directly by promoting cell proliferation.	Bile Acids and Salts	114-116	fibroblast growth factor 15	Mus musculus	75-80
29672888-5	2018	In this study, we aimed to clarify these relationships by generating Fgf15 Tet-Off, transgenic mice (Fgf15 Tg) that had very low BA levels as a result from overexpressed Fgf15-mediated suppression of BA synthesis.	Bile Acids and Salts	129-131	fibroblast growth factor 15	Mus musculus	101-106
29973237-8	2018	Increased levels of FGF15/FGFR4/beta-klotho, aberrant epithelial-mesenchymal transition (EMT) and Wnt/beta-catenin signaling were detected in DEN+HFD mice.	Diethylnitrosamine	142-145	fibroblast growth factor 15	Mus musculus	20-25
30127091-3	2018	Despite the physiological role of FGF21 and FGF19 being quite different, both lower blood glucose (BG) when administered to diabetic mice.	Blood Glucose	84-97	fibroblast growth factor 15	Mus musculus	44-49
30127091-3	2018	Despite the physiological role of FGF21 and FGF19 being quite different, both lower blood glucose (BG) when administered to diabetic mice.	Blood Glucose	99-101	fibroblast growth factor 15	Mus musculus	44-49
29876009-1	2018	Fibroblast growth factor-19 (human FGF19; murine FGF15) suppresses bile acid synthesis.	Bile Acids and Salts	67-76	fibroblast growth factor 15	Mus musculus	49-54
29159825-6	2018	Mediated by a lower farnesoid X receptor (FXR) activity in enterocytes, lower fibroblast growth factor (FGF)-15 protein secretion was associated with increased hepatic cytochrome P450 enzyme (Cyp)-7a1 protein expression and circulating bile acid levels.	Bile Acids and Salts	236-245	fibroblast growth factor 15	Mus musculus	78-111
29159825-13	2018	Targeted interventions improve bile acid-FXR-FGF15 signaling by modulation of hepatic Cyp7a1 and lipid metabolism, and reduce ethanol-induced liver disease in mice.	Bile Acids and Salts	31-40	fibroblast growth factor 15	Mus musculus	45-50
29876009-10	2018	These findings confirm FGF15, the murine homolog of FGF19, plays a key role in modulating gallbladder filling and bile acid homeostasis.	Bile Acids and Salts	114-123	fibroblast growth factor 15	Mus musculus	23-28
29876009-10	2018	These findings confirm FGF15, the murine homolog of FGF19, plays a key role in modulating gallbladder filling and bile acid homeostasis.	Bile Acids and Salts	114-123	fibroblast growth factor 15	Mus musculus	52-57
28498614-8	2017	Fgf15 (mouse counterpart of FGF19) expression was induced in hypercholanemic OATP and NTCP knockout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced in humans treated with myrcludex B.	myrcludex-B	120-131	fibroblast growth factor 15	Mus musculus	0-5
29295820-1	2018	Diet1 modulates intestinal production of the hormone, fibroblast growth factor (FGF)15, which signals in liver to regulate bile acid synthesis.	Bile Acids and Salts	123-132	fibroblast growth factor 15	Mus musculus	80-86
29416063-2	2018	Here, we show that Pemt and Gnmt, key one-carbon cycle genes regulating PC/SAM levels, are downregulated after feeding, leading to decreased PC and increased SAM levels, but these effects are blunted in small heterodimer partner (SHP)-null or FGF15-null mice.	Carbon	42-48	fibroblast growth factor 15	Mus musculus	243-248
29290621-2	2018	We have previously shown that FGF19 can modulate glucose handling by suppressing the activity of hypothalamic AGRP/NPY neurons.	Glucose	49-56	fibroblast growth factor 15	Mus musculus	30-35
29290621-3	2018	As bile acids stimulate the release of FGF19/FGF15 into the circulation, we pursued the potential of bile acids to improve glucose tolerance via a gut-brain axis involving FXR and FGF15/FGF19 within enterocytes and FGF receptors on hypothalamic AGRP/NPY neurons.	Bile Acids and Salts	3-13	fibroblast growth factor 15	Mus musculus	39-44
29290621-3	2018	As bile acids stimulate the release of FGF19/FGF15 into the circulation, we pursued the potential of bile acids to improve glucose tolerance via a gut-brain axis involving FXR and FGF15/FGF19 within enterocytes and FGF receptors on hypothalamic AGRP/NPY neurons.	Bile Acids and Salts	3-13	fibroblast growth factor 15	Mus musculus	45-50
29290621-6	2018	RESULTS: The taurocholic acid gavage led to increased serum concentrations of taurocholic acid as well as increases of FGF15 mRNA in the ileum and improved oral glucose tolerance in obese (ob/ob) mice.	Taurocholic Acid	13-29	fibroblast growth factor 15	Mus musculus	119-124
29290621-16	2018	From the intestine, bile acids stimulate FGF15 secretion, leading to activation of the FGF receptors in hypothalamic AGRP/NPY neurons.	Bile Acids and Salts	20-30	fibroblast growth factor 15	Mus musculus	41-46
28888832-10	2017	By the suppression of intestinal FXR/FGF-15 signaling, hepatic bile-acid synthesis gene expression was increased leading to an elevation of secondary and hydrophobic bile acids in liver, bile, and intestine.	Bile Acids and Salts	63-72	fibroblast growth factor 15	Mus musculus	37-43
28888832-10	2017	By the suppression of intestinal FXR/FGF-15 signaling, hepatic bile-acid synthesis gene expression was increased leading to an elevation of secondary and hydrophobic bile acids in liver, bile, and intestine.	Bile Acids and Salts	166-176	fibroblast growth factor 15	Mus musculus	37-43
28498614-8	2017	Fgf15 (mouse counterpart of FGF19) expression was induced in hypercholanemic OATP and NTCP knockout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced in humans treated with myrcludex B.	myrcludex-B	120-131	fibroblast growth factor 15	Mus musculus	28-33
28498614-8	2017	Fgf15 (mouse counterpart of FGF19) expression was induced in hypercholanemic OATP and NTCP knockout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced in humans treated with myrcludex B.	myrcludex-B	218-229	fibroblast growth factor 15	Mus musculus	0-5
28498614-8	2017	Fgf15 (mouse counterpart of FGF19) expression was induced in hypercholanemic OATP and NTCP knockout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced in humans treated with myrcludex B.	myrcludex-B	218-229	fibroblast growth factor 15	Mus musculus	28-33
28498614-9	2017	Fgf15/FGF19 expression was induced in polarized human enterocyte-models and mouse organoids by basolateral incubation with a high concentration (1 mM) of conjugated bile acids.	Bile Acids and Salts	165-175	fibroblast growth factor 15	Mus musculus	0-5
28498614-11	2017	Enterocytes sense highly elevated levels of (conjugated) bile acids in the systemic circulation to induce FGF15/19, which modulates hepatic bile acid synthesis and uptake.	Bile Acids and Salts	57-67	fibroblast growth factor 15	Mus musculus	106-114
28498614-11	2017	Enterocytes sense highly elevated levels of (conjugated) bile acids in the systemic circulation to induce FGF15/19, which modulates hepatic bile acid synthesis and uptake.	Bile Acids and Salts	57-66	fibroblast growth factor 15	Mus musculus	106-114
28981086-0	2017	Engineered fibroblast growth factor 19 protects from acetaminophen-induced liver injury and stimulates aged liver regeneration in mice.	Acetaminophen	53-66	fibroblast growth factor 15	Mus musculus	11-38
