PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30695317-9 2016 Large cholesterol-rich HDL2 is inversely associated with plasma TG and insulin resistance, whereas small cholesterol-poor HDL3 is not. Triglycerides 64-66 junctophilin 3 Homo sapiens 23-27 21251287-6 2011 Furthermore, despite of in the apoB-100/A-I < 0.9 group, the contents of prebeta1-HDL increased, and those of HDL2b decreased significantly for subjects in both high and very high TG levels compared to that in normal TG levels. Triglycerides 183-185 junctophilin 3 Homo sapiens 113-117 24972700-8 2015 In contrast, the same exercise training program was effective in increasing contents of cholesterol, triglyceride, and phospholipid in the HDL2 subfraction in the C-TR group (p = 0.036, ES = 2.06; p = 0.038, ES = 1.77; and p = 0.0021, ES = 2.37, respectively, within-group comparisons), whereas no changes were observed in the composition of the HDL3 subfraction. Triglycerides 101-113 junctophilin 3 Homo sapiens 139-143 25201260-9 2014 The HDL2-C/HDL3-C ratio exhibited moderate negative correlations with the body mass index, waist circumference, and triglyceride level. Triglycerides 116-128 junctophilin 3 Homo sapiens 4-8 23833575-8 2012 HDL mean particle size and HDL2/HDL3 ratio had negative correlation with body mass index (BMI), waist hip ratio (WHR), and serum triglyceride (TG) levels, and positive correlation with serum HDL-C levels. Triglycerides 129-141 junctophilin 3 Homo sapiens 27-31 23833575-8 2012 HDL mean particle size and HDL2/HDL3 ratio had negative correlation with body mass index (BMI), waist hip ratio (WHR), and serum triglyceride (TG) levels, and positive correlation with serum HDL-C levels. Triglycerides 143-145 junctophilin 3 Homo sapiens 27-31 22659528-7 2012 Additionally, HDL2-C was more closely correlated than total HDL-C or HDL3-C with sdLDL-C, LDL-C, triglycerides (TG), and apolipoprotein B (apoB). Triglycerides 97-110 junctophilin 3 Homo sapiens 14-18 22659528-7 2012 Additionally, HDL2-C was more closely correlated than total HDL-C or HDL3-C with sdLDL-C, LDL-C, triglycerides (TG), and apolipoprotein B (apoB). Triglycerides 112-114 junctophilin 3 Homo sapiens 14-18 21251287-6 2011 Furthermore, despite of in the apoB-100/A-I < 0.9 group, the contents of prebeta1-HDL increased, and those of HDL2b decreased significantly for subjects in both high and very high TG levels compared to that in normal TG levels. Triglycerides 220-222 junctophilin 3 Homo sapiens 113-117 15277993-11 2004 Increases in HDL2-unesterified cholesterol (UC) and HDL3-UC were obtained at T2 and T3 (P<0.05), and high HDL2-triacylglycerols (TG) and HDL3-TG were noted at T1, T2, and T3 (P<0.001). Triglycerides 114-130 junctophilin 3 Homo sapiens 109-113 19287187-5 2009 LDL and HDL2 fraction of the MI group were more enriched with TG than those of AP group. Triglycerides 62-64 junctophilin 3 Homo sapiens 8-12 17311515-7 2007 The latter was positively correlated with HDL2 triglycerides and negatively with HDL3 total cholesterol. Triglycerides 47-60 junctophilin 3 Homo sapiens 42-46 16721834-4 2006 Their fasting plasma lipid, lipoproteins, apolipoproteins, and the cholesterol and triglyceride concentrations in HDL2 and HDL3, isolated by microultracentrifugation, were determined by enzymatic-colorimetric methods. Triglycerides 83-95 junctophilin 3 Homo sapiens 114-118 16721834-6 2006 HDL2 triglyceride levels (HDL2Tg) in men were 1-26 mg/dL and in women 2-28 mg/dL; moreover, the HDL3 triglyceride (HDL3Tg) intervals were established as 4-46 mg/dL for both sexes. Triglycerides 5-17 junctophilin 3 Homo sapiens 0-4 15733886-7 2005 CONCLUSIONS: These results indicate that menopausal status not only increases plasma LDL-cholesterol and triglyceride levels, but also increases the HDL2/HDL3 ratio when associated with elevation of plasma triglyceride levels. Triglycerides 206-218 junctophilin 3 Homo sapiens 149-153 16024023-9 2006 Postprandial cholesteryl ester/triglyceride ratios were lower in VLDL1 and VLDL2 and higher in HDL2 following exercise. Triglycerides 31-43 junctophilin 3 Homo