PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16549444-0 2006 Triglyceride-rich HDL3 from patients with familial hypercholesterolemia are less able to inhibit cytokine release or to promote cholesterol efflux. Triglycerides 0-12 HDL3 Homo sapiens 18-22 17868679-0 2008 Metabolic syndrome features small, apolipoprotein A-I-poor, triglyceride-rich HDL3 particles with defective anti-apoptotic activity. Triglycerides 60-72 HDL3 Homo sapiens 78-82 16111685-7 2006 The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation. Triglycerides 149-161 HDL3 Homo sapiens 72-76 16111685-7 2006 The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation. Triglycerides 149-161 HDL3 Homo sapiens 117-121 16111685-7 2006 The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation. Triglycerides 149-161 HDL3 Homo sapiens 117-121 16111685-7 2006 The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation. Triglycerides 149-161 HDL3 Homo sapiens 117-121 16111685-7 2006 The results demonstrated that (i) E2 esterification occurring mainly in HDL3 was significantly more efficient in HTG-HDL3 compared to NTG-HDL3, (ii) triglyceride content in HDL3 correlated positively with E2 esterification rate, and (iii) addition of both exogenous LCAT and E2 into the incubation prolonged lag time of HDL3 oxidation. Triglycerides 149-161 HDL3 Homo sapiens 117-121 16549444-7 2006 In conclusion, compared with healthy controls, FH-patients are characterized by higher levels of low-grade proinflammatory markers, and FH-derived HDL3 with high triglyceride content may be more proatherogenic. Triglycerides 162-174 HDL3 Homo sapiens 147-151 16549444-8 2006 These triglyceride rich-HDL3 might be partly responsible for the phenotypic variation among FH-patients with identical LDL-receptor mutations. Triglycerides 6-18 HDL3 Homo sapiens 24-28 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 101-113 HDL3 Homo sapiens 96-100 15936009-9 2005 HDL3 isolated from FH with body mass index(BMI)>25 and from FH subjects with premature CAD contained higher content of triglycerides compared to the HDL3 from FH subjects with BMI<25 and without CAD, respectively. Triglycerides 122-135 HDL3 Homo sapiens 0-4 15231851-6 2004 CETP could also mediate the selective uptake of HDL3-derived triacylglycerol (TG) and phospholipid (PL). Triglycerides 61-76 HDL3 Homo sapiens 48-52 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 HDL3 Homo sapiens 154-158 12479869-5 2003 Therefore, we have studied the effect of HOCl on the function of HDL subclass 3 (HDL3) and triglyceride-enriched HDL3 (TG-HDL3) in PLTP-mediated processes in vitro. Triglycerides 91-103 HDL3 Homo sapiens 113-117 12479869-5 2003 Therefore, we have studied the effect of HOCl on the function of HDL subclass 3 (HDL3) and triglyceride-enriched HDL3 (TG-HDL3) in PLTP-mediated processes in vitro. Triglycerides 91-103 HDL3 Homo sapiens 113-117 12370852-7 2002 In univariate analyses, BMI significantly negatively correlated with HDL-C and HDL2-C. LCAT activity significantly positively correlated with HDL3-C, LDL-C, total cholesterol (TC) and triglycerides (TG). Triglycerides 199-201 HDL3 Homo sapiens 142-146 10488970-15 1999 In addition, higher levels of serum HDL3 triglyceride on lipid-lowering therapy (6 months) appear to be a common predictor of regression of Achilles" tendon xanthoma in the treatment with either pravastatin or probucol. Triglycerides 41-53 HDL3 Homo sapiens 36-40 8640403-7 1996 HDL3, particularly apoA-II-containing HDL3, reduced lipolysis of triglyceride and total fatty acid liberation in small VLDL. Triglycerides 65-77 HDL3 Homo sapiens 0-4 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 HDL3 Homo sapiens 136-140 9472977-6 1998 Fasting HDL was triglyceride-rich with a preponderance of HDL3, and became more enriched with triglycerides postprandially. Triglycerides 16-28 HDL3 Homo sapiens 58-62 8944748-3 1996 Following incubation with LPDP and TGRP, unmodified HDL3 are mainly converted into large, HDL2 particles (diameter: 9.90 +/- 0.07 nm), enriched in triglycerides and depleted