29404440-0	2017	Engineered FGF19 eliminates bile acid toxicity and lipotoxicity leading to resolution of steatohepatitis and fibrosis in mice.	Bile Acids and Salts	28-37	fibroblast growth factor 15	Mus musculus	11-16
29404440-6	2017	Mass spectrometry-based lipidomics analysis of livers from mice treated with FGF19 or M70 revealed significant reductions in the levels of toxic lipid species (i.e., diacylglycerols, ceramides and free cholesterol) and an increase in levels of unoxidized cardiolipins, an important component of the inner mitochondrial membrane.	Diglycerides	166-181	fibroblast growth factor 15	Mus musculus	77-82
29404440-6	2017	Mass spectrometry-based lipidomics analysis of livers from mice treated with FGF19 or M70 revealed significant reductions in the levels of toxic lipid species (i.e., diacylglycerols, ceramides and free cholesterol) and an increase in levels of unoxidized cardiolipins, an important component of the inner mitochondrial membrane.	Ceramides	183-192	fibroblast growth factor 15	Mus musculus	77-82
29404440-6	2017	Mass spectrometry-based lipidomics analysis of livers from mice treated with FGF19 or M70 revealed significant reductions in the levels of toxic lipid species (i.e., diacylglycerols, ceramides and free cholesterol) and an increase in levels of unoxidized cardiolipins, an important component of the inner mitochondrial membrane.	Cholesterol	202-213	fibroblast growth factor 15	Mus musculus	77-82
29404440-6	2017	Mass spectrometry-based lipidomics analysis of livers from mice treated with FGF19 or M70 revealed significant reductions in the levels of toxic lipid species (i.e., diacylglycerols, ceramides and free cholesterol) and an increase in levels of unoxidized cardiolipins, an important component of the inner mitochondrial membrane.	Cardiolipins	255-267	fibroblast growth factor 15	Mus musculus	77-82
28981086-3	2017	Fibroblast growth factor 19 (FGF19, rodent FGF15) is an enterokine that regulates liver bile acid and lipid metabolism, and stimulates hepatocellular protein synthesis and proliferation.	Bile Acids and Salts	88-97	fibroblast growth factor 15	Mus musculus	0-27
28981086-3	2017	Fibroblast growth factor 19 (FGF19, rodent FGF15) is an enterokine that regulates liver bile acid and lipid metabolism, and stimulates hepatocellular protein synthesis and proliferation.	Bile Acids and Salts	88-97	fibroblast growth factor 15	Mus musculus	29-34
28981086-3	2017	Fibroblast growth factor 19 (FGF19, rodent FGF15) is an enterokine that regulates liver bile acid and lipid metabolism, and stimulates hepatocellular protein synthesis and proliferation.	Bile Acids and Salts	88-97	fibroblast growth factor 15	Mus musculus	43-48
28119353-1	2017	OBJECTIVE: Fibroblast growth factor 15/19 (FGF15/19), an enterokine that regulates synthesis of hepatic bile acids (BA), has been proposed to influence fat metabolism.	Bile Acids and Salts	104-114	fibroblast growth factor 15	Mus musculus	43-51
28119353-3	2017	We studied the role of FGF15/19 in response to a high fat diet (HFD) and its regulation by saturated fatty acids.	Fatty Acids	91-112	fibroblast growth factor 15	Mus musculus	23-31
28119353-7	2017	Influence of palmitic acid (PA) on FGF15/19 expression was determined in mice and in human liver cell lines.	Palmitic Acid	13-26	fibroblast growth factor 15	Mus musculus	35-43
28119353-7	2017	Influence of palmitic acid (PA) on FGF15/19 expression was determined in mice and in human liver cell lines.	Palmitic Acid	28-30	fibroblast growth factor 15	Mus musculus	35-43
28119353-12	2017	PA induced FGF15/19 expression in mouse ileum and human liver cells, and FGF19 protected from PA-mediated ER stress and cytotoxicity.	Palmitic Acid	0-2	fibroblast growth factor 15	Mus musculus	11-19
28189755-9	2017	RESULTS: Both FGF15 and FGF19 hormones repressed bile acid synthesis (p&lt;0.001 for both).	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	14-19
28673684-2	2017	Fibroblast growth factor 15 (FGF15), an endocrine factor mainly produced in the distal part of small intestine, has emerged to be a critical factor in regulating bile acid homeostasis, energy metabolism, and liver regeneration.	Bile Acids and Salts	162-171	fibroblast growth factor 15	Mus musculus	0-27
28673684-2	2017	Fibroblast growth factor 15 (FGF15), an endocrine factor mainly produced in the distal part of small intestine, has emerged to be a critical factor in regulating bile acid homeostasis, energy metabolism, and liver regeneration.	Bile Acids and Salts	162-171	fibroblast growth factor 15	Mus musculus	29-34
28673684-7	2017	Furthermore, FGF15 deficiency resulted in abnormal bile acid homeostasis, increased insulin resistance, increased HFD-induced serum triglycerides, decreased inductions of hepatic cholesterol content by HFD, and altered gene expression of lipid metabolic enzymes.	Bile Acids and Salts	51-60	fibroblast growth factor 15	Mus musculus	13-18
28673684-7	2017	Furthermore, FGF15 deficiency resulted in abnormal bile acid homeostasis, increased insulin resistance, increased HFD-induced serum triglycerides, decreased inductions of hepatic cholesterol content by HFD, and altered gene expression of lipid metabolic enzymes.	Triglycerides	132-145	fibroblast growth factor 15	Mus musculus	13-18
28673684-7	2017	Furthermore, FGF15 deficiency resulted in abnormal bile acid homeostasis, increased insulin resistance, increased HFD-induced serum triglycerides, decreased inductions of hepatic cholesterol content by HFD, and altered gene expression of lipid metabolic enzymes.	Cholesterol	179-190	fibroblast growth factor 15	Mus musculus	13-18
28673684-8	2017	These data suggest that FGF15 improves lipid homeostasis and reduces bile acid synthesis, but promotes fibrosis during the development of NASH.	Bile Acids and Salts	69-78	fibroblast growth factor 15	Mus musculus	24-29
28872123-3	2017	After ileal resection, circulating blood is permanently devoid of the ileum-specific endocrine hormone fibroblast growth factor 15 (FGF15), which releases its endocrinal inhibition of bile acid synthesis in the liver.	Bile Acids and Salts	184-193	fibroblast growth factor 15	Mus musculus	103-130
28872123-3	2017	After ileal resection, circulating blood is permanently devoid of the ileum-specific endocrine hormone fibroblast growth factor 15 (FGF15), which releases its endocrinal inhibition of bile acid synthesis in the liver.	Bile Acids and Salts	184-193	fibroblast growth factor 15	Mus musculus	132-137
28474246-0	2017	Pectin Penta-Oligogalacturonide Suppresses Intestinal Bile Acids Absorption and Downregulates the FXR-FGF15 Axis in High-Cholesterol Fed Mice.	penta-oligogalacturonide	7-31	fibroblast growth factor 15	Mus musculus	102-107
28487440-1	2017	Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose.	Bile Acids and Salts	0-9	fibroblast growth factor 15	Mus musculus	98-131
28487440-1	2017	Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose.	Bile Acids and Salts	11-13	fibroblast growth factor 15	Mus musculus	98-131