sapiens 95-99 12562872-6 2003 HDL2 stimulates HL-mediated hydrolysis of VLDL-triacylglycerol, while HDL3 is inhibitory. Triglycerides 47-62 junctophilin 3 Homo sapiens 0-4 12777471-8 2003 Multivariate regression analysis demonstrated that gender, HL activity, TG, and body mass index have independent contributions to HDL2 cholesterol levels. Triglycerides 72-74 junctophilin 3 Homo sapiens 130-134 12777471-9 2003 We suggest that in FCHL, TG enrichment of HDL particles and enhanced HL activity lead to the reduction of HDL cholesterol and HDL2 cholesterol. Triglycerides 25-27 junctophilin 3 Homo sapiens 126-130 12562872-8 2003 This study suggests that high HDL2 levels are positively related to efficient triacylglycerol hydrolysis by their ability to enhance the liberation of HL into the plasma compartment and by a direct stimulation of VLDL-triacylglycerol hydrolysis. Triglycerides 78-93 junctophilin 3 Homo sapiens 30-34 12562872-8 2003 This study suggests that high HDL2 levels are positively related to efficient triacylglycerol hydrolysis by their ability to enhance the liberation of HL into the plasma compartment and by a direct stimulation of VLDL-triacylglycerol hydrolysis. Triglycerides 218-233 junctophilin 3 Homo sapiens 30-34 10319421-4 1999 An increase in triglycerides and a decrease in HDL-cholesterol, especially in the HDL2 subfraction, were observed in patients with breast cancer. Triglycerides 15-28 junctophilin 3 Homo sapiens 82-86 11678968-5 2001 Age and HbA1c adjusted values of triglyceride, total cholesterol, LDL-C, HDL-C and HDL3-C in men and triglyceride and HDL2-C in women showed significant associations with central obesity, measured as the waist to hip ratio (WHR). Triglycerides 101-113 junctophilin 3 Homo sapiens 118-122 10781640-6 2000 Estrogen and combination therapy significantly increased the levels of cholesterol in the HDL2 subfraction, triglyceride in the HDL2 and HDL3 subfractions, and apolipoprotein A-I and A-II. Triglycerides 108-120 junctophilin 3 Homo sapiens 128-132 10421991-5 1999 The main quantitative abnormalities are increased triglyceride levels related to elevated VLDL and IDL and decreased HDL-cholesterol levels due to a drop in the HDL2 subfraction. Triglycerides 50-62 junctophilin 3 Homo sapiens 161-165 9778375-8 1998 First, while triglyceride rich HDL2 particles were able to bind only the low-affinity binding sites, the remaining particle generated after hepatic lipase lipolysis the remnant HDL2 was further able to bind to the high-affinity binding sites. Triglycerides 13-25 junctophilin 3 Homo sapiens 31-35 9859151-5 1998 RESULTS: Most of the measured parameters were significantly higher in patients receiving carbamazepine or phenytoin; carbamazepine-treated subjects showed specifically an increase in HDL2 lipoprotein cholesterol, whereas phenytoin-treated subjects showed specifically an increase of triglycerides; all of the observed alterations, save the increase in HDL lipoprotein cholesterol and apolipoprotein A1, were significant in women but not in men. Triglycerides 283-296 junctophilin 3 Homo sapiens 183-187 9778375-12 1998 Second, following binding on those two binding sites, the remnant HDL2 were faster internalized and in higher amounts than the native triglyceride rich HDL2. Triglycerides 134-146 junctophilin 3 Homo sapiens 66-70 9778375-12 1998 Second, following binding on those two binding sites, the remnant HDL2 were faster internalized and in higher amounts than the native triglyceride rich HDL2. Triglycerides 134-146 junctophilin 3 Homo sapiens 152-156 8761524-7 1996 In serum, total phospholipids and HDL2 components (cholesterol, phospholipids and protein) were higher in persons with high HDL, whereas non-esterified fatty acids (NEFA) and very low density lipoprotein (VLDL) components (triglycerides, cholesterol, phospholipids and protein) were lower. Triglycerides 223-236 junctophilin 3 Homo sapiens 34-38 9568735-8 1998 In control subjects the triglyceride levels increased in both HDL2 (0.10+/-0.06-0.17+/-0.06 mmol/l; P=0.0005) and to a lesser extent in HDL3 (0.10+/-0.03-0.12+/-0.02 