of cholesteryl esters. Triglycerides 147-160 HDL3 Homo sapiens 52-56 8769365-4 1996 The composition of HDL, HDL2, and HDL3 was significantly altered in the postprandial state in IDDM subjects and controls with an increase in triglyceride content at 4 to 8 hours and a reciprocal decrease in cholesteryl ester, reflecting exchange of lipid constituents of HDL with triglyceride (TG)-rich lipoproteins. Triglycerides 141-153 HDL3 Homo sapiens 34-38 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 HDL3 Homo sapiens 38-42 8847483-7 1995 Even in the absence of VLDL, HDL3 continued to donate CE to LDL and HDL2 to almost the same degree as in intact plasma (plasma minus VLDL: 17.5 +/- 5.9 nmol/ml per h vs. intact plasma: 20.2 +/- 7.5 nmol/ml per h) without accepting any TG. Triglycerides 235-237 HDL3 Homo sapiens 29-33 7670941-10 1995 However, in heterozygotes the cholesterol-to-triglyceride ratios in VLDL2, LDL1, LDL3, HDL2b, HDL2a, and HDL3a were 8% to 54% lower than in unaffected family members (P < .05). Triglycerides 45-57 HDL3 Homo sapiens 105-109 8199177-6 1994 In the group with elevated plasma cholesterol and triglyceride, subjects possessing the 6.6-kbp allele exhibited a greater carotid artery intimal-medial thickness (P = .034) and higher plasma levels of apoA-I, high-density lipoprotein (HDL) cholesterol, and HDL3 cholesterol (P < .02) than subjects homozygous for the 8.3-kbp allele. Triglycerides 50-62 HDL3 Homo sapiens 258-262 7755644-9 1995 Furthermore, gemfibrozil increased HDL cholesterol (P < 0.05) and normalised the elevated HDL2 and HDL3 TG content. Triglycerides 107-109 HDL3 Homo sapiens 102-106 7942573-2 1994 Significant correlations emerged between body mass index and sum of glucose during oral glucose load and HDL3 triglycerides and also between visceral abdominal fat and triglycerides, apolipoprotein B, sum of insulin during oral glucose load, very-low-density-lipoprotein (VLDL) cholesterol, and VLDL and low-density-lipoprotein (LDL) triglycerides. Triglycerides 110-123 HDL3 Homo sapiens 105-109 1501422-8 1992 HDL3 cholesterol was associated positively with LPL, HTGL and LCAT and inversely with VLDL triglyceride. Triglycerides 91-103 HDL3 Homo sapiens 0-4 8169333-8 1994 Using multivariate analysis, both HDL2-C and HDL3-C (in females) were inversely correlated with triglyceride, body weight, and fasting insulin; HDL3-C was inversely correlated with central fat distribution in women. Triglycerides 96-108 HDL3 Homo sapiens 45-49 8306464-7 1993 The triglyceride percent content of LDL2 and HDL3 is increased, while that of esterified cholesterol is reduced in hypertriglyceridemic patients. Triglycerides 4-16 HDL3 Homo sapiens 45-49 8474323-10 1993 The major preprandial HDL subclass in HP subjects was HDL3, which showed a relative decrease in cholesterol esters (CE) and an increase in TG levels following the SFA meal. Triglycerides 139-141 HDL3 Homo sapiens 54-58 1402396-7 1992 Triglyceride transfer from triglyceride-rich lipoproteins to HDL2 and subsequent lipolysis by hepatic lipase are thought to mediate the conversion of HDL2 into HDL3. Triglycerides 0-12 HDL3 Homo sapiens 160-164 1613316-2 1992 At baseline the patients with familial hypercholesterolemia had a markedly reduced or missing HDL2 subfraction and their HDL3 was more dense with reduced content of cholesteryl ester and increased content of triglyceride compared with HDL of control subjects with normal lipid values. Triglycerides 208-220 HDL3 Homo sapiens 121-125 8354252-7 1993 In HDL3 the relative amounts of cholesterol increased (unesterified free cholesterol; FC) before vs 20 h after, P < 0.05; cholesterylester (CE), before vs 20 h after, P < 0.01) and TG and PL decreased (TG and PL, before vs 20 h after, P < 0.05). Triglycerides 187-189 HDL3 Homo sapiens 3-7 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 HDL3 Homo sapiens 45-49 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 HDL3 Homo sapiens 44-48 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 HDL3 Homo sapiens 173-177 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 