28487440-1	2017	Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose.	Bile Acids and Salts	169-171	fibroblast growth factor 15	Mus musculus	98-131
28487440-1	2017	Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose.	Triglycerides	206-219	fibroblast growth factor 15	Mus musculus	98-131
28487440-1	2017	Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose.	Glucose	224-231	fibroblast growth factor 15	Mus musculus	98-131
28189755-9	2017	RESULTS: Both FGF15 and FGF19 hormones repressed bile acid synthesis (p&lt;0.001 for both).	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	24-29
28315901-8	2017	Sitagliptin treatment depressed blood lipid levels, increased serum FGF-21 and FGF-19 levels, PPAR-alpha, CREBH, and CPT1 expression, and suppressed FAS expression (p&lt;0.05).	Sitagliptin Phosphate	0-11	fibroblast growth factor 15	Mus musculus	79-85
28969019-0	2017	Repression of intestinal transporters and FXR-FGF15 signaling explains bile acids dysregulation in experimental colitis-associated colon cancer.	Bile Acids and Salts	71-81	fibroblast growth factor 15	Mus musculus	46-51
28969019-5	2017	CAC mice were characterized by an accumulation of BAs in various compartments except ileum, which is in line with repressed ileal FXR-FGF15 feedback signaling and the increased expression of hepatic CYP7A1.	Bile Acids and Salts	50-53	fibroblast growth factor 15	Mus musculus	134-139
28508871-6	2017	We show that the hepatocyte-specific deletion of Stat3, genetic ablation of Il6, treatment with a neutralizing anti-IL-6 antibody or administration of a small-molecule JAK inhibitor, abolishes FGF19-induced tumorigenesis, while the regulatory functions of FGF19 in bile acid, glucose and energy metabolism remain intact.	Bile Acids and Salts	265-274	fibroblast growth factor 15	Mus musculus	193-198
28508871-6	2017	We show that the hepatocyte-specific deletion of Stat3, genetic ablation of Il6, treatment with a neutralizing anti-IL-6 antibody or administration of a small-molecule JAK inhibitor, abolishes FGF19-induced tumorigenesis, while the regulatory functions of FGF19 in bile acid, glucose and energy metabolism remain intact.	Glucose	276-283	fibroblast growth factor 15	Mus musculus	193-198
28065787-14	2017	PX20606 and FGF19 each increased the ratio of muricholate:cholate in bile, inducing a more hydrophilic bile salt pool.	Muricholic acid	46-57	fibroblast growth factor 15	Mus musculus	12-17
28065787-14	2017	PX20606 and FGF19 each increased the ratio of muricholate:cholate in bile, inducing a more hydrophilic bile salt pool.	Cholates	50-57	fibroblast growth factor 15	Mus musculus	12-17
28065787-14	2017	PX20606 and FGF19 each increased the ratio of muricholate:cholate in bile, inducing a more hydrophilic bile salt pool.	Bile Acids and Salts	103-112	fibroblast growth factor 15	Mus musculus	12-17
28065787-17	2017	CONCLUSIONS: Hydrophilicity of the bile salt pool, controlled by FXR and FGF15/19, is an important determinant of cholesterol removal via TICE.	Bile Acids and Salts	35-44	fibroblast growth factor 15	Mus musculus	73-81
28065787-17	2017	CONCLUSIONS: Hydrophilicity of the bile salt pool, controlled by FXR and FGF15/19, is an important determinant of cholesterol removal via TICE.	Cholesterol	114-125	fibroblast growth factor 15	Mus musculus	73-81
28315901-9	2017	CONCLUSIONS Sitagliptin can protect liver tissue and modulate lipid metabolism in NAFLD mice via elevating FGF-21 and FGF-19, upregulating liver PPAR-a and CREBH levels, and mediating expression levels of key enzymes for lipid metabolism.	Sitagliptin Phosphate	12-23	fibroblast growth factor 15	Mus musculus	118-124
27609522-7	2016	Treatment of pregnant mice with GW4064 induced ileal Fgf15, Shp and Ostalpha/beta mRNAs, and restored hepatic Shp, Bal, Ntcp, and Bsep back to vehicle-treated virgin levels.	GW 4064	32-38	fibroblast growth factor 15	Mus musculus	53-58
28130274-5	2017	The absence of gut microbiota changed the bile acid composition in the ileum, which was associated with activation of the enterohepatic fibroblast growth factor 15, fibroblast growth factor receptor 4 axis, and reduction of cholesterol 7alpha-hydroxylase and hepatic bile acid synthesis, resulting in the accumulation of liver cholesterol content.	Bile Acids and Salts	42-51	fibroblast growth factor 15	Mus musculus	136-163
28202906-7	2017	BAR502 increased the expression of SHP and ABCG5 in the liver and SHP, FGF15 and GLP1 in intestine.	BAR502	0-6	fibroblast growth factor 15	Mus musculus	71-76
28178326-2	2017	FGF19 is secreted and signals to the liver, where it contributes to the homeostasis of bile acid (BA), lipid and carbohydrate metabolism.	Bile Acids and Salts	87-96	fibroblast growth factor 15	Mus musculus	0-5
28178326-2	2017	FGF19 is secreted and signals to the liver, where it contributes to the homeostasis of bile acid (BA), lipid and carbohydrate metabolism.	Bile Acids and Salts	98-100	fibroblast growth factor 15	Mus musculus	0-5
28178326-2	2017	FGF19 is secreted and signals to the liver, where it contributes to the homeostasis of bile acid (BA), lipid and carbohydrate metabolism.	Carbohydrates	113-125	fibroblast growth factor 15	Mus musculus	0-5
28178326-9	2017	FGF19 treatment decreased the expression of proteins involved in fatty acid (FA) synthesis, i.e., Fabp5, Scd1, and Acsl3 and increased the expression of Acox1, involved in FA oxidation.	Fatty Acids	65-75	fibroblast growth factor 15	Mus musculus	0-5
28041926-5	2017	We elucidate that the mechanism of FGF21 induced bile acid changes is mainly through antagonizing FGF15/19 function on liver betaKlotho/FGFR4 receptor complex; thus inhibiting FGF15/19-mediated suppression of Cyp7a1 expression.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	98-106
28041926-5	2017	We elucidate that the mechanism of FGF21 induced bile acid changes is mainly through antagonizing FGF15/19 function on liver betaKlotho/FGFR4 receptor complex; thus inhibiting FGF15/19-mediated suppression of Cyp7a1 expression.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	98-103
27895309-8	2016	Additionally, disturbed bile acid regulation through the FXR-FGF15-FGFR4 pathway was observed in mice with activated beta-catenin.	Bile Acids and Salts	24-33	fibroblast growth factor 15	Mus musculus	61-66
27573244-5	2016	Mechanistic studies demonstrated that ethanol administration to mNTKO mice induced two pivotal endocrine hormones, namely, adipose-derived adiponectin and gut-derived fibroblast growth factor 15 (Fgf15).	Ethanol	38-45	fibroblast growth factor 15	Mus musculus	167-194
27573244-5	2016	Mechanistic studies demonstrated that ethanol administration to mNTKO mice induced two pivotal endocrine hormones, namely, adipose-derived adiponectin and gut-derived fibroblast growth factor 15 (Fgf15).	Ethanol	38-45	fibroblast growth factor 15	Mus musculus	196-201
27573244-6	2016	The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNTKO mice.	Bile Acids and Salts	107-117	fibroblast growth factor 15	Mus musculus	55-60