mmol/l, P=0.0017). Triglycerides 24-36 junctophilin 3 Homo sapiens 62-66 9425934-9 1998 Because this observed relative increase in larger cholesteryl ester-rich HDL particles (HDL2) may result from inhibition of cholesteryl ester-triglyceride transfer processes, cholesteryl ester transfer protein activity was assayed. Triglycerides 142-154 junctophilin 3 Homo sapiens 88-92 9101097-5 1997 The plasma concentration of triglycerides was 46% higher in patients during the acute phase of Kawasaki disease than in the control subjects, which may be ascribed to the increase of triglycerides in very low density lipoprotein (VLDL), low density lipoprotein (LDL) and HDL2. Triglycerides 28-41 junctophilin 3 Homo sapiens 271-275 9101097-8 1997 Furthermore, the levels of cholesterol, apoA-I and apoA-II in HDL2, but not in HDL3, were inversely correlated with the levels of triglyceride. Triglycerides 130-142 junctophilin 3 Homo sapiens 62-66 8979650-9 1996 Additionally, the total area under the TG curve was positively correlated with baseline TG concentrations (r = 0.53) and inversely correlated with baseline HDL2 concentrations (r = 0.64). Triglycerides 39-41 junctophilin 3 Homo sapiens 156-160 8692021-7 1996 KT-R, in contrast, showed no changes in lipoprotein surface composition but a substantial triglyceride enrichment of HDL2 as compared with PKT-R and healthy controls (both P < .05). Triglycerides 90-102 junctophilin 3 Homo sapiens 117-121 8692021-11 1996 We explain the increase in HDL2 cholesterol and LDL size in PKT-R by their high lipoprotein lipase (LPL) activity conferring an excellent capacity to clear chylomicron triglycerides. Triglycerides 168-181 junctophilin 3 Homo sapiens 27-31 7728839-11 1995 Besides decreasing triglycerides, it increases significantly HDL-2 cholesterol. Triglycerides 19-32 junctophilin 3 Homo sapiens 61-66 8743899-2 1996 Hepatic lipase plays a central role in the hydrolysis of HDL2 triglycerides and phospholipids and in the concomitant apolipoprotein A-I efflux from this density class. Triglycerides 62-75 junctophilin 3 Homo sapiens 57-61 8548415-6 1996 In contrast, the relationship between fibrinogen and HDL2 cholesterol was primarily influenced by triglycerides and cholesterol and not independently influenced by fibrinogen. Triglycerides 98-111 junctophilin 3 Homo sapiens 53-57 7551826-9 1995 In the latter group, the labeled HDL2/HDL3 ratio was increased, indicating a more complete conversion that was correlated with the triglyceride/cholesterol ester ratio in HDL. Triglycerides 131-143 junctophilin 3 Homo sapiens 33-37 7857379-4 1994 Rapid lipolysis of TG-rich lipoproteins produces increased lipid uptake, formation of HDL2 and may protect the arterial wall; delayed lipolysis increases transfer of TG from TG-rich lipoproteins into HDL. Triglycerides 19-21 junctophilin 3 Homo sapiens 86-90 7775869-7 1995 Both HDL2 and HDL3 particles in group 1 were significantly depleted of unesterified cholesterol, and their HDL2 was TG-enriched (P = 0.053). Triglycerides 116-118 junctophilin 3 Homo sapiens 107-111 7822240-5 1994 Apolipoprotein (apo) E-free HDL2 from the patients, separated by heparin-Sepharose column chromatography, was rich in CE, poor in triglycerides (TG), and enlarged in size on 4-30% nondenaturing polyacrylamide gradient gel electrophoresis. Triglycerides 130-143 junctophilin 3 Homo sapiens 28-32 7822240-5 1994 Apolipoprotein (apo) E-free HDL2 from the patients, separated by heparin-Sepharose column chromatography, was rich in CE, poor in triglycerides (TG), and enlarged in size on 4-30% nondenaturing polyacrylamide gradient gel electrophoresis. Triglycerides 145-147 junctophilin 3 Homo sapiens 28-32 8147032-6 1993 It is concluded that there are metabolic relations between the observed low HDL2 cholesterol concentrations in the group of older subjects and in patients with arteriosclerotic diseases and the high magnitude of HDL triglyceride increase in the postprandial state which are relevant within the risk syndrome hypertriglyceridaemia-low HDL2 levels. Triglycerides 216-228 junctophilin 3 Homo