PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2507377-1	1989	Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation.	Glucose	210-217	interleukin 1 alpha	Homo sapiens	18-37	
2507377-1	1989	Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation.	Glucose	210-217	interleukin 1 alpha	Homo sapiens	39-43	
2507377-1	1989	Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation.	Glucose	254-261	interleukin 1 alpha	Homo sapiens	18-37	
2507377-1	1989	Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation.	Glucose	254-261	interleukin 1 alpha	Homo sapiens	39-43	
2507377-4	1989	Islets that had been pretreated with IL-1 for 18 h showed elevated rates of PGE2 production at basal (3-mM) and stimulatory (16.5-mM) glucose concentrations and converted exogenous arachidonic acid to PGE2 at twice the maximal rate of control islets.	Glucose	134-141	interleukin 1 alpha	Homo sapiens	37-41	
2668949-3	1989	In these animal models, a single injection of a low dose of human recombinant IL-1 normalized glucose blood levels for several hours.	Glucose	94-101	interleukin 1 alpha	Homo sapiens	78-82	
2666106-15	1989	These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism.	Glucose	93-100	interleukin 1 alpha	Homo sapiens	53-57	
2666106-17	1989	It is conceivable that the IL-1-induced suppression and shift in islet metabolism can be an explanation for the beta-cell insensitivity to glucose observed in the early phases of human and experimental insulin-dependent diabetes mellitus.	Glucose	139-146	interleukin 1 alpha	Homo sapiens	27-31	
2539976-0	1989	Interleukin-1 alpha exerts glucose-dependent stimulatory and inhibitory effects on islet cell phosphoinositide hydrolysis and insulin secretion.	Glucose	27-34	interleukin 1 alpha	Homo sapiens	0-19	
2539976-5	1989	1) In islets labeled for 2 h with [3H]inositol in the presence of 2.75 mM glucose, subsequent perifusion with 5.0 nM IL-1 increased insulin output, [3H]inositol efflux, and [3H]inositol phosphate accumulation in the simultaneous presence of 7 mM, but not 2.75 mM, glucose.	Glucose	264-271	interleukin 1 alpha	Homo sapiens	117-121	
2539976-6	1989	2) Mannoheptulose, a competitive inhibitor of islet glucokinase, blocked the stimulatory effects of IL-1 noted in the presence of 7 mM glucose.	Glucose	135-142	interleukin 1 alpha	Homo sapiens	100-104	
2539976-12	1989	6) These inhibitory effects of IL-1 were abolished if mannoheptulose was included during the 2-h incubation with 7 mM glucose plus 5.0 nM <protein-id="3605">IL-1.	Glucose	118-125	interleukin 1 alpha	Homo sapiens	31-35	
2539976-13	1989	7</protein-id>) The diacylglycerol kinase inhibitor 1-monooleoylglycerol (100 microM) significantly restored insulin output after IL-1 exposure (with 7 mM glucose).	Glucose	155-162	interleukin 1 alpha	Homo sapiens	130-134	
2539976-14	1989	8) Similar to the results obtained with 7 mM glucose plus IL-1, incubation of islets with 8-10 mM glucose alone produced dose-dependent impairments of [3H]inositol efflux patterns and inositol phosphate accumulation.	Glucose	98-105	interleukin 1 alpha	Homo sapiens	58-62	
2539976-16	1989	These results demonstrate that IL-1 has glucose-dependent stimulatory and inhibitory effects on beta-cell function.	Glucose	40-47	interleukin 1 alpha	Homo sapiens	31-35	
3308437-5	1987	IL-1 was found to reduce insulin release in culture and totally inhibit glucose-stimulated insulin release in short-term incubations.	Glucose	72-79	interleukin 1 alpha	Homo sapiens	0-4	
2689826-2	1989	Since an enhanced rate of whole-body glucose utilization is a consistent feature of the hypermetabolic phase of infection, the purpose of the present study was to determine whether IL-1 could increase glucose uptake and whether that increase was dependent on the concomitant elevation in plasma insulin.	Glucose	201-208	interleukin 1 alpha	Homo sapiens	181-185	