26634251-2	2015	The unusual orphan nuclear receptor, small heterodimer partner (SHP), acts as a co-repressor for many transcriptional factors and has been implicated in diverse biological pathways including FGF19-mediated repression of bile acid synthesis.	Bile Acids and Salts	220-229	fibroblast growth factor 15	Mus musculus	191-196
27573244-6	2016	The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNTKO mice.	Ethanol	228-235	fibroblast growth factor 15	Mus musculus	55-60
26505219-3	2016	Activation of FXR by a synthetic agonist, GW4064, in mice increased occupancy of FXR and its DNA-binding partner, retinoid X receptor-alpha, at FGF15-signaling component genes, particularly betaKL, and induced expression of these genes.	GW 4064	42-48	fibroblast growth factor 15	Mus musculus	144-149
26505219-7	2016	In mice, transient inductions of intestinal Fgf15 and hepatic betaKL were temporally correlated after GW4064 treatment, and pretreatment of hepatocytes with GW4064 before FGF19 treatment enhanced FGF19 signaling, which was abolished by transcriptional inhibition or betaKL down-regulation.	GW 4064	157-163	fibroblast growth factor 15	Mus musculus	44-49
26505219-7	2016	In mice, transient inductions of intestinal Fgf15 and hepatic betaKL were temporally correlated after GW4064 treatment, and pretreatment of hepatocytes with GW4064 before FGF19 treatment enhanced FGF19 signaling, which was abolished by transcriptional inhibition or betaKL down-regulation.	GW 4064	157-163	fibroblast growth factor 15	Mus musculus	196-201
27580383-7	2016	RESULTS: Dextran sulfate sodium-treated mice with ileum-sparing colitis showed higher Fgf15 serum levels.	Dextran Sulfate	9-31	fibroblast growth factor 15	Mus musculus	86-91
27580383-10	2016	Fibroblast growth factor receptor 4 up-regulation was in line with higher Fgf15 serum levels in dextran sulfate sodium-treated mice.	Dextran Sulfate	96-118	fibroblast growth factor 15	Mus musculus	74-79
27048804-8	2016	An FXR antagonist had the same effect on FGF15 and CYP7A1 expression as RSV, while an FXR agonist abolished RSV-induced alterations in FGF15 and CYP7A1 expression.	Resveratrol	108-111	fibroblast growth factor 15	Mus musculus	135-140
27048804-11	2016	In conclusion, RSV attenuated TMAO-induced AS by decreasing TMAO levels and increasing hepatic BA neosynthesis via gut microbiota remodeling, and the BA neosynthesis was partially mediated through the enterohepatic FXR-FGF15 axis.	Resveratrol	15-18	fibroblast growth factor 15	Mus musculus	219-224
27048804-17	2016	And RSV-induced hepatic BA neosynthesis was partially mediated through downregulating the enterohepatic farnesoid X receptor-fibroblast growth factor 15 axis.	Resveratrol	4-7	fibroblast growth factor 15	Mus musculus	125-152
26418580-3	2016	We hypothesized that modulating bile acid metabolism by the gut hormone fibroblast growth factor 19 (FGF19) may represent a novel approach for treating cholangiopathy and comorbidities.	Bile Acids and Salts	32-41	fibroblast growth factor 15	Mus musculus	72-99
26418580-3	2016	We hypothesized that modulating bile acid metabolism by the gut hormone fibroblast growth factor 19 (FGF19) may represent a novel approach for treating cholangiopathy and comorbidities.	Bile Acids and Salts	32-41	fibroblast growth factor 15	Mus musculus	101-106
26418580-7	2016	Mechanistically, FGF19 and M70 significantly inhibited hepatic expression of Cyp7a1 and Cyp27a1, which encode enzymes responsible for the rate-limiting steps in the classic and alternate bile acid synthetic pathways, thereby reducing the hepatic bile acid pool and blood levels of bile acids.	Bile Acids and Salts	187-196	fibroblast growth factor 15	Mus musculus	17-22
26418580-7	2016	Mechanistically, FGF19 and M70 significantly inhibited hepatic expression of Cyp7a1 and Cyp27a1, which encode enzymes responsible for the rate-limiting steps in the classic and alternate bile acid synthetic pathways, thereby reducing the hepatic bile acid pool and blood levels of bile acids.	Bile Acids and Salts	246-255	fibroblast growth factor 15	Mus musculus	17-22
26418580-7	2016	Mechanistically, FGF19 and M70 significantly inhibited hepatic expression of Cyp7a1 and Cyp27a1, which encode enzymes responsible for the rate-limiting steps in the classic and alternate bile acid synthetic pathways, thereby reducing the hepatic bile acid pool and blood levels of bile acids.	Bile Acids and Salts	281-291	fibroblast growth factor 15	Mus musculus	17-22
26418580-10	2016	CONCLUSION: These results demonstrate the potential for treating cholangiopathy by safely harnessing FGF19 biology to suppress bile acid synthesis.	Bile Acids and Salts	127-136	fibroblast growth factor 15	Mus musculus	101-106
26723851-3	2016	In mice, FGF15 expression (ortholog of human FGF19) is induced by vitamin A (VitA) in an FXR-dependent manner.	Vitamin A	66-75	fibroblast growth factor 15	Mus musculus	9-14
26634251-8	2015	Furthermore, FGF19-induced phosphorylation of SHP at Thr-55 is shown to be important for its functional interaction with SREBP-2 and reduction of liver/serum cholesterol levels.	Threonine	53-56	fibroblast growth factor 15	Mus musculus	13-18
26634251-8	2015	Furthermore, FGF19-induced phosphorylation of SHP at Thr-55 is shown to be important for its functional interaction with SREBP-2 and reduction of liver/serum cholesterol levels.	Cholesterol	158-169	fibroblast growth factor 15	Mus musculus	13-18
26634251-9	2015	CONCLUSION: This study reveals SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19.	Sterols	99-105	fibroblast growth factor 15	Mus musculus	203-208
26634251-9	2015	CONCLUSION: This study reveals SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19.	Cholesterol	172-183	fibroblast growth factor 15	Mus musculus	203-208
26039452-1	2015	Fibroblast growth factor 15 (FGF15) has been proposed as a postprandial hormone that signals from intestine to liver to regulate bile acid and carbohydrate homeostasis.	Bile Acids and Salts	129-138	fibroblast growth factor 15	Mus musculus	0-27
26040986-0	2015	Circadian control of bile acid synthesis by a KLF15-Fgf15 axis.	Bile Acids and Salts	21-30	fibroblast growth factor 15	Mus musculus	52-57
26040986-6	2015	Ileal Fgf15 is a potent inhibitor of BA synthesis.	Bile Acids and Salts	37-39	fibroblast growth factor 15	Mus musculus	6-11
26028580-13	2015	CONCLUSIONS: In mice with humanized livers, expression of an FGF19 transgene corrects bile acid signaling defects, resulting in normalization of bile acid synthesis, the bile acid pool, and liver size.	Bile Acids and Salts	86-95	fibroblast growth factor 15	Mus musculus	61-66
26028580-13	2015	CONCLUSIONS: In mice with humanized livers, expression of an FGF19 transgene corrects bile acid signaling defects, resulting in normalization of bile acid synthesis, the bile acid pool, and liver size.	Bile Acids and Salts	145-154	fibroblast growth factor 15	Mus musculus	61-66
26028580-13	2015	CONCLUSIONS: In mice with humanized livers, expression of an FGF19 transgene corrects bile acid signaling defects, resulting in normalization of bile acid synthesis, the bile acid pool, and liver size.	Bile Acids and Salts	145-154	fibroblast growth factor 15	Mus musculus	61-66