sapiens 76-80 7907227-7 1994 Multivariate analysis demonstrated that the TaqI B polymorphism had an effect on HDL cholesterol and HDL2 that was independent of age, sex, body mass index, oral contraceptive use, exercise, alcohol consumption, and plasma triglycerides. Triglycerides 223-236 junctophilin 3 Homo sapiens 101-105 7907227-9 1994 We conclude that the TaqI B RFLP is associated with a quantitatively significant effect on plasma HDL2 levels that is independent of plasma triglycerides and interacts with lifestyle factors. Triglycerides 140-153 junctophilin 3 Homo sapiens 98-102 8139473-6 1994 The magnitude of the PP triglyceridemic area showed a negative correlation with HDL2 cholesterol (r = .66, P < .001) and a positive correlation with PP HDL2 TG enrichment (r = .80, P < .001). Triglycerides 160-162 junctophilin 3 Homo sapiens 155-159 8147032-6 1993 It is concluded that there are metabolic relations between the observed low HDL2 cholesterol concentrations in the group of older subjects and in patients with arteriosclerotic diseases and the high magnitude of HDL triglyceride increase in the postprandial state which are relevant within the risk syndrome hypertriglyceridaemia-low HDL2 levels. Triglycerides 216-228 junctophilin 3 Homo sapiens 334-338 1501422-7 1992 HDL2 cholesterol was associated positively with LPL and negatively with VLDL triglyceride in the model. Triglycerides 77-89 junctophilin 3 Homo sapiens 0-4 8272699-13 1993 Triglycerides lower HDL2 levels and thereby exert indirect atherogenicity. Triglycerides 0-13 junctophilin 3 Homo sapiens 20-24 8111077-6 1993 With improving metabolic control HDL2 lipid levels increased more than twofold and the compositional changes in HDL2 were reflected by an increased apo A-I:apo A-II ratio (P < 0.05) and a decreased triglyceride:apo A-I ratio (P < 0.05). Triglycerides 201-213 junctophilin 3 Homo sapiens 112-116 8215234-10 1993 HDL2 cholesterol levels were negatively correlated with HL, posthepatic plasma lipolytic activity, sigma glucose, plasma triglycerides and BMI. Triglycerides 121-134 junctophilin 3 Homo sapiens 0-4 1452137-5 1992 HTG HDL2 and HDL3 were rich in TG. Triglycerides 1-3 junctophilin 3 Homo sapiens 4-8 8432854-3 1993 The carriers" impaired triglyceride tolerance, as evident in the postprandial state of challenge only, was associated with a fasting lipoprotein constellation characterized by (a) enrichment of HDL2 with triglycerides, (b) reduced HDL2-cholesterol, (c) enrichment of VLDL and intermediate density lipoprotein (IDL) with cholesteryl esters, (d) elevated IDL levels, and (e) small-sized LDL. Triglycerides 23-35 junctophilin 3 Homo sapiens 194-198 8432854-3 1993 The carriers" impaired triglyceride tolerance, as evident in the postprandial state of challenge only, was associated with a fasting lipoprotein constellation characterized by (a) enrichment of HDL2 with triglycerides, (b) reduced HDL2-cholesterol, (c) enrichment of VLDL and intermediate density lipoprotein (IDL) with cholesteryl esters, (d) elevated IDL levels, and (e) small-sized LDL. Triglycerides 23-35 junctophilin 3 Homo sapiens 231-235 8432854-3 1993 The carriers" impaired triglyceride tolerance, as evident in the postprandial state of challenge only, was associated with a fasting lipoprotein constellation characterized by (a) enrichment of HDL2 with triglycerides, (b) reduced HDL2-cholesterol, (c) enrichment of VLDL and intermediate density lipoprotein (IDL) with cholesteryl esters, (d) elevated IDL levels, and (e) small-sized LDL. Triglycerides 204-217 junctophilin 3 Homo sapiens 194-198 1961121-6 1991 After omega-3 supplementation, both HDL2 and HDL3 became cholesteryl ester (CE)- and TG-enriched and free cholesterol (FC)- and phospholipid (PL)-depleted. Triglycerides 85-87 junctophilin 3 Homo sapiens 36-40 1845100-2 1991 Risk associated to increased triglyceride levels (above 200 mg/dl) must be judged in relation to associated factors such as family history of coronary heart disease, presence of remnants (type III hyperlipidemia), presence of Lp(a), increased levels of Apo B, reduced