ライフサイエンスコーパス: triglyceride

1 = -0.25 with body mass index and -0.20 with triglycerides).

2 abolic disease (phosphatidylethanolamine and triglycerides).

3 neogenesis rather than being reesterified to triglyceride.

4 = 0.017) were independently associated with triglycerides.

5 ference, serum gamma-glutamyltransferase and triglycerides.

6 ell tolerated, without an increase in plasma triglycerides.

7 omarkers including serum LDL cholesterol and triglycerides.

8 sensitivity, and decreases plasma levels of triglycerides.

9 gh-density lipoprotein (HDL) cholesterol and triglycerides.

10 in oleic acid (OA, 18:1), diglycerides, and triglycerides.

11 ained stable after adjustments for LDL-C and triglycerides.

12 ucose, and an almost complete lack of stored triglycerides.

13 igh lipolysis, INSR subjects had low hepatic triglycerides (0.5% [interquartile range 0.1%-0.5%]), in

14 t on predictions (9.5% for glucose, 0.8% for triglyceride, 0.2% for C-peptide).

15 mean, %)) in postprandial responses of blood triglyceride (103%), glucose (68%) and insulin (59%) fol

16 signed statin-treated patients with elevated triglycerides (135-499 mg/dL), controlled low-density li

17 9%), insulin (20%), physical activity (15%), triglycerides (14%), and red meat consumption (7%). Conc

18 Those with FLD had higher median triglyceride (171 versus 100 mg/dL, P<.01) and sdLDL (44

19 ith obesity (2.29 [95% CI, 2.02-2.56]), high triglycerides (2.67 [95% CI, 2.38-2.95]), or low high-de

20 bition in lipo-toxicity by decreasing 40% of triglyceride, 30% of diacylglycerol and 50% of PKC level

21 uced ALT (mean 71.6 vs 44.6 IU/l, p < 0.01), triglycerides (38.8 vs 28.1 mg/dl, p < 0.05), LDL-C (39.

22 olesterol (220), apolipoprotein B (n = 255), triglycerides (440), HDL cholesterol (534), and apolipop

23 sterol, 1.19 (95% CI: 1.14 to 1.25) for VLDL triglycerides, 5.38 (95% CI: 3.73 to 7.75) for IDL chole

24 A), 3,4-DHBA, ribonic acid, ribitol, and the triglycerides 50:1 and 50:2 significantly correlated (P

25 rast, p16 overexpression was associated with triglyceride accumulation and increased lipid droplet nu

26 lipoprotein (LDL), high-density lipoprotein, triglycerides, alanine aminotransferase (ALT), and aspar

27 nsity lipoprotein, high-density lipoprotein, triglycerides, albumin excretion rate, and DCCT/EDIC mea

28 Notably, a decline in liver triglycerides alongside increased activities of NAD(P)H:

29 viability as well as internal LDs' protein, triglyceride and cholesterol level.

30 ysregulation in CD36KO mice, and circulating triglyceride and cholesterol levels in PPARalphaKO mice.

31 e visceral adipose tissue hydrolyzed adipose triglyceride and generated excess nonesterified fatty ac

32 by multiple mechanisms, hydrolyzing adipose triglyceride and generating excess NEFAs.

33 ate decreased the elevated hepatic and renal triglyceride and hepatic glycogen levels found in contro

34 omes were baseline and day 3 compliance with triglyceride and lipase laboratory monitoring per protoc

35 ort tool to enforce protocol compliance with triglyceride and lipase level monitoring and mitigate pr

36 ene ANGPTL4 for association with trait serum triglyceride and used ethnicity as a covariate.

37 iscontinuation of propofol in the setting of triglyceride and/or lipase levels exceeding protocol cut

38 , ~0.1 mmol/l higher non-HDL cholesterol and triglycerides and 0.2 mmol/l higher non-fasting glucose,

39 cg09637273) were associated with cord blood triglycerides and birth weight, respectively (FDR < 0.1)

40 re consistent with correspondingly increased triglycerides and cholesterol and altered expression of

41 studies indicate that circulating levels of triglycerides and cholesterol transported in triglycerid

42 lic risk (higher values of insulin, glucose, triglycerides and cholesterol).

43 ene significantly (p < 0.01) elevated plasma triglycerides and cholesterol, treatment with MSU-42011

44 lipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol levels, is a

45 ted hemoglobin (HbA1c), triglyceride levels, triglycerides and glucose (TyG) index, and TyG-WC decrea

46 ication and different ratios of medium-chain-triglycerides and glycerol monostearate (lipid phase) we

47 is as strongly related to genetic risk from triglycerides and HDL-C as from LDL-C.

48 ssociated with reciprocal genetic effects on triglycerides and HDL-C.

49 omic Epidemiology consortium, fasting plasma triglycerides and high- and low-density lipoprotein chol

50 ons in statin-treated patients with elevated triglycerides and increased cardiovascular risk.