HDL3 Homo sapiens 293-297 2044643-3 1991 HDL subfractions were only slightly modified, with an increase of dense, cholesteryl ester-enriched and triglyceride-poor HDL3 particles. Triglycerides 104-116 HDL3 Homo sapiens 122-126 2248619-6 1990 By contrast, triglyceridemia was negatively correlated with the HDL3 flotation rate, both in healthy subjects and coronary patients at all triglyceride levels. Triglycerides 13-25 HDL3 Homo sapiens 64-68 2115514-7 1990 Following transformation of the apoAIM homo- and heterodimers into their normal counterparts, i.e. monomeric apoAI and -AII, by reduction and carboxamidomethylation of AIM HDL3, the modified HDL3 behave like control HDL3 during incubation with lipoprotein-depleted plasma and triglyceride-rich particles. Triglycerides 276-288 HDL3 Homo sapiens 191-195 2115514-7 1990 Following transformation of the apoAIM homo- and heterodimers into their normal counterparts, i.e. monomeric apoAI and -AII, by reduction and carboxamidomethylation of AIM HDL3, the modified HDL3 behave like control HDL3 during incubation with lipoprotein-depleted plasma and triglyceride-rich particles. Triglycerides 276-288 HDL3 Homo sapiens 191-195 2930766-11 1989 Coincident with the hepatic lipase-induced hydrolysis of LDL and HDL triacylglycerol, there were marked reductions in the particle size of both lipoprotein fractions, which were now comparable to those of human LDL and HDL3, respectively. Triglycerides 69-84 HDL3 Homo sapiens 219-223 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 HDL3 Homo sapiens 156-160 2804054-6 1989 (2) HDL3 were modified in the presence of VLDL by inducing triacylglycerol lipolysis with a semipurified lipoprotein lipase from bovine milk. Triglycerides 59-74 HDL3 Homo sapiens 4-8 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 HDL3 Homo sapiens 68-72 2917147-8 1989 Lipolysis-modified HDL3 (LIP-HDL3) were mostly enriched in free cholesterol (+80%, P less than 0.05) and to a lesser extent in triacylglycerol (+33%). Triglycerides 127-142 HDL3 Homo sapiens 19-23 2917147-15 1989 The modified HDL3 (CET-HDL3) were depleted in esterified cholesterol (-25%, P less than 0.05) and enriched in triacylglycerol (+70%, P less than 0.05). Triglycerides 110-125 HDL3 Homo sapiens 13-17 2917147-7 1989 (2) HDL3 were modified in the presence of VLDL by inducing triacylglycerol lipolysis in VLDL with a semi-purified human plasma or bovine milk lipoprotein lipase (LPL). Triglycerides 59-74 HDL3 Homo sapiens 4-8 2917147-15 1989 The modified HDL3 (CET-HDL3) were depleted in esterified cholesterol (-25%, P less than 0.05) and enriched in triacylglycerol (+70%, P less than 0.05). Triglycerides 110-125 HDL3 Homo sapiens 19-27 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 HDL3 Homo sapiens 21-25 3145750-7 1988 An increase in HDL3 triglyceride was observed. Triglycerides 20-32 HDL3 Homo sapiens 15-19 3401291-6 1988 HDL3 was the only HDL population identified and was also triglyceride- and protein-rich and cholesteryl ester-poor. Triglycerides 57-69 HDL3 Homo sapiens 0-4 3150123-5 1988 The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. Triglycerides 4-16 HDL3 Homo sapiens 37-41 3150123-5 1988 The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. Triglycerides 70-83 HDL3 Homo sapiens 37-41 3126747-7 1988 The associations of HDL3 cholesterol and apo A-II with LCAT were strengthened when allowance was made by multiple regression for the effect of log plasma triglyceride; under these circumstances variation in LCAT explained statistically 8% of the variance in HDL3-cholesterol, and 10% of that in apo A-II. Triglycerides 154-166 HDL3 Homo sapiens 20-24 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 HDL3 Homo sapiens 93-97 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 HDL3 Homo sapiens 93-97 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 HDL3 Homo sapiens 62-66 3036237-4 1987 When the movement of cholesterol between cells and HDL3 particles was allowed to approach equilibrium, the lipid composition of HDL3 became an important