2689826-7	1989	SRIF prevented the IL-1 induced increase in insulin and tissue glucose utilization.	Glucose	63-70	interleukin 1 alpha	Homo sapiens	19-23	
2689826-9	1989	These data suggest that the administration of IL-1 increases organ glucose utilization by insulin-dependent mechanisms.	Glucose	67-74	interleukin 1 alpha	Homo sapiens	46-50	
3046964-4	1988	Several studies have convincingly demonstrated that IL-1 is a potent modulator of beta-cell function and can potentiate or inhibit glucose-induced insulin secretion, depending on the concentration and length of exposure to IL-1.	Glucose	131-138	interleukin 1 alpha	Homo sapiens	52-56	
3046964-4	1988	Several studies have convincingly demonstrated that IL-1 is a potent modulator of beta-cell function and can potentiate or inhibit glucose-induced insulin secretion, depending on the concentration and length of exposure to IL-1.	Glucose	131-138	interleukin 1 alpha	Homo sapiens	223-227	
3128273-1	1988	Recombinant-derived human interleukin 1 (IL1) alpha and beta and interferon gamma (IFN-gamma) each produced similar increases in rheumatoid synovial cell (RSC) glycolysis, as judged by increased values for glucose uptake, lactate production and cellular fructose 2,6-bisphosphate [Fru(2,6)P2].	Glucose	206-213	interleukin 1 alpha	Homo sapiens	26-51	
2783675-0	1989	Modification of tissue-factor mRNA and protein response to thrombin and interleukin 1 by high glucose in cultured human endothelial cells.	Glucose	94-101	interleukin 1 alpha	Homo sapiens	72-85	
2783675-6	1989	In contrast, the tissue-factor response to interleukin 1, a modulator of endothelial function in the context of host defense, was decreased in cells cultured in high glucose (P = .04).	Glucose	166-173	interleukin 1 alpha	Homo sapiens	43-56	
2783675-8	1989	The reciprocal effects of high glucose on the tissue-factor response to thrombin and interleukin 1 points to different pathways of tissue-factor stimulation by the two agents and suggests functional consequences pertinent to the increased thrombin activity and compromised host-defense mechanisms observed in diabetes.	Glucose	31-38	interleukin 1 alpha	Homo sapiens	85-98	
2510238-5	1989	Glycolysis, estimated by glucose utilisation and measurements of the glycolytic regulatory metabolite fructose 2,6-bisphosphate was significantly stimulated by TGF beta, IL-1 alpha and IFN-gamma, but less so by TGF alpha.	Glucose	25-32	interleukin 1 alpha	Homo sapiens	170-180	
3259727-0	1988	Cachectin/TNF and IL-1 induced by glucose-modified proteins: role in normal tissue remodeling.	Glucose	34-41	interleukin 1 alpha	Homo sapiens	18-22	
3308437-6	1987	Islet (pro)insulin biosynthesis, glucose oxidation, and oxygen uptake at 16.7 mM glucose were partially inhibited by IL-1.	Glucose	33-40	interleukin 1 alpha	Homo sapiens	117-121	
3093048-3	1986	In some cancer patients with weight loss there are many similarities to an interleukin-1 response including increases in resting energy expenditure, whole-body protein flux and synthesis and glucose flux and recycling, hypoalbuminemia and increased albumin catabolic rates, and an adaptive low T3 state that suggest a similar injury/infection response.	Glucose	191-198	interleukin 1 alpha	Homo sapiens	75-88	
3297891-1	1987	The effects of interleukin 1 (IL-1) on glucose-induced insulin secretion from isolated rat islets of Langerhans have been examined.	Glucose	39-46	interleukin 1 alpha	Homo sapiens	30-34	