25416068-5	2015	RESULTS: siRNA-mediated knockdown of Fgfr4 severely affected liver regeneration due to impairment of hepatocyte proliferation combined with liver necrosis.Mechanistically, the proliferation defect resulted from inhibition of an Fgf15-Fgfr4-Stat3 signalling pathway,which is required for injury-induced expression of the Foxm1 transcription factor and subsequent cell cycle progression, while elevated levels of intrahepatic toxicbile acids were identified as the likely cause of the necrotic damage.	toxicbile acids	424-439	fibroblast growth factor 15	Mus musculus	228-233
26039452-1	2015	Fibroblast growth factor 15 (FGF15) has been proposed as a postprandial hormone that signals from intestine to liver to regulate bile acid and carbohydrate homeostasis.	Bile Acids and Salts	129-138	fibroblast growth factor 15	Mus musculus	29-34
26039452-1	2015	Fibroblast growth factor 15 (FGF15) has been proposed as a postprandial hormone that signals from intestine to liver to regulate bile acid and carbohydrate homeostasis.	Carbohydrates	143-155	fibroblast growth factor 15	Mus musculus	0-27
26039452-1	2015	Fibroblast growth factor 15 (FGF15) has been proposed as a postprandial hormone that signals from intestine to liver to regulate bile acid and carbohydrate homeostasis.	Carbohydrates	143-155	fibroblast growth factor 15	Mus musculus	29-34
26039452-5	2015	Consistent with the proposed endocrine role for FGF15 in liver, mice lacking hepatocyte expression of the obligate FGF15 co-receptor, beta-Klotho, have increased bile acid synthesis and reduced glycogen storage despite having supraphysiological plasma FGF15 concentrations.	Bile Acids and Salts	162-171	fibroblast growth factor 15	Mus musculus	115-120
26039452-5	2015	Consistent with the proposed endocrine role for FGF15 in liver, mice lacking hepatocyte expression of the obligate FGF15 co-receptor, beta-Klotho, have increased bile acid synthesis and reduced glycogen storage despite having supraphysiological plasma FGF15 concentrations.	Bile Acids and Salts	162-171	fibroblast growth factor 15	Mus musculus	115-120
26039452-5	2015	Consistent with the proposed endocrine role for FGF15 in liver, mice lacking hepatocyte expression of the obligate FGF15 co-receptor, beta-Klotho, have increased bile acid synthesis and reduced glycogen storage despite having supraphysiological plasma FGF15 concentrations.	Glycogen	194-202	fibroblast growth factor 15	Mus musculus	115-120
26039452-5	2015	Consistent with the proposed endocrine role for FGF15 in liver, mice lacking hepatocyte expression of the obligate FGF15 co-receptor, beta-Klotho, have increased bile acid synthesis and reduced glycogen storage despite having supraphysiological plasma FGF15 concentrations.	Glycogen	194-202	fibroblast growth factor 15	Mus musculus	115-120
26045273-4	2015	Blocking ileal apical membrane bile acid transport (Asbt-null mice) increases fecal bile acid excretion, hepatic Cyp7a1 expression, and the relative proportion of taurocholate in the bile acid pool, but decreases ileal FGF15 expression, bile acid pool size, and hepatic cholesterol content.	asbt	52-56	fibroblast growth factor 15	Mus musculus	219-224
25346390-1	2015	Fibroblast growth factor 15 (FGF15), FGF19 in humans, is a gut-derived hormone and a key regulator of bile acids and carbohydrate metabolism.	Bile Acids and Salts	102-112	fibroblast growth factor 15	Mus musculus	29-34
25346390-1	2015	Fibroblast growth factor 15 (FGF15), FGF19 in humans, is a gut-derived hormone and a key regulator of bile acids and carbohydrate metabolism.	Carbohydrates	117-129	fibroblast growth factor 15	Mus musculus	29-34
25604607-3	2015	FGF19 regulates bile acid biosynthesis in the bile duct, glucose metabolism and vitamin D and phosphate homeostasis, raises the metabolic rate, reduces body weight, and ameliorates diabetes in mice.	Bile Acids and Salts	16-25	fibroblast growth factor 15	Mus musculus	0-5
25604607-3	2015	FGF19 regulates bile acid biosynthesis in the bile duct, glucose metabolism and vitamin D and phosphate homeostasis, raises the metabolic rate, reduces body weight, and ameliorates diabetes in mice.	Vitamin D	80-89	fibroblast growth factor 15	Mus musculus	0-5
25604607-3	2015	FGF19 regulates bile acid biosynthesis in the bile duct, glucose metabolism and vitamin D and phosphate homeostasis, raises the metabolic rate, reduces body weight, and ameliorates diabetes in mice.	Phosphates	94-103	fibroblast growth factor 15	Mus musculus	0-5
25582706-1	2015	Bile acids (BAs) are known to regulate BA synthesis and transport by the farnesoid X receptor in the liver (FXR-SHP) and intestine (FXR-Fgf15).	Bile Acids and Salts	0-10	fibroblast growth factor 15	Mus musculus	136-141
25582706-1	2015	Bile acids (BAs) are known to regulate BA synthesis and transport by the farnesoid X receptor in the liver (FXR-SHP) and intestine (FXR-Fgf15).	Bile Acids and Salts	12-14	fibroblast growth factor 15	Mus musculus	136-141
25582706-6	2015	In the ileum, the mRNA of the intestinal FXR target gene Fgf15 was increased at lower doses and to a higher extent by CA and DCA than by CDCA and LCA.	dichloroacetylene	125-128	fibroblast growth factor 15	Mus musculus	57-62
25582706-6	2015	In the ileum, the mRNA of the intestinal FXR target gene Fgf15 was increased at lower doses and to a higher extent by CA and DCA than by CDCA and LCA.	Chenodeoxycholic Acid	137-141	fibroblast growth factor 15	Mus musculus	57-62
25582706-6	2015	In the ileum, the mRNA of the intestinal FXR target gene Fgf15 was increased at lower doses and to a higher extent by CA and DCA than by CDCA and LCA.	Lithocholic Acid	146-149	fibroblast growth factor 15	Mus musculus	57-62
26045262-0	2015	Diet1 is a regulator of fibroblast growth factor 15/19-dependent bile acid synthesis.	Bile Acids and Salts	65-74	fibroblast growth factor 15	Mus musculus	24-51
26045262-2	2015	In response to bile acid uptake in enterocytes, farnesoid X receptor is activated and induces transcription of fibroblast growth factor (FGF)15 in mice, or FGF19 in humans.	Bile Acids and Salts	15-24	fibroblast growth factor 15	Mus musculus	137-143
26045262-2	2015	In response to bile acid uptake in enterocytes, farnesoid X receptor is activated and induces transcription of fibroblast growth factor (FGF)15 in mice, or FGF19 in humans.	Bile Acids and Salts	15-24	fibroblast growth factor 15	Mus musculus	156-161
26045262-3	2015	FGF15/19 is secreted into the enterohepatic circulation, and through activation of hepatic receptors, leads to repression of Cyp7a1, a rate-limiting enzyme for bile acid synthesis.	Bile Acids and Salts	160-169	fibroblast growth factor 15	Mus musculus	0-8
26045262-8	2015	Diet1 appears to be a control point for the production of FGF15/19 in enterocytes, and thus a regulator of bile acid and lipid homeostasis.	Bile Acids and Salts	107-116	fibroblast growth factor 15	Mus musculus	58-66
26045262-10	2015	CONCLUSIONS: Further elucidation of the Diet1-FGF15/19 interaction will provide new insights into the intricate regulatory mechanisms underlying bile acid metabolism.	Bile Acids and Salts	145-154	fibroblast growth factor 15	Mus musculus	46-54