factor in determining the net amount of cholesterol removed from cells, with cholesterol-deficient triacylglycerol-rich HDL3 particles having the best capacity to promote net transport of cholesterol from cells. Triglycerides 252-267 HDL3 Homo sapiens 128-132 3036237-4 1987 When the movement of cholesterol between cells and HDL3 particles was allowed to approach equilibrium, the lipid composition of HDL3 became an important factor in determining the net amount of cholesterol removed from cells, with cholesterol-deficient triacylglycerol-rich HDL3 particles having the best capacity to promote net transport of cholesterol from cells. Triglycerides 252-267 HDL3 Homo sapiens 128-132 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 HDL3 Homo sapiens 24-28 3606461-4 1987 HDL3 was negatively correlated with cigarette smoking, body mass index, and triglycerides and positively associated with exercise level and alcohol consumption. Triglycerides 76-89 HDL3 Homo sapiens 0-4 2897239-3 1987 The decrease in HDL triglycerides was a result of the decrease in HDL3 triglyceride levels. Triglycerides 20-33 HDL3 Homo sapiens 66-70 2897239-3 1987 The decrease in HDL triglycerides was a result of the decrease in HDL3 triglyceride levels. Triglycerides 20-32 HDL3 Homo sapiens 66-70 3559390-3 1986 On the other hand, HDL3 that had first been depleted of cholesteryl ester and enriched with triglyceride and phospholipid, during prior incubation with Intralipid and a source of lipid transfer protein, were much more susceptible to the action of hepatic lipase. Triglycerides 92-104 HDL3 Homo sapiens 19-23 3559390-4 1986 When these modified HDL3 were incubated with hepatic lipase there was a depletion of the triglyceride and phospholipid content and a conversion into much smaller particles the same size as those predominant in hypertriglyceridemic subjects. Triglycerides 89-101 HDL3 Homo sapiens 20-24 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 HDL3 Homo sapiens 24-28 3957920-12 1986 After lipolysis of acquired triglyceride, HDL2 is remodeled, in both composition and flotation parameters, toward HDL3. Triglycerides 28-40 HDL3 Homo sapiens 114-118 6413216-7 1983 Since te rise in HDL3-lipids follows the fall in serum TG, this provides further indication that the metabolism of these fractions in mutually related. Triglycerides 55-57 HDL3 Homo sapiens 17-21 3708859-4 1986 The triacylglycerol moieties of the HDL3 subfraction had a higher proportion of unsaturated fatty acyl components than HDL2, but there was no difference in the average chain length between the two subfractions. Triglycerides 4-19 HDL3 Homo sapiens 36-40 4026936-6 1985 At low concentrations of plasma triglyceride the predominant subpopulation of HDL3 comprised particles of mean radius 4.3 nm. Triglycerides 32-44 HDL3 Homo sapiens 78-82 4026936-7 1985 As the triglyceride concentration increased, however, there was a progressive appearance of HDL3 particles of radius 3.9 nm; in plasma samples with the highest concentrations of triglyceride there was an almost complete disappearance of the 4.3-nm particles, with the population of 3.9-nm particles now predominant. Triglycerides 7-19 HDL3 Homo sapiens 92-96 3964340-7 1986 The decrease of HDL2-C and HDL3-PL were significant also after allowance for the influences of obesity and triglyceride level. Triglycerides 107-119 HDL3 Homo sapiens 27-31 3964341-8 1986 Also in HDL3 the cholesterol, phospholipid and protein contents decreased to a similar extent but the triglyceride content rose. Triglycerides 102-114 HDL3 Homo sapiens 8-12 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 HDL3 Homo sapiens 18-22 6439739-9 1984 By contrast, a major fraction of triglyceride-richer pp-HDL2 was converted to particles with density, size, and apoprotein composition of native HDL3. Triglycerides 33-45 HDL3 Homo sapiens 145-149 7066084-5 1982 At higher concentrations of VLDL-triglyceride relative to HDL3-protein (1.8 or 2.4 mg of VLDL-triglyceride and 0.1 mg of HDL3-protein) the amount of lipid and apoprotein isolated in the