3297891-9	1987	In addition to the inhibitory effects of IL-1 on glucose-induced insulin secretion, purified IL-1 and human rIL-1 had stimulatory effects on glucose-induced insulin secretion under the following conditions: a 90-min incubation with purified IL-1 (10% vol/vol) or in the presence of human rIL-1 (1400 pM) or a 15-h incubation with relatively low concentrations of human rIL-1 (0.5 or 5 pM).	Glucose	141-148	interleukin 1 alpha	Homo sapiens	93-97	
3297891-9	1987	In addition to the inhibitory effects of IL-1 on glucose-induced insulin secretion, purified IL-1 and human rIL-1 had stimulatory effects on glucose-induced insulin secretion under the following conditions: a 90-min incubation with purified IL-1 (10% vol/vol) or in the presence of human rIL-1 (1400 pM) or a 15-h incubation with relatively low concentrations of human rIL-1 (0.5 or 5 pM).	Glucose	141-148	interleukin 1 alpha	Homo sapiens	93-97	
33989405-7	2021	TNFalpha measurably increased secretion of IL-8 and IL-1beta, which was enhanced at 60 mM glucose.	Glucose	90-97	interleukin 1 alpha	Homo sapiens	52-60	
3514344-1	1986	Addition of highly purified human Interleukin-1 to the culture medium of isolated rat islets of Langerhans for 6 days led to 88% inhibition of glucose-induced insulin-release, reduction of islet contents of insulin and glucagon to 31% and 8% respectively, and disintegration of the islets.	Glucose	143-150	interleukin 1 alpha	Homo sapiens	34-47	
32968210-9	2021	Cultured human and mouse podocytes were treated with high glucose (30 mM), which significantly increased the expression levels of caspase-11 or caspase-4 (the homolog of caspase-11 in human), GSDMD-N, NF-kappaB, IL-1beta, and IL-18, and decreased the expression of nephrin and podocin.	Glucose	58-65	interleukin 1 alpha	Homo sapiens	212-220	
33979025-7	2021	Together, this suggests that the IL-1beta-stimulated energy shift is driven by shunting of glucose-derived pyruvate into mitochondria to maintain elevated oxygen consumption in HUVECs.	Glucose	91-98	interleukin 1 alpha	Homo sapiens	33-41	
33729569-10	2021	RESULTS: High glucose could induce IL-1beta-driven inflammatory responses in HGFs via the activation of NLRP3 inflammasome regulated by TLR2/TLR4 coupled ROS in NF-kappaB-dependent manner.	Glucose	14-21	interleukin 1 alpha	Homo sapiens	35-43	
33739224-8	2022	Logistic regression analysis identified the CC+CT genotype as an independent risk factor for the development of diabetes in patients with normal glucose metabolism (OR = 2.457, 95% CI: 1.238-4.877).Conclusions: The IL-1beta gene rs16944 C/T polymorphism may cause genetic susceptibility to T2DM in the Luzhou population.	Glucose	145-152	interleukin 1 alpha	Homo sapiens	215-223	
33729569-12	2021	CONCLUSION: Taiwanese green propolis could elicit protective effects against IL-1beta-driven inflammation in high glucose-exposed HGFs through TLR2/TLR4 combined ROS/NF-kappaB/NLRP3 inflammasome pathway.	Glucose	114-121	interleukin 1 alpha	Homo sapiens	77-85	
32908567-11	2020	There were medium-to-strong correlation between CML with SOD (r = 0.58, p < 0.05) and IL-1alpha with SOD (r = 0.70, p < 0.05) in well-controlled blood glucose.	Glucose	151-158	interleukin 1 alpha	Homo sapiens	86-95	
33629290-8	2021	RESULTS: HIF-1alpha and Runx2 were increased, and glucose uptake and ATP generation were decreased in the degenerative CHs from both OA and IL-1beta conditions.	Glucose	50-57	interleukin 1 alpha	Homo sapiens	140-148	
33354576-0	2020	Tangeretin Inhibition of High-Glucose-Induced IL-1beta, IL-6, TGF-beta1, and VEGF Expression in Human RPE Cells.	Glucose	30-37	interleukin 1 alpha	Homo sapiens	46-54	
33136275-7	2022	HBMVECs were injured by exposure to glucose and/or hypoxia, as assessed by release of LDH, interleukin (IL)-1beta, and reactive oxygen species (ROS).	Glucose	36-43	interleukin 1 alpha	Homo sapiens	91-113	