24954587-9	2015	CONCLUSION: Intestinal FXR is sufficient to restore BA homeostasis through the FGF15 axis and prevent progression of liver damage to HCC even in the absence of hepatic FXR.	Bile Acids and Salts	52-54	fibroblast growth factor 15	Mus musculus	79-84
25278499-9	2014	Noticeably, atorvastatin suppressed the expression of BA nuclear receptor farnesoid X receptor (FXR) target genes, namely small heterodimer partner (liver) and fibroblast growth factor 15 (ileum).	Atorvastatin	12-24	fibroblast growth factor 15	Mus musculus	160-187
26045273-5	2015	In contrast, blocking ileal basolateral membrane bile acid transport (Ostalpha-null mice) increases ileal FGF15 expression, reduces hepatic Cyp7a1 expression, and increases the proportion of tauro-beta-muricholic acid in the bile acid pool.	Bile Acids and Salts	49-58	fibroblast growth factor 15	Mus musculus	106-111
25204652-3	2014	Mechanism of action studies in FGFR4-deficient mice suggest that the effects are mediated in part by increased plasma levels of adiponectin and the endocrine FGF factors FGF21 and FGF15, the latter of which increase in response to an elevated bile acid pool.	Bile Acids and Salts	243-252	fibroblast growth factor 15	Mus musculus	180-185
25214402-6	2014	Moreover, administration of a bile acid-sequestering agent suppressed ileal fibroblast growth factor 15 expression, leading to increased iASBT expression to restore bile filling in the liver and biliary tree, which ameliorates steatosis and inflammation in the liver.	Bile Acids and Salts	30-39	fibroblast growth factor 15	Mus musculus	76-103
24033844-1	2014	AIM: Bile acid synthesis is regulated by nuclear receptors including farnesoid X receptor (FXR) and small heterodimer partner (SHP), and by fibroblast growth factor 15/19 (FGF15/19).	Bile Acids and Salts	5-14	fibroblast growth factor 15	Mus musculus	172-180
25175738-9	2014	Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15.	Tretinoin	20-22	fibroblast growth factor 15	Mus musculus	167-172
25080475-4	2014	We describe a nontumorigenic FGF19 variant, M70, which regulates bile acid metabolism and, through inhibition of bile acid synthesis and reduction of excess hepatic bile acid accumulation, protects mice from liver injury induced by either extrahepatic or intrahepatic cholestasis.	Bile Acids and Salts	65-74	fibroblast growth factor 15	Mus musculus	29-34
24981838-0	2014	Cytoplasmic tyrosine phosphatase Shp2 coordinates hepatic regulation of bile acid and FGF15/19 signaling to repress bile acid synthesis.	Bile Acids and Salts	116-125	fibroblast growth factor 15	Mus musculus	86-94
24981838-1	2014	Bile acid (BA) biosynthesis is tightly controlled by intrahepatic negative feedback signaling elicited by BA binding to farnesoid X receptor (FXR) and also by enterohepatic communication involving ileal BA reabsorption and FGF15/19 secretion.	Bile Acids and Salts	0-9	fibroblast growth factor 15	Mus musculus	223-231
24981838-1	2014	Bile acid (BA) biosynthesis is tightly controlled by intrahepatic negative feedback signaling elicited by BA binding to farnesoid X receptor (FXR) and also by enterohepatic communication involving ileal BA reabsorption and FGF15/19 secretion.	Bile Acids and Salts	11-13	fibroblast growth factor 15	Mus musculus	223-231
25080475-4	2014	We describe a nontumorigenic FGF19 variant, M70, which regulates bile acid metabolism and, through inhibition of bile acid synthesis and reduction of excess hepatic bile acid accumulation, protects mice from liver injury induced by either extrahepatic or intrahepatic cholestasis.	Bile Acids and Salts	113-122	fibroblast growth factor 15	Mus musculus	29-34
25080475-4	2014	We describe a nontumorigenic FGF19 variant, M70, which regulates bile acid metabolism and, through inhibition of bile acid synthesis and reduction of excess hepatic bile acid accumulation, protects mice from liver injury induced by either extrahepatic or intrahepatic cholestasis.	Bile Acids and Salts	113-122	fibroblast growth factor 15	Mus musculus	29-34
24535283-2	2014	In this review, we focus on the role of the intestinal FGF15/19 hormone in modulating bile acid levels, and additional metabolic effects on glucose metabolism, nonalcoholic liver disease (NAFLD), and liver regeneration.	Bile Acids and Salts	86-95	fibroblast growth factor 15	Mus musculus	55-63
24068255-10	2014	Thus, the results collectively suggest that cholangiocytes may be able to actively regulate bile acid biosynthesis in cholangiocytes and even hepatocyte by secreting FGF15/19.	Bile Acids and Salts	92-101	fibroblast growth factor 15	Mus musculus	166-174
24535283-0	2014	Regulation of bile acid homeostasis by the intestinal Diet1-FGF15/19 axis.	Bile Acids and Salts	14-23	fibroblast growth factor 15	Mus musculus	60-68
24688219-0	2014	Short-term dietary phosphate restriction up-regulates ileal fibroblast growth factor 15 gene expression in mice.	Phosphates	19-28	fibroblast growth factor 15	Mus musculus	60-87
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	inorganic	165-174	fibroblast growth factor 15	Mus musculus	41-44
24688219-8	2014	Furthermore, diurnal variations of plasma triglyceride concentrations and hepatic mRNA expression of the bile acid synthesis enzyme Cyp7a1 as one of Fgf15 negative target genes was influenced by dietary Pi restriction.	Bile Acids and Salts	105-114	fibroblast growth factor 15	Mus musculus	149-154
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	inorganic	165-174	fibroblast growth factor 15	Mus musculus	77-85
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Phosphates	175-184	fibroblast growth factor 15	Mus musculus	41-44
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Phosphates	175-184	fibroblast growth factor 15	Mus musculus	77-85
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Vitamin D	194-203	fibroblast growth factor 15	Mus musculus	41-44
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Vitamin D	194-203	fibroblast growth factor 15	Mus musculus	77-85
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Bile Acids and Salts	205-214	fibroblast growth factor 15	Mus musculus	41-44
24688219-1	2014	Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy.	Bile Acids and Salts	205-214	fibroblast growth factor 15	Mus musculus	77-85
24465767-0	2014	Soluble expression of disulfide bond containing proteins FGF15 and FGF19 in the cytoplasm of Escherichia coli.	Disulfides	22-31	fibroblast growth factor 15	Mus musculus	57-62
24465767-0	2014	Soluble expression of disulfide bond containing proteins FGF15 and FGF19 in the cytoplasm of Escherichia coli.	Disulfides	22-31	fibroblast growth factor 15	Mus musculus	67-72
24465767-2	2014	FGF15/FGF19 protein contains two disulfide bonds.	Disulfides	33-42	fibroblast growth factor 15	Mus musculus	0-5
24465767-2	2014	FGF15/FGF19 protein contains two disulfide bonds.	Disulfides	33-42	fibroblast growth factor 15	Mus musculus	6-11