51 Unsaturated triglycerides and phosphatidylethanolamines decreased in

52 While elevated triglycerides and prediabetes were more frequent among L

53 This study evaluated the association of triglycerides and remnant cholesterol (remnant-C) with m

54 jects at high cardiovascular risk, levels of triglycerides and remnant-C, but not LDL-C, were associa

55 Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate as

56 ities (low high-density lipoprotein and high triglycerides) and hypertension were both independently

57 body mass index (BMI), waist circumference, triglyceride, and gamma-glutamyl transferase (GGT).

58 mice had reduced weight gain, lowered serum triglyceride, and increased serum cholesterol levels and

59 ower diglycerides, lysophosphatidylcholines, triglycerides, and alanine before GADA-first.

60 nsity lipoprotein (LDL and HDL) cholesterol, triglycerides, and apolipoprotein A-I and B (apoA-I and

61 r low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B to identify lipid-as

62 sure, insulin resistance, total cholesterol, triglycerides, and C-reactive protein concentrations (P

63 pressure, LDL cholesterol, HDL cholesterol, triglycerides, and fasting glucose) to dietary fat.

64 es, including type 2 diabetes, low HDL, high triglycerides, and female-specific overweight and obesit

65 od pressure and higher levels of circulating triglycerides, and having lower levels of HDL cholestero

66 ty on 1-year change in BMI, fasting glucose, triglycerides, and HDL cholesterol in individuals random

67 high-density-lipoprotein cholesterol or high triglycerides, and high insulin concentrations.

68 ted increased body and liver weight, hepatic triglycerides, and inflammatory gene expression compared

69 PHIV had higher waist-hip ratio, triglycerides, and insulin resistance (P <= .03).

70 ers had higher BMI, higher concentrations of triglycerides, and lower insulin sensitivity compared wi

71 djustment for age, BMI, sex, CD4 cell count, triglycerides, and separately adding sCD163, sCD14, and

72 GL) in human pseudoislets (shATGL) increased triglycerides, and the number and size of LDs indicating

73 intracellular transport of FA, synthesis of triglycerides, and transcription factors.

74 % confidence interval [CI], 1.04-1.59), high triglycerides (aOR, 1.34; 95% CI, 1.11-1.63), and high A

75 fidence interval [CI], 1.10-3.20; P = 0.04), triglycerides (AOR, 2.84 per mmol/L; 95% CI, 1.06-4.35 p

76 Cholesterol and triglycerides are among the most well-known risk factors

77 alysis demonstrates that LDL cholesterol and triglycerides are associated with adverse changes in car

78 IL-6, CRP and triglycerides are likely to be causally linked with depr

79 In black women, triglycerides are paradoxically normal in the presence o

80 Triglycerides are the major form of stored fat in all an

81 VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids and at

82 r grade of DR in type 1 diabetes and several triglycerides being negatively correlated.

83 nificant associations were found for HDL and triglycerides (both p > 0.05).

84 umerous traditional risk factors (especially triglycerides), both associations were attenuated and on

85 storage and abolishes the sex difference in triglyceride breakdown via strongly male-biased effects.

86 This meant genotype-specific triglyceride changes could not move in parallel when tri

87 including lipoproteins (HDL, LDL), neutral (triglycerides, cholesterol) and polar lipids (sphingo- a

88 The milk and cheese diets increased triglycerides compared with the control diet (+9.9%, P =

89 L-C), and triglycerides, for cholesterol and triglycerides components of size-defined lipoprotein par

90 ipid droplets, by measurement of basolateral triglyceride concentration and by analysing the expressi

91 cg11250194 (FADS2) was associated with lower triglyceride concentrations (MR, P=1.5x10(-14)).and hype

92 )) for each one-percent decrement in fasting triglyceride concentrations, i.e., h(2) +/- SE were: 0.4

93 in glycated hemoglobin, HDL-cholesterol, or triglyceride concentrations.

94 (post-treatment) than higher (pre-treatment) triglyceride concentrations.

95 id solutions (nonhuman samples) with varying triglyceride content (145-19 000 mg/dL [1.64-214.7 mmol/

96 In vivo fat fraction was correlated with triglyceride content (r = 0.96, P < .001).

97 Fat fraction was correlated with triglyceride content (r = 0.96, P < .001).

98 wed that fat fraction values correlated with triglyceride content (r = 0.99, P < .001).

99 either of two BMP inhibitors reduced hepatic triglyceride content in diabetic (db/db) mice.

100 controls also had significant reductions in triglyceride content in the liver and skeletal muscle an

101 containing lipoproteins) and cholesterol and triglyceride content of VLDL, intermediate-density lipop

102 tended to decrease with elevation, and that triglyceride contents decreased with distance from the s

103 yceride levels necessarily created a greater triglyceride decrease for the genotype with a higher pre

104 l lipase (MGL) is the last enzymatic step in triglyceride degradation, hydrolyzing monoglycerides int

105 ew we define RLPs as postlipolytic partially triglyceride-depleted particles derived from chylomicron

106 Patients with elevated triglycerides despite statin therapy have increased risk

107 ing, and IDL + LDL cholesterol, whereas VLDL triglycerides did not enter the model.