levels of HDL2 or Apo A1. Triglycerides 29-41 junctophilin 3 Homo sapiens 278-282 1856575-5 1991 Moreover, their very-low-density lipoprotein (VLDL) and HDL2 tended to have reduced amounts of free (unesterified) cholesterol (FC) relative to lecithin, and their HDL2 and HDL3 tended to be triglyceride enriched. Triglycerides 191-203 junctophilin 3 Homo sapiens 56-60 1856575-5 1991 Moreover, their very-low-density lipoprotein (VLDL) and HDL2 tended to have reduced amounts of free (unesterified) cholesterol (FC) relative to lecithin, and their HDL2 and HDL3 tended to be triglyceride enriched. Triglycerides 191-203 junctophilin 3 Homo sapiens 164-168 2060089-5 1991 Adjustments for obesity, ischemic heart disease, other cardiovascular disease, maximal oxygen uptake, systolic blood pressure, antihypertensive medication, serum low density lipoprotein cholesterol, and triglyceride concentrations reduced the excess risks associated with serum HDL, HDL2, and HDL3 cholesterol in the lowest quartiles by 52%, 48%, and 41%, respectively. Triglycerides 203-215 junctophilin 3 Homo sapiens 283-287 2180397-6 1990 Lipoprotein core lipid abnormalities were also present before treatment: the TG/cholesteryl ester ratio was reduced in VLDL and increased in LDL, HDL2, and HDL3. Triglycerides 77-79 junctophilin 3 Homo sapiens 146-150 1884874-6 1991 Through the action of cholesterol ester transfer protein, HDL2 become enriched in triglycerides and transfer cholesterol esters to LDL. Triglycerides 82-95 junctophilin 3 Homo sapiens 58-62 2244851-7 1990 The DZ/MZ variance ratio decreased 9% after adjustment of HDL2 for correlations with plasma triglycerides, alcohol consumption, smoking, exercise, and body mass index measured at the third exam. Triglycerides 92-105 junctophilin 3 Homo sapiens 58-62 2397247-9 1990 The number of phosphatidylethanolamine molecules hydrolysed exceeded that of triacylglycerol by 30% in HDL2 and by 70% in HDL3. Triglycerides 77-92 junctophilin 3 Homo sapiens 103-107 2242098-8 1990 Multiple partial correlation analysis demonstrated, however, that the nicotinic acid induced increase in HDL-2b concentration showed a highly significant inverse correlation to the decrease in LDL cholesterol, but not to the decrease in VLDL triglyceride levels. Triglycerides 242-254 junctophilin 3 Homo sapiens 105-110 2397247-10 1990 HDL2 were 2- and 4-times more reactive than HDL3 for the hydrolysis of phosphatidylethanolamine and triacylglycerol, respectively, taking the Vmax/Km ratio as an indicator of catalytic efficiency. Triglycerides 100-115 junctophilin 3 Homo sapiens 0-4 2680233-10 1989 Analysis of variance revealed that differences in gender and triacylglycerol concentrations were the most important determinants of HDL and HDL2 cholesterol levels. Triglycerides 61-76 junctophilin 3 Homo sapiens 140-144 2327147-2 1990 A decrease of HDL- and HDL2-cholesterol levels and an increase of HDL- and HDL2-triglyceride concentrations are seen in the group of older persons. Triglycerides 80-92 junctophilin 3 Homo sapiens 75-79 2327147-4 1990 The content of triglycerides and the relation triglyceride/cholesterol of the subfraction HDL2, but not of HDL3, show positive correlations with the level of serum triglycerides. Triglycerides 15-28 junctophilin 3 Homo sapiens 90-94 2327147-4 1990 The content of triglycerides and the relation triglyceride/cholesterol of the subfraction HDL2, but not of HDL3, show positive correlations with the level of serum triglycerides. Triglycerides 15-27 junctophilin 3 Homo sapiens 90-94 2327147-4 1990 The content of triglycerides and the relation triglyceride/cholesterol of the subfraction HDL2, but not of HDL3, show positive correlations with the level of serum triglycerides. Triglycerides 164-177 junctophilin 3 Homo sapiens 90-94 3178932-4 1988 The decrease was most marked in the HDL2 subfraction in which cholesterol and protein contents were decreased by 50%; it was independent of triglyceride levels and not related to the severity of overweight. Triglycerides 140-152 junctophilin 3 Homo sapiens 36-40 3150123-5 1988 