24465767-6	2014	Several commercial available strains with the disruption of thiol-redox pathways, and/or co-expression of redoxase or refolding chaperones were used to develop this novel method for expression of FGF15/FGF19 in E. coli.	Sulfhydryl Compounds	60-65	fibroblast growth factor 15	Mus musculus	196-201
24465767-6	2014	Several commercial available strains with the disruption of thiol-redox pathways, and/or co-expression of redoxase or refolding chaperones were used to develop this novel method for expression of FGF15/FGF19 in E. coli.	Sulfhydryl Compounds	60-65	fibroblast growth factor 15	Mus musculus	202-207
24465767-8	2014	However, TRX fusion protein improved FGF19 solubility in strains of thiol-redox system mutants.	Sulfhydryl Compounds	68-73	fibroblast growth factor 15	Mus musculus	37-42
24465767-9	2014	In addition, DsbC co-expressed in thiol-redox system mutants alone improved and further enhanced FGF19 solubility with combination of TRX fusion tag.	Sulfhydryl Compounds	34-39	fibroblast growth factor 15	Mus musculus	97-102
24465767-10	2014	The soluble FGF19 proteins were easily purified through Ni-NTA affinity chromatography and anion exchange chromatography, and the purified protein maintained its biological activities, confirmed by suppressing hepatic Cyp7a1 gene transcription in mice and by activating ERK1/2 signaling pathway in HepG2 cells.	ni-nta	56-62	fibroblast growth factor 15	Mus musculus	12-17
24465767-12	2014	In summary, we have successfully developed a method to express functional FGF19 protein in prokaryotic cells, and this strategy may be adapted for the expression of other disulfide-containing proteins.	Disulfides	171-180	fibroblast growth factor 15	Mus musculus	74-79
24309182-1	2014	Fibroblast growth factor-19 (FGF-19), a bile acid-responsive enterokine, is secreted by the ileum and regulates a variety of metabolic processes.	Bile Acids and Salts	40-49	fibroblast growth factor 15	Mus musculus	0-27
24309182-1	2014	Fibroblast growth factor-19 (FGF-19), a bile acid-responsive enterokine, is secreted by the ileum and regulates a variety of metabolic processes.	Bile Acids and Salts	40-49	fibroblast growth factor 15	Mus musculus	29-35
25056539-1	2014	In addition to being positively regulated by prandial activity, bile acid production is also negatively controlled by the endocrine fibroblast growth factor 19 (FGF19) or the mouse ortholog FGF15 from the ileum that represses hepatic cholesterol 7 alpha-hydroxylase (Cyp7a1) expression through activating FGF receptor four (FGFR4).	Bile Acids and Salts	64-73	fibroblast growth factor 15	Mus musculus	132-159
25056539-1	2014	In addition to being positively regulated by prandial activity, bile acid production is also negatively controlled by the endocrine fibroblast growth factor 19 (FGF19) or the mouse ortholog FGF15 from the ileum that represses hepatic cholesterol 7 alpha-hydroxylase (Cyp7a1) expression through activating FGF receptor four (FGFR4).	Bile Acids and Salts	64-73	fibroblast growth factor 15	Mus musculus	161-166
25056539-1	2014	In addition to being positively regulated by prandial activity, bile acid production is also negatively controlled by the endocrine fibroblast growth factor 19 (FGF19) or the mouse ortholog FGF15 from the ileum that represses hepatic cholesterol 7 alpha-hydroxylase (Cyp7a1) expression through activating FGF receptor four (FGFR4).	Bile Acids and Salts	64-73	fibroblast growth factor 15	Mus musculus	190-195
25056539-3	2014	Here we report that hepatocyte FGFR substrate 2alpha (FRS2alpha), a scaffold protein essential for canonical FGFRs to activate the ERK and AKT pathways, was required for the regulation of bile acid production by the FGF15/19-FGFR4 signaling axis.	Bile Acids and Salts	188-197	fibroblast growth factor 15	Mus musculus	216-224
25056539-7	2014	Together, the results demonstrate that FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis.	Bile Acids and Salts	133-142	fibroblast growth factor 15	Mus musculus	89-94
25056539-7	2014	Together, the results demonstrate that FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis.	Bile Acids and Salts	133-142	fibroblast growth factor 15	Mus musculus	95-100
24118394-4	2014	Studies on such mice have concluded BA synthesis is induced due to reduced hormonal signalling by fibroblast growth factor (FGF)15 from intestine to liver.	Bile Acids and Salts	36-38	fibroblast growth factor 15	Mus musculus	124-130
23801799-2	2013	In mice, fibroblast growth factor (FGF) 15 (FGF19 in humans) regulates hepatic bile acid (BA) production and can also resolve diabetes.	Bile Acids and Salts	79-88	fibroblast growth factor 15	Mus musculus	9-42
24084738-0	2013	FGF19 action in the brain induces  insulin-independent glucose lowering.	Glucose	55-62	fibroblast growth factor 15	Mus musculus	0-5
24084738-6	2013	injection of FGF19 dramatically improved glucose intolerance within 2 hours.	Glucose	41-48	fibroblast growth factor 15	Mus musculus	13-18
23880190-8	2013	Ileal FGF15 expression was directly correlated with plasma cholesterol levels and aortic cholesterol content.	Cholesterol	59-70	fibroblast growth factor 15	Mus musculus	6-11
23880190-8	2013	Ileal FGF15 expression was directly correlated with plasma cholesterol levels and aortic cholesterol content.	Cholesterol	89-100	fibroblast growth factor 15	Mus musculus	6-11
23880190-10	2013	CONCLUSIONS: Decreases in ileal FGF15, with subsequent increases in hepatic Cyp7a1 expression and bile acid synthesis appear to be necessary for the plasma cholesterol-lowering and atheroprotective effects associated with blocking intestinal bile acid absorption.	Cholesterol	156-167	fibroblast growth factor 15	Mus musculus	32-37
23880190-10	2013	CONCLUSIONS: Decreases in ileal FGF15, with subsequent increases in hepatic Cyp7a1 expression and bile acid synthesis appear to be necessary for the plasma cholesterol-lowering and atheroprotective effects associated with blocking intestinal bile acid absorption.	Bile Acids and Salts	242-251	fibroblast growth factor 15	Mus musculus	32-37
23922646-9	2013	Mechanistic studies indicated that anti-obesity effect of FGFR4 ASO was mediated at least in part through an induction of plasma FGF15 level resulted from reduction of hepatic FGFR4 expression.	Oligonucleotides, Antisense	64-67	fibroblast growth factor 15	Mus musculus	129-134
24184963-5	2014	Furthermore, treatment of mice with FGF19 (the human counterpart of mouse FGF15) abolished the difference between WT and LCN mice in small intestinal (SI) CYP3A levels at 6 hours after the treatment.	1,5-Anhydro-D-Arabino-Hex-1-Enitol	121-124	fibroblast growth factor 15	Mus musculus	36-41
24184963-5	2014	Furthermore, treatment of mice with FGF19 (the human counterpart of mouse FGF15) abolished the difference between WT and LCN mice in small intestinal (SI) CYP3A levels at 6 hours after the treatment.	1,5-Anhydro-D-Arabino-Hex-1-Enitol	121-124	fibroblast growth factor 15	Mus musculus	74-79
24279986-1	2013	BACKGROUND: Endocrine FGF21 and FGF19 target adipocytes and hepatocytes through betaKlotho (KLB) and FGFR tyrosine kinases effecting glucose, lipid and energy metabolism.	Glucose	133-140	fibroblast growth factor 15	Mus musculus	32-37