33655586-9	2021	After high glucose induction, the expression of TNF-alpha, IL-1beta, and IL-6 was increased and the expression of MCP-1, NLPR3, and ASC proteins was also increased (p < .001).	Glucose	11-18	interleukin 1 alpha	Homo sapiens	59-67	
32455427-4	2021	Specifically, we provide evidence that the key diabetogenic cytokine IL-1beta disrupts functionality of the beta cell circadian clock and impairs circadian regulation of glucose-stimulated insulin secretion.	Glucose	170-177	interleukin 1 alpha	Homo sapiens	69-77	
33038372-4	2020	KEY FINDINGS: Data indicated that high glucose increased the expression of interleukin-1beta (IL-1beta), an upstream regulator of nuclear factor-kappaB (NF-kappaB) pathway, through the nuclear localization of NF-kappaB.	Glucose	39-46	interleukin 1 alpha	Homo sapiens	94-102	
32699039-8	2020	CONCLUSION: In conclusion, we demonstrated that GLUT1-mediated glucose uptake is instrumental during the inflammatory IL-1beta response induced by MSU and CPP crystals.	Glucose	63-70	interleukin 1 alpha	Homo sapiens	118-126	
32806763-12	2020	RIH/glucose fluctuations also induced M1 polarization and an inflammatory profile (CD11c, IL-1beta, TNF-alpha, IL-6, and monocyte chemoattractant protein (MCP)-1) in macrophages.	Glucose	4-11	interleukin 1 alpha	Homo sapiens	90-98	
32561825-2	2020	At basal time, the T polymorphic allele of the rs16944 was associated with lower IL-1beta mRNA expression (p = 0.006); and higher glucose level was positive correlated to IL-1beta protein levels (p = 0.015).	Glucose	130-137	interleukin 1 alpha	Homo sapiens	171-179	
32650532-4	2020	Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D.	Glucose	125-132	interleukin 1 alpha	Homo sapiens	178-186	
32350565-11	2020	GPR44 inhibition antagonised the reduction in glucose-stimulated insulin secretion induced by HG and IL-1beta in human islets.	Glucose	46-53	interleukin 1 alpha	Homo sapiens	101-109	
32733443-0	2020	Glucose Induces IL-1alpha-Dependent Inflammation and Extracellular Matrix Proteins Expression and Deposition in Renal Tubular Epithelial Cells in Diabetic Kidney Disease.	Glucose	0-7	interleukin 1 alpha	Homo sapiens	16-25	
32733443-4	2020	Human proximal tubular kidney HK-2 cells exposed to high glucose (HG) gradually increase the expression of IL-1alpha but not IL-1beta and induce the expression and deposition of extracellular matrix (ECM) proteins.	Glucose	57-64	interleukin 1 alpha	Homo sapiens	107-116	
32733443-5	2020	We further demonstrate that in vitro ectopic addition of recombinant IL-1alpha in low glucose concentration leads to a similar effect as in HG, while supplementing excess amounts of IL-1Ra in HG significantly attenuates the ECM protein overexpression and deposition.	Glucose	86-93	interleukin 1 alpha	Homo sapiens	69-78	
32561825-4	2020	Surprisingly, we observed that the greater decreases in glucose level were associated to increased IL-1beta serum levels (p = 0.040).	Glucose	56-63	interleukin 1 alpha	Homo sapiens	99-107	
32439949-5	2020	An in vitro study indicated that high glucose increased IL-1beta and IL-18 expression and activated the NLRP3 inflammasome via upregulation of MARK4 in human umbilical vein endothelial cells (HUVECs).	Glucose	38-45	interleukin 1 alpha	Homo sapiens	56-64	
32587797-11	2020	Moreover, the highest ROS and the lowest insulin secretion were found in FAC combined with IL-1beta and TNF-alpha in the high-glucose condition of human pancreatic beta cell, which could be involved in the mechanism of DM development in beta-thalassemia patients.	Glucose	126-133	interleukin 1 alpha	Homo sapiens	91-99	