The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. Triglycerides 4-16 junctophilin 3 Homo sapiens 28-32 3150123-5 1988 The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. Triglycerides 70-83 junctophilin 3 Homo sapiens 28-32 2769073-4 1989 Similarly, although triglyceride enrichment of VLDL, LDL, HDL2, and HDL3 with a concomitant reduction of cholesteryl esters from all particles except HDL2 was observed in both CF groups, it was more sizable in the EFAD patients. Triglycerides 20-32 junctophilin 3 Homo sapiens 58-62 3145749-10 1988 Both uremic HDL2 and HDL3 were relatively enriched in TG, and uremic HDL3 were poorer in EC than normal HDL3. Triglycerides 54-56 junctophilin 3 Homo sapiens 12-16 3145750-6 1988 HDL2 as well as triglyceride, phospholipid, free cholesterol and protein within the HDL2 increased, while HDL3 decreased. Triglycerides 16-28 junctophilin 3 Homo sapiens 84-88 3608116-5 1987 Serum triglycerides were inversely related to both HDL2-C and HDL3-C only in white children (p less than .001). Triglycerides 6-19 junctophilin 3 Homo sapiens 51-55 3392355-7 1988 Levels of triglycerides (TG) were slightly reduced in HDL2 but showed a greater reduction in HDL3 in both diets. Triglycerides 10-23 junctophilin 3 Homo sapiens 54-58 3392355-7 1988 Levels of triglycerides (TG) were slightly reduced in HDL2 but showed a greater reduction in HDL3 in both diets. Triglycerides 25-27 junctophilin 3 Homo sapiens 54-58 3391217-7 1988 TG and CHOL in the VLDL, IDL, LDL, and CHOL in HDL2, but not HDL3 were inversely correlated with the serum albumin level. Triglycerides 0-2 junctophilin 3 Homo sapiens 47-51 3330423-4 1987 In contrast, low LPL activity impedes the removal of triglyceride-rich particles, resulting in the elevation of serum triglycerides and a decrease of HDL (HDL2). Triglycerides 53-65 junctophilin 3 Homo sapiens 150-153 3330423-4 1987 In contrast, low LPL activity impedes the removal of triglyceride-rich particles, resulting in the elevation of serum triglycerides and a decrease of HDL (HDL2). Triglycerides 53-65 junctophilin 3 Homo sapiens 155-159 3409630-4 1988 Triglyceride (TG) levels increased by 180% 4-6 h after fat plus ethanol intake, the hypertriglyceridaemic response being inversely correlated with the basal HDL2 mass (r = -0.82). Triglycerides 0-12 junctophilin 3 Homo sapiens 157-161 3409630-4 1988 Triglyceride (TG) levels increased by 180% 4-6 h after fat plus ethanol intake, the hypertriglyceridaemic response being inversely correlated with the basal HDL2 mass (r = -0.82). Triglycerides 14-16 junctophilin 3 Homo sapiens 157-161 3608116-6 1987 A black-white difference in HDL2-C persisted only among boys and girls in the older age group after adjusting for the covariates (sexual maturation, age, adiposity, oral contraceptive use, cigarette smoking, alcohol use, and serum triglycerides). Triglycerides 231-244 junctophilin 3 Homo sapiens 28-32 3964341-6 1986 The HDL2 cholesterol, phospholipid and protein concentrations decreased in approximately similar proportions, whereas the HDL2 triglyceride increased by 40%. Triglycerides 127-139 junctophilin 3 Homo sapiens 122-126 3606461-3 1987 HDL2 showed an inverse relationship with cigarette consumption, body mass index, triglycerides, and systolic blood pressure and a positive relationship with age. Triglycerides 81-94 junctophilin 3 Homo sapiens 0-4 3730047-8 1986 There was a significant negative correlation between the concentrations of HDL2 cholesterol and VLDL triglyceride. Triglycerides 101-113 junctophilin 3 Homo sapiens 75-79 3746133-9 1986 Contraceptive steroids also caused a decrease in the HDL2/HDL3 cholesterol ratio (P less than 0.05), implying impaired peripheral lipoprotein triglyceride hydrolysis and/or increased HDL2 clearance by hepatic triglyceride lipase. Triglycerides 142-154 junctophilin 3 Homo sapiens 53-57 3957920-5 1986 In modified M-HDL2 or M-HDL3, triglyceride becomes the major core lipid as the triglyceride/cholesterol ester weight ratio increases 8-10-fold relative to native HDL. Triglycerides 30-42 junctophilin 3 Homo sapiens 14-18 3957920-5 