HDL3 density fraction decreased after lipolysis and there was an increase in the amount isolated between d 1.063-1.120 g/ml. Triglycerides 33-45 HDL3 Homo sapiens 121-125 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 HDL3 Homo sapiens 104-108 6809752-6 1982 All the anomalous HDL3 particles are triglyceride enriched, with a decreased cholesterol ester content. Triglycerides 37-49 HDL3 Homo sapiens 18-22 7104306-4 1982 More than 90% of the [14C]cholesterol in donor HDL3 is transferred to LDL in a first-order process whose half-time is 2.9 min at 37 degrees C. This indicates that transfer of cholesterol molecules from the cholesterol ester/triglyceride core of HDL to the phospholipid/apoprotein monolayer at the surface of the particle is not rate limiting for exchange. Triglycerides 224-236 HDL3 Homo sapiens 47-51 7066084-5 1982 At higher concentrations of VLDL-triglyceride relative to HDL3-protein (1.8 or 2.4 mg of VLDL-triglyceride and 0.1 mg of HDL3-protein) the amount of lipid and apoprotein isolated in the HDL3 density fraction decreased after lipolysis and there was an increase in the amount isolated between d 1.063-1.120 g/ml. Triglycerides 33-45 HDL3 Homo sapiens 121-125 7426099-5 1980 An increase in phospholipid and triglyceride as well as a slight reduction in cholesterol was evident in HDL after 4.5 h. At the same time both lipids and proteins were decreased in HDL3 and increased in HDL2. Triglycerides 32-44 HDL3 Homo sapiens 105-108 221605-6 1979 HDL(3), which contain the main LCAT substrates, revealed increased triglycerides and generally reduced cholesteryl esters which were reciprocally correlated, demonstrating a phenomenon previously observed in vitro by others. Triglycerides 67-80 HDL3 Homo sapiens 0-5 24972700-6 2015 SLE patients showed significantly lower contents of Apo A-I, phospholipid, and triglyceride in the HDL3 subfraction (p < 0.05, between-group comparisons) than healthy controls at baseline. Triglycerides 79-91 HDL3 Homo sapiens 99-103 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 HDL3 Homo sapiens 114-118 33515552-9 2021 HDL were TG enriched, CE depleted, and much smaller, causing the HDL3:HDL2 ratio to increase 3-fold. Triglycerides 9-11 HDL3 Homo sapiens 65-69 32067428-5 2020 RESULTS: HDL3-C levels and HDL3-C proportion had a weak positive correlation with low-density lipoprotein cholesterol (LDL-C) and triglycerides (r=0.21, r=0.25; r=0.26, r=0.34, respectively, all P<0.001); in contrast, non-HDL3-C levels had a weak negative correlation with these parameters (r=-0.17 and r=-0.25, respectively, both P<0.005). Triglycerides 130-143 HDL3 Homo sapiens 9-13 32067428-5 2020 RESULTS: HDL3-C levels and HDL3-C proportion had a weak positive correlation with low-density lipoprotein cholesterol (LDL-C) and triglycerides (r=0.21, r=0.25; r=0.26, r=0.34, respectively, all P<0.001); in contrast, non-HDL3-C levels had a weak negative correlation with these parameters (r=-0.17 and r=-0.25, respectively, both P<0.005). Triglycerides 130-143 HDL3 Homo sapiens 27-31 32067428-5 2020 RESULTS: HDL3-C levels and HDL3-C proportion had a weak positive correlation with low-density lipoprotein cholesterol (LDL-C) and triglycerides (r=0.21, r=0.25; r=0.26, r=0.34, respectively, all P<0.001); in contrast, non-HDL3-C levels had a weak negative correlation with these parameters (r=-0.17 and r=-0.25, respectively, both P<0.005). Triglycerides 130-143 HDL3 Homo sapiens 27-31 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 HDL3 Homo sapiens 11-15 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 HDL3 Homo sapiens 32-36 24055774-4 2014 METHODS: Triglyceride (TG) rich lipoproteins (TRLs), low-density lipoprotein (LDL), HDL2, and HDL3 were used for screening of surfactants and enzymes to react selectively with HDL3-C and to decompose other lipoproteins. Triglycerides 9-21 HDL3 Homo sapiens 176-180 22234951-5 2012 In multivariate analysis, only plasma triglycerides and waist circumference remained independent predictors of HDL3c percentage. Triglycerides 38-51 HDL3 Homo sapiens 111-115