32028854-2	2020	Biological function experiments showed that miR-218 and inflammatory factors TNF-alpha and IL-1beta were highly expressed in renal proximal tubule under high-glucose conditions.	Glucose	158-165	interleukin 1 alpha	Homo sapiens	91-99	
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	173-180	interleukin 1 alpha	Homo sapiens	110-118	
32429534-9	2020	Finally, NTS and MSM inhibited the high glucose-induced expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha and binding of NF-kappaB protein to the DNA of proinflammatory cytokines.	Glucose	40-47	interleukin 1 alpha	Homo sapiens	70-92	
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	28-35	interleukin 1 alpha	Homo sapiens	110-118	
32197070-0	2020	Postprandial Hypoglycemia in Patients after Gastric Bypass Surgery Is Mediated by Glucose-Induced IL-1beta.	Glucose	82-89	interleukin 1 alpha	Homo sapiens	98-106	
32420343-6	2020	Our data showed that high glucose induced NLRP3-caspase-1-GSDMD activation and pore formation in a dose- and time-dependent manner (p < 0.05) and resulted in the inflammatory cytokines IL-1beta and IL-18 and lactate dehydrogenase (LDH) release from HRPs (p < 0.05), which are all signs of HRP pyroptosis.	Glucose	26-33	interleukin 1 alpha	Homo sapiens	185-193	
32550560-2	2020	In this study, we investigated whether high glucose and/or tumor necrosis factor (TNF) would enhance pro-inflammatory cytokine expression of tumor necrosis factor (TNF) and interleukin (IL)-1beta (IL1B) by altering histone modifications in U937, a juvenile macrophage cell line.	Glucose	44-51	interleukin 1 alpha	Homo sapiens	173-195	
32197070-7	2020	Our study proposes a role for glucose-induced IL-1beta in postprandial hypoglycemia after gastric bypass surgery and suggests that SGLT2-inhibitors and IL-1 antagonism may improve this condition.	Glucose	30-37	interleukin 1 alpha	Homo sapiens	46-54	
32197070-3	2020	Here, we hypothesized that glucose-induced IL-1beta leads to an exaggerated insulin response in this condition.	Glucose	27-34	interleukin 1 alpha	Homo sapiens	43-51	
32062019-7	2020	Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1beta pathway, which could be reversed by activated Nrf2-HO-1 pathway.	Glucose	31-38	interleukin 1 alpha	Homo sapiens	282-290	
31850631-4	2020	High levels of glucose, reactive oxygen species, and advanced glycation end-products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor-kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin-1.	Glucose	15-22	interleukin 1 alpha	Homo sapiens	273-286	
32209983-8	2020	IL-1beta secretion did not differ between conditions but was lower 60 min post-glucose ingestion compared to the fasting baseline (main effect of time, p = 0.014).	Glucose	79-86	interleukin 1 alpha	Homo sapiens	0-8	
31705795-0	2020	Allopurinol inhibits excess glucose-induced trophoblast IL-1beta and ROS production.	Glucose	28-35	interleukin 1 alpha	Homo sapiens	56-64	
31705795-2	2020	Using an in vitro model, we previously reported that hyperglycemic levels of glucose induced a pro-inflammatory (IL-1beta, IL-8, RANTES, GRO-alpha), anti-angiogenic (sFlt-1) and anti-migratory profile in a human trophoblast cell line.	Glucose	77-84	interleukin 1 alpha	Homo sapiens	113-121	
31705795-3	2020	The IL-1beta response to excess glucose was mediated by uric acid-induced activation of the NLRP3 inflammasome.	Glucose	32-39	interleukin 1 alpha	Homo sapiens	4-12	
31705795-5	2020	Thus, we sought to test the effects of allopurinol on the IL-1beta and other inflammatory, angiogenic and migratory responses that are triggered in the trophoblast by excess glucose.	Glucose	174-181	interleukin 1 alpha	Homo sapiens	58-66	