1986 In modified M-HDL2 or M-HDL3, triglyceride becomes the major core lipid as the triglyceride/cholesterol ester weight ratio increases 8-10-fold relative to native HDL. Triglycerides 79-91 junctophilin 3 Homo sapiens 14-18 3957920-10 1986 After depletion of cholesterol ester from HDL, most but not all, exchanged triglyceride can be removed by lipolysis with either hepatic or lipoprotein lipase, resulting in a post-lipolysis HDL2 with an increased triglyceride content relative to normal HDL. Triglycerides 75-87 junctophilin 3 Homo sapiens 189-193 3957920-10 1986 After depletion of cholesterol ester from HDL, most but not all, exchanged triglyceride can be removed by lipolysis with either hepatic or lipoprotein lipase, resulting in a post-lipolysis HDL2 with an increased triglyceride content relative to normal HDL. Triglycerides 212-224 junctophilin 3 Homo sapiens 189-193 3957920-12 1986 After lipolysis of acquired triglyceride, HDL2 is remodeled, in both composition and flotation parameters, toward HDL3. Triglycerides 28-40 junctophilin 3 Homo sapiens 42-46 3544771-5 1987 Hepatic lipase has a central role in the removal of phospholipids and triglycerides from subfractions of high-density lipoprotein (HDL2) particles, but it may also function in the lipolysis of triglyceride-rich particles. Triglycerides 70-83 junctophilin 3 Homo sapiens 131-135 3544771-5 1987 Hepatic lipase has a central role in the removal of phospholipids and triglycerides from subfractions of high-density lipoprotein (HDL2) particles, but it may also function in the lipolysis of triglyceride-rich particles. Triglycerides 70-82 junctophilin 3 Homo sapiens 131-135 3767284-3 1986 HDL2 was found to show a stronger negative correlation with serum triglyceride and a stronger positive correlation with total HDL than HDL3. Triglycerides 66-78 junctophilin 3 Homo sapiens 0-4 6517974-8 1984 The per cent decrease in HDL2 cholesterol during abstinence was positively correlated to the respective fall of VLDL triglyceride fractional catabolic rate (r = +0.51). Triglycerides 117-129 junctophilin 3 Homo sapiens 25-29 2415036-4 1985 We have also shown that subjects with high serum triglyceride levels tend to have low plasma HDL2 concentrations, a finding which is consistent with an inverse relationship between these two parameters. Triglycerides 49-61 junctophilin 3 Homo sapiens 93-97 4026936-4 1985 It was also confirmed that the proportion of HDL subfraction 2 (HDL2) declines as the plasma triglyceride increases. Triglycerides 93-105 junctophilin 3 Homo sapiens 45-62 4026936-4 1985 It was also confirmed that the proportion of HDL subfraction 2 (HDL2) declines as the plasma triglyceride increases. Triglycerides 93-105 junctophilin 3 Homo sapiens 64-68 3935096-6 1985 In HDL2 the percentage content of cholesterol and triglyceride decreased, while that of phospholipid increased. Triglycerides 50-62 junctophilin 3 Homo sapiens 3-7 3973511-11 1985 The addition of increasing amounts of human HDL2 to the incubations caused the progressive dissociation of apoA-IV from the triglyceride-rich particles. Triglycerides 124-136 junctophilin 3 Homo sapiens 44-48 3705064-7 1986 In either HDL2 or HDL3, the percent content of triglyceride was higher and that of phospholipid was lower in survivors than in controls. Triglycerides 47-59 junctophilin 3 Homo sapiens 10-14 4063921-6 1985 Stratification of plasma triglyceride levels for all age groups showed that mean HDL2 levels decreased rapidly with moderate rises in triglyceride levels. Triglycerides 25-37 junctophilin 3 Homo sapiens 81-85 4063921-6 1985 Stratification of plasma triglyceride levels for all age groups showed that mean HDL2 levels decreased rapidly with moderate rises in triglyceride levels. Triglycerides 134-146 junctophilin 3 Homo sapiens 81-85 3969013-11 1985 The increment of HDL2 concentration was due to a rise of its triglycerides, phospholipids, and apoproteins A-I and A-II but not to a rise of cholesterol. Triglycerides 61-74 junctophilin 3 Homo sapiens 17-21 6697533-5 1984 The results obtained confirmed both the difference