24007882-6	2013	CSA-fed mice exhibited significantly higher activation of c-Jun N-terminal protein kinases and a significant decrease in intestinal fibroblast growth factor 15 mRNA after APAP treatment.	Cholestyramine Resin	0-3	fibroblast growth factor 15	Mus musculus	132-159
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Glucose	118-125	fibroblast growth factor 15	Mus musculus	0-27
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Glucose	118-125	fibroblast growth factor 15	Mus musculus	32-37
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Glucose	118-125	fibroblast growth factor 15	Mus musculus	47-52
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Bile Acids and Salts	137-146	fibroblast growth factor 15	Mus musculus	0-27
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Bile Acids and Salts	137-146	fibroblast growth factor 15	Mus musculus	32-37
24165751-2	2013	Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism.	Bile Acids and Salts	137-146	fibroblast growth factor 15	Mus musculus	47-52
23801799-2	2013	In mice, fibroblast growth factor (FGF) 15 (FGF19 in humans) regulates hepatic bile acid (BA) production and can also resolve diabetes.	Bile Acids and Salts	79-88	fibroblast growth factor 15	Mus musculus	44-49
23801799-2	2013	In mice, fibroblast growth factor (FGF) 15 (FGF19 in humans) regulates hepatic bile acid (BA) production and can also resolve diabetes.	Bile Acids and Salts	90-92	fibroblast growth factor 15	Mus musculus	9-42
23801799-2	2013	In mice, fibroblast growth factor (FGF) 15 (FGF19 in humans) regulates hepatic bile acid (BA) production and can also resolve diabetes.	Bile Acids and Salts	90-92	fibroblast growth factor 15	Mus musculus	44-49
23106963-2	2012	Ileal FGF19 regulates bile acid metabolism through specifically FGFR4-KLB in hepatocytes where FGFR1 is not significant.	Bile Acids and Salts	22-31	fibroblast growth factor 15	Mus musculus	6-11
23292666-2	2013	Fibroblast growth factor 15 (Fgf15, human FGF19) is a BA-induced ileum-derived enterokine that governs BA metabolism.	Bile Acids and Salts	54-56	fibroblast growth factor 15	Mus musculus	0-27
23292666-2	2013	Fibroblast growth factor 15 (Fgf15, human FGF19) is a BA-induced ileum-derived enterokine that governs BA metabolism.	Bile Acids and Salts	54-56	fibroblast growth factor 15	Mus musculus	29-34
23292666-3	2013	We evaluated the relevance of Fgf15 in the preservation of BA homeostasis after PH and its potential role in the regenerative process.	Bile Acids and Salts	59-61	fibroblast growth factor 15	Mus musculus	30-35
23292666-8	2013	RESULTS: Fgf15 (-/-) mice showed marked liver injury and mortality after PH accompanied by persistently elevated intrahepatic BA levels.	Bile Acids and Salts	126-128	fibroblast growth factor 15	Mus musculus	9-14
23292666-9	2013	Cholestyramine feeding and adenovirally delivered Fgf15 reduced BA levels and significantly prevented this lethal outcome.	Bile Acids and Salts	64-66	fibroblast growth factor 15	Mus musculus	50-55
23292666-14	2013	CONCLUSIONS: Fgf15 is necessary to maintain BA homeostasis and prevent liver injury during liver regeneration.	Bile Acids and Salts	44-46	fibroblast growth factor 15	Mus musculus	13-18
23292666-15	2013	Moreover, Fgf15 is an essential mediator of the liver growth-promoting effects of BA.	Bile Acids and Salts	82-84	fibroblast growth factor 15	Mus musculus	10-15
23747249-0	2013	Diet1 functions in the FGF15/19 enterohepatic signaling axis to modulate bile acid and lipid levels.	Bile Acids and Salts	73-82	fibroblast growth factor 15	Mus musculus	23-31
23204296-5	2013	FGF19 and FGF21 equally improved glucose parameters; however, we observed increased serum TG and cholesterol levels after treatment with FGF19 but not with FGF21.	Glucose	33-40	fibroblast growth factor 15	Mus musculus	0-5
23204296-5	2013	FGF19 and FGF21 equally improved glucose parameters; however, we observed increased serum TG and cholesterol levels after treatment with FGF19 but not with FGF21.	Triglycerides	90-92	fibroblast growth factor 15	Mus musculus	137-142
23204296-5	2013	FGF19 and FGF21 equally improved glucose parameters; however, we observed increased serum TG and cholesterol levels after treatment with FGF19 but not with FGF21.	Cholesterol	97-108	fibroblast growth factor 15	Mus musculus	137-142
23338060-0	2013	Liver: Fgf15 maintains bile acid homeostasis and is a key mediator of liver regeneration in mice.	Bile Acids and Salts	23-32	fibroblast growth factor 15	Mus musculus	7-12
22396169-6	2012	Mouse Fgf15 and human FGF19 play key roles in enterohepatic signaling, regulation of liver bile acid biosynthesis, gallbladder motility and metabolic homeostasis.	Bile Acids and Salts	91-100	fibroblast growth factor 15	Mus musculus	6-11
22370560-2	2012	FGF19 and FGF21 can regulate glucose, lipid, and energy metabolism, while FGF23 regulates phosphate homeostasis.	Glucose	29-36	fibroblast growth factor 15	Mus musculus	0-5
22661717-6	2012	FGF19, a gut hormone whose expression and secretion is induced by intestinal bile acids, also increased hepatic FGF21 secretion.	Bile Acids and Salts	77-87	fibroblast growth factor 15	Mus musculus	0-5
22661717-9	2012	We propose that the enhanced enterohepatic flux of bile acids during HF-LC consumption leads to activation of hepatic FXR and FGF19 signaling activity and an increase in FGF21 gene expression and secretion.	Bile Acids and Salts	51-61	fibroblast growth factor 15	Mus musculus	126-131
22617565-2	2012	FGF19 improves glucose tolerance when overexpressed in mice with impaired glucose tolerance or diabetes.	Glucose	15-22	fibroblast growth factor 15	Mus musculus	0-5
22617565-5	2012	Its cognate receptor in the liver (FGFR4) mediated the effects of FGF19 on proliferation and bile salt synthesis, while this receptor was dispensable for its effects on glucose homeostasis.	Bile Acids and Salts	93-102	fibroblast growth factor 15	Mus musculus	66-71
22617565-7	2012	FGF19 signaling was shown to stimulate glycogen and protein synthesis, and inhibit gluconeogenesis.	Glycogen	39-47	fibroblast growth factor 15	Mus musculus	0-5
22617565-9	2012	Mice with genetic disruption of Fgf15 (the mouse FGF19 ortholog) were glucose intolerant but had normal insulin levels and normal insulin sensitivity.	Glucose	70-77	fibroblast growth factor 15	Mus musculus	32-37
22617565-9	2012	Mice with genetic disruption of Fgf15 (the mouse FGF19 ortholog) were glucose intolerant but had normal insulin levels and normal insulin sensitivity.	Glucose	70-77	fibroblast growth factor 15	Mus musculus	49-54
22457778-0	2012	Characterization of a FGF19 variant with altered receptor specificity revealed a central role for FGFR1c in the regulation of glucose metabolism.	Glucose	126-133	fibroblast growth factor 15	Mus musculus	22-27
22457778-7	2012	We show that FGF19-7 is equally efficacious as wild type FGF19 in regulating glucose, lipid, and energy metabolism in both diet-induced obesity and leptin-deficient mouse models.	Glucose	77-84	fibroblast growth factor 15	Mus musculus	13-18