31705795-10	2020	Together, our findings indicate that the xanthine oxidase inhibitor allopurinol inhibited excess glucose-induced trophoblast IL-1beta secretion.	Glucose	97-104	interleukin 1 alpha	Homo sapiens	125-133	
31473434-7	2019	We found high glucose could increase Propidium Iodide (PI) positive cells and elevate release of lactate dehydrogenase (LDH), Interleukin 1 beta (IL-1beta) and Interleukin 18 (IL-18); protein levels of GSDMD, GSDMD N-terminal domain (GSDMD-N) and cleaved-caspase-1 were also elevated.	Glucose	14-21	interleukin 1 alpha	Homo sapiens	146-154	
31229280-10	2019	Co-incubation of high-glucose-treated endothelial cells with milk extracts from group S15 improved cell viability compared with cells treated with high glucose only; it also reduced intracellular lipid peroxidation (144.3 +- 0.4 vs. 177.5 +- 1.9%), reactive oxygen species (141.3 +- 0.9 vs. 189.3 +- 4.7 optical density units), and cytokine release (tumor necrosis factor-alpha, IL-1beta, IL-6).	Glucose	22-29	interleukin 1 alpha	Homo sapiens	379-387	
28553653-6	2017	Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha).	Glucose	116-123	interleukin 1 alpha	Homo sapiens	308-317	
31302140-7	2019	Notably, dulaglutide treatment suppressed high glucose- induced maturation of IL-1beta and IL-18.	Glucose	47-54	interleukin 1 alpha	Homo sapiens	78-86	
31485193-7	2019	In addition, levels of ROS, caspase1, and IL-1beta increased in a time- and dose-dependent manner in the high glucose group, even with an increased expression of LC3 (p < 0.01).	Glucose	110-117	interleukin 1 alpha	Homo sapiens	42-50	
30919933-7	2019	High levels of D-fructose compared to D-glucose led to activation of DCs in vitro by promoting interleukin (IL)-6 and IL-1beta production.	Glucose	40-47	interleukin 1 alpha	Homo sapiens	118-126	
31178664-5	2019	The results demonstrate that compared with the low-glucose culture, high glucose triggered higher cell death and increased IL-18 and IL-1beta mRNA expression and protein production.	Glucose	73-80	interleukin 1 alpha	Homo sapiens	133-141	
31178664-7	2019	Notably, NAC, a ROS scavenger, could attenuate high glucose-induced ROS formation and IL-18 and IL-1beta mRNA and protein expression and block inflammasome activation.	Glucose	52-59	interleukin 1 alpha	Homo sapiens	96-104	
31178664-9	2019	Intrudingly, H2S could ameliorate high glucose-induced ROS formation, IL-18 and IL-1beta expression, and inflammasome activation.	Glucose	39-46	interleukin 1 alpha	Homo sapiens	80-88	
29142506-8	2017	Glycated hemoglobin levels measured after 6-month glucose-lowering treatment appeared to be inversely correlated with plasma anti-IL1alpha IgG (r=-0.477, df=17, p=0.039) and anti-IL6 IgG (r=-0.519, df=17, p=0.023) although such correlation failed to survive the Bonferroni correction.	Glucose	50-57	interleukin 1 alpha	Homo sapiens	130-138	
20019678-7	2010	Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor.	Glucose	8-15	interleukin 1 alpha	Homo sapiens	83-92	
24588826-3	2014	These aspects are complementary because stimulatory actions of IL-1 may be due to its capacity to increase glucose uptake by immune cells in the periphery and to affect the control of glucose homeostasis at brain levels, so as to deviate this main fuel to immune cells during inflammatory and infectious diseases.	Glucose	107-114	interleukin 1 alpha	Homo sapiens	63-67	
21233852-4	2011	Preliminary results from clinical trials with salicylates and interleukin-1 antagonists support this notion and have opened the door for immunomodulatory strategies for the treatment of T2D that simultaneously lower blood glucose levels and potentially reduce the severity and prevalence of the associated complications of this disease.	Glucose	222-229	interleukin 1 alpha	Homo sapiens	62-75	