in HDL and particularly HDL2 levels between the sexes which other authors had observed with reference methods, and the significant negative correlation between plasma triglycerides and HDL2 levels. Triglycerides 218-231 junctophilin 3 Homo sapiens 236-240 6852443-5 1983 Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. Triglycerides 79-92 junctophilin 3 Homo sapiens 138-142 6651616-5 1983 The HDL2 triglyceride and phospholipids increased, while the HDL3 esterified cholesterol and protein decreased. Triglycerides 9-21 junctophilin 3 Homo sapiens 4-8 6365116-4 1983 Only HDL2-cholesterol, but not HDL3-cholesterol, raised; moreover, we found a significant inverse relationship between HDL-cholesterol (and also HDL2-cholesterol) and triglycerides. Triglycerides 167-180 junctophilin 3 Homo sapiens 145-149 7284422-1 1981 We studied the interaction of apolipoproteins A-I, C, and HDL2 with phospholipid-stabilized, triacylglycerol-rich particles to learn more about the molecular mechanisms that underlie the metabolism of chylomicrons. Triglycerides 93-108 junctophilin 3 Homo sapiens 58-62 6760874-6 1982 Among factors influencing serum HDL2-C concentration, the most important was the negative association with the level of very low density lipoprotein-triglycerides. Triglycerides 149-162 junctophilin 3 Homo sapiens 32-36 7284422-6 1981 Unexpectedly, previous binding of apolipoprotein A-I to triacylglycerol-rich particles nearly tripled the ability of these particles to bind apolipoprotein C. Destabilization of triacylglycerol-rich particles by apolipoprotein A-I was prevented by HDL2. Triglycerides 178-193 junctophilin 3 Homo sapiens 248-252 7421421-9 1980 There was also an inverse correlation between triglyceride concentration and HDL2. Triglycerides 46-58 junctophilin 3 Homo sapiens 77-81 7284053-3 1981 The results differ from other societies in which HDL2 concentration is lower in men than women, and are thought to provide further evidence for interaction between hormonal status and factors such as adiposity and triglyceride concentration with respect to HDL concentration. Triglycerides 214-226 junctophilin 3 Homo sapiens 49-53 33934596-9 2021 These results suggest that both apoC-II and apoC-III transfer disproportionately from VLDL to HDL2 and the larger HDL3, and these transfers might be involved in individual triglyceride metabolism. Triglycerides 172-184 junctophilin 3 Homo sapiens 94-98 27227658-6 2016 Pearson correlation analysis revealed that serum HDL2b level was negatively correlated with body mass index, waist circumference, waist-to-hip ratio, INS0, HOMA-IR, T, estradiol, triglyceride (TG) and low-density lipoprotein (LDL)-C; and the ratio of HDL2b/HDL was negatively correlated with T, TG and LDL-C. Stepwise multiple regression analyses showed a reverse correlation for HDL2b and its ratio to HDL with hyperandrogenism. Triglycerides 179-191 junctophilin 3 Homo sapiens 49-53 27227658-6 2016 Pearson correlation analysis revealed that serum HDL2b level was negatively correlated with body mass index, waist circumference, waist-to-hip ratio, INS0, HOMA-IR, T, estradiol, triglyceride (TG) and low-density lipoprotein (LDL)-C; and the ratio of HDL2b/HDL was negatively correlated with T, TG and LDL-C. Stepwise multiple regression analyses showed a reverse correlation for HDL2b and its ratio to HDL with hyperandrogenism. Triglycerides 193-195 junctophilin 3 Homo sapiens 49-53 27227658-6 2016 Pearson correlation analysis revealed that serum HDL2b level was negatively correlated with body mass index, waist circumference, waist-to-hip ratio, INS0, HOMA-IR, T, estradiol, triglyceride (TG) and low-density lipoprotein (LDL)-C; and the ratio of HDL2b/HDL was negatively correlated with T, TG and LDL-C. Stepwise multiple regression analyses showed a reverse correlation for HDL2b and its ratio to HDL with hyperandrogenism. Triglycerides 295-297 junctophilin 3 Homo sapiens 49-53 33515552-9 2021 HDL were TG enriched, CE depleted, and much smaller, causing the HDL3:HDL2 ratio to increase 3-fold. Triglycerides 9-11 junctophilin 3 Homo sapiens 70-74