108 d apoB-containing lipoproteins, whereas VLDL triglycerides did not explain risk.

109 m apoB-containing lipoproteins, whereas VLDL triglycerides did not explain risk.

110 demonstrated that saroglitazar also reduced triglycerides, diglycerides, sphingomyelins and ceramide

111 B, very-low-density lipoprotein cholesterol, triglycerides, diglycerides, total and monounsaturated f

112 5th, 50th, 25th, and 10th percentiles of the triglyceride distribution, respectively.

113 In fact, VSG corrected hepatic triglyceride dysregulation in CD36KO mice, and circulati

114 ted the hypothesis that VLDL cholesterol and triglycerides each explain part of the myocardial infarc

115 rial respiration, lipid droplet content, and triglyceride excretion.

116 tive, but not statistically significant, for triglycerides, fasting glucose, and non-HDL cholesterol.

117 sformed blood pressure, waist circumference, triglycerides, fasting glucose, and non-high-density lip

118 density lipoprotein cholesterol (LDL-C), and triglycerides, for cholesterol and triglycerides compone

119 le in preventing dyslipidemia by hydrolyzing triglycerides from packaged lipoproteins.

120 asma due to a reduced level of VLDL-secreted triglycerides from the liver.

121 methylation with metabolic phenotypes (BMI, triglyceride, glucose) and diseases in all 3 populations

122 High carbohydrate intake raises blood triglycerides, glucose, and insulin; reduces HDLs; and m

123 Atherogenic dyslipidemia (triglycerides >150 mg/dl [1.69 mmol/l] and HDL-C <40 mg/

124 8179 statin-treated patients with qualifying triglycerides >=135 and <500 mg/dL and low-density lipop

125 0 mg/dL for males and <50 mg/dL for females; triglycerides >=150 mg/dL, and glucose >=100 mg/dL.

126 In multivariable-adjusted analyses, triglycerides (hazard ratio [HR]: 1.04; 95% confidence i

127 .04), but there were no group differences in triglycerides, HDL cholesterol, glucose, insulin, insuli

128 exposure duration was associated with worse triglycerides-, HDL-, blood pressure-, fasting glucose-

129 cular disease risk factors (body mass index, triglycerides, high-density lipoprotein cholesterol conc

130 2D progression included age, sex, race, BMI, triglycerides, high-density lipoprotein, blood pressure,

131 rtiles, which were determined by the log of (triglyceride/high-density lipoprotein cholesterol).

132 neral content; and higher plasma insulin and triglycerides, higher homeostatic model assessment of in

133 tify bmm as a link between the regulation of triglyceride homeostasis and biological sex.

134 d in neurons in the regulation of whole-body triglyceride homeostasis.

135 e cell types in the regulation of whole-body triglyceride homeostasis.

136 bmm) in the regulation of sex differences in triglyceride homeostasis.

137 rea focused on accumulation of intramuscular triglyceride; however, bioactive lipids such as diacylgl

138 Deficiencies in either LPL or GPIHBP1 impair triglyceride hydrolysis, resulting in severe hypertrigly

139 : (a) lean subjects with normal intrahepatic triglyceride (IHTG) and glucose tolerance (lean-NL; n =

140 BACKGROUNDAn increase in intrahepatic triglyceride (IHTG) is the hallmark feature of nonalcoho

141 main substrate for synthesis of intrahepatic triglycerides (IHTG).

142 ectroscopy, yielding data on intramyocardial triglyceride (IMTG) content (a continuous marker for myo

143 ike certain lipid metabolites, intramuscular triglyceride (IMTG) stored within lipid droplets (LDs) d

144 of the lipid droplets storing intramuscular triglyceride (IMTG).

145 One significant gene-alcohol interaction on triglycerides in a novel locus was significantly discove

146 , inhibited autophagy, and increased hepatic triglycerides in Acox1-LKO mice.

147 e presence of Scia induced a 50% decrease in triglycerides in blood plasma due to a reduced level of

148 i.e., a dramatic increase of cholesterol and triglycerides in circulation).

149 njury, cell death, and the saponification of triglycerides in ex vivo porcine adipose tissue.

150 ogical intervention can acutely lower plasma triglycerides in FCS.

151 ession were positively correlated with liver triglycerides in female mice.

152 nd Cd36 was positively correlated with liver triglycerides in male mice, and Mogat1 and Cd36 expressi

153 l as lowered the serum levels of insulin and triglycerides in male offspring at weaning.

154 his fusion protein effectively lowers plasma triglycerides in mice and represents a promising new app

155 esents a promising new approach for lowering triglycerides in patients with familial chylomicronemia

156 ological basis of apoB, LDL cholesterol, and triglycerides in relation to ischemic stroke, in particu

157 dministrations of the fusion protein lowered triglycerides in several mouse strains without causing a

158 ipase (LPL) is responsible for breaking down triglycerides in the blood.

159 nalysis including apoB, LDL cholesterol, and triglycerides in the same model, apoB retained a robust

160 These measures, as well as triglycerides, increased on the delayed compared to the