17189875-6	2007	Proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) also stimulated NF-kappaB-dependent transcription and showed an additive effect with high glucose.	Glucose	182-189	interleukin 1 alpha	Homo sapiens	34-79	
18290856-7	2008	RESULTS: Hyperglycaemia reduced LPS-induced mRNA expression of nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (NFKBIA), interleukin-1 alpha (IL1A) and chemokine (C-C motif) ligand 3 (CCL3), whereas during hyperinsulinaemia enhanced mRNA levels occurred in six out of eight measured inflammation-related genes, irrespective of plasma glucose levels.	Glucose	369-376	interleukin 1 alpha	Homo sapiens	177-181	
15070811-9	2004	We conclude that IL-1 cytokines can regulate cellular Glc phosphorylating capacity via an IL-1 receptor-, Ras-, and classic MAPK pathway-mediated increase in HKII abundance.	Glucose	54-57	interleukin 1 alpha	Homo sapiens	17-21	
16249450-0	2005	Is there a role for locally produced interleukin-1 in the deleterious effects of high glucose or the type 2 diabetes milieu to human pancreatic islets?	Glucose	86-93	interleukin 1 alpha	Homo sapiens	37-50	
15070811-9	2004	We conclude that IL-1 cytokines can regulate cellular Glc phosphorylating capacity via an IL-1 receptor-, Ras-, and classic MAPK pathway-mediated increase in HKII abundance.	Glucose	54-57	interleukin 1 alpha	Homo sapiens	90-94	
15001844-5	2004	Neu5Ac-Gal-IL-1alpha exhibited reduction in activities in vivo, including induction of serum amyloid A and NOx, and down-regulation of serum glucose.	Glucose	141-148	interleukin 1 alpha	Homo sapiens	11-20	
9151802-6	1997	The ability of IL-1 to upregulate Glut1 and Glut3 transcripts proved time-, dose-, nitric oxide-, and protein biosynthesis-dependent but glucose independent.	Glucose	137-144	interleukin 1 alpha	Homo sapiens	15-19	
9828188-4	1998	First, IL-1alpha was shown to increase the uptake of glucose substrate in a time- and dose-dependent manner.	Glucose	53-60	interleukin 1 alpha	Homo sapiens	7-16	
10506586-9	1999	When cells were incubated in 25 mM glucose to mimic the diabetic state, IL-1beta induction was inhibited in all cases, but to a significantly lesser extent with the 14-repeat allele.	Glucose	35-42	interleukin 1 alpha	Homo sapiens	72-80	
7487926-6	1995	These results imply that the activation of distinct MAP kinase pathways is required for the stimulation of glucose transport by IL1/anisomycin and IGF1 in KB cells, and suggest that the combined use of SB 203580 and PD 98059 is a powerful new approach to explore the roles of different MAP kinase cascades in cell regulation.	Glucose	107-114	interleukin 1 alpha	Homo sapiens	128-131	
1478189-2	1992	IL-1 significantly reduced serum insulin levels in ADX rats only, while it similarly decreased plasma glucose levels.	Glucose	102-109	interleukin 1 alpha	Homo sapiens	0-4	
1665456-3	1991	In perifused islets, insulin secretion in response to IL-1 in the presence of 7 mM glucose averaged 313 +/- 43 pg/islet/min 35-40 min after the onset of stimulation.	Glucose	83-90	interleukin 1 alpha	Homo sapiens	54-58	
1477295-0	1992	The effects of interleukin-1 on pancreatic beta cell function in vitro depend on the glucose concentration.	Glucose	85-92	interleukin 1 alpha	Homo sapiens	15-28	
1511500-5	1992	Thus, the inflammatory cytokines IL-1 and TNF alpha reportedly detected in the circulation during severe sepsis may directly affect not only glucose uptake but also its subsequent metabolism within tissue fibroblasts.	Glucose	141-148	interleukin 1 alpha	Homo sapiens	33-37	
1665456-1	1991	The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis.	Glucose	50-57	interleukin 1 alpha	Homo sapiens	13-32	
1665456-1	1991	The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis.	Glucose	50-57	interleukin 1 alpha	Homo sapiens	34-38	
1665456-6	1991	This level of IL-1 caused significant increases in inositol phosphate accumulation in the presence of 7 mM glucose but not 2.75 mM glucose.	Glucose	107-114	interleukin 1 alpha	Homo sapiens	14-18	
34576117-1	2021	We aimed to investigate the effect of acute glucose shift on the activation of the NLRP3 inflammasome, IL-1beta secretion, and underlying signaling pathways in THP-1 cells.	Glucose	44-51	interleukin 1 alpha	Homo sapiens	103-111	
34651203-15	2022	HIF-1 activation increased IL-1beta and IL-8 in human uroepithelial cells treated with high glucose concentration.	Glucose	92-99	interleukin 1 alpha	Homo sapiens	27-35	
34858390-4	2021	We now describe that the macrophage molecular clock, through Bmal1, regulates the uptake of glucose, its flux through glycolysis and the Krebs cycle, including the production of the metabolite succinate to drive Il-1beta production.	Glucose	92-99	interleukin 1 alpha	Homo sapiens	212-220	
34831052-3	2021	One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis.	Glucose	131-138	interleukin 1 alpha	Homo sapiens	150-154	
34402957-4	2021	Long-term exposure to high glucose significantly enhanced the increase in the production of pro-inflammatory cytokines, including tumor necrosis-alpha, interleukin (IL)-1beta, and IL-6, when macrophages were stimulated with LPS.	Glucose	27-34	interleukin 1 alpha	Homo sapiens	152-174	
34576117-6	2021	Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells.	Glucose	87-94	interleukin 1 alpha	Homo sapiens	111-119	
34139004-0	2021	Glucose regulates expression of pro-inflammatory genes IL-1beta and IL-12 through a mechanism involving hexosamine biosynthesis pathway dependent regulation of alphaEcatenin.	Glucose	0-7	interleukin 1 alpha	Homo sapiens	55-63	
34139004-7	2021	We find that the reduction of alpha-E catenin level using siRNA attenuates the glucose induced changes of both IL-1beta and IL-12 mRNA levels under LPS stimulated condition but does not affect TNF-alpha expression.	Glucose	79-86	interleukin 1 alpha	Homo sapiens	111-119	
34139004-8	2021	Together this indicates that alpha-E catenin can sense the changes in glucose levels in macrophages via hexosamine biosynthesis pathway and also can modulate the glucose induced gene expression of inflammatory markers such as IL-1beta and IL-12.	Glucose	162-169	interleukin 1 alpha	Homo sapiens	226-234	
34185112-6	2021	RESULTS: Compared with the high glucose group, the proliferation rate, migration rate, and the expression of alpha-SMA, bcl-2, TLR4, NF-kappaB, TNF-alpha, IL-6, IL- and IL-1 were significantly decreased in the high glucose + MSC-Exo-miR-26a mimics group, while the apoptosis rate and the expression of miR-26a, cleaved-caspase 3, cleaved-caspase 9 and Bax were significantly increased.	Glucose	215-222	interleukin 1 alpha	Homo sapiens	161-173	
34198548-3	2021	Macrophage-specific deletion of Glucose Transporter 1 (GLUT1) significantly reduced tumor burden, which was accompanied by increased Natural Killer and CD8+ T cell activity and suppression of the NLRP3-IL1beta inflammasome axis.	Glucose	32-39	interleukin 1 alpha	Homo sapiens	202-209	
34247997-0	2021	Association of IL-6 & IL-1beta (pro-inflammatory cytokines) and related biochemical indexes in newly diagnosed diabetics subjected to glucose tolerance test.	Glucose	134-141	interleukin 1 alpha	Homo sapiens	22-30	
35513427-4	2022	Stimulation of human mesangial cells with high glucose primed the inflammasome-driven interleukin 1 beta (IL-1beta) secretion, which in turn stimulated platelet-derived growth factor (PDGF-BB) release.	Glucose	47-54	interleukin 1 alpha	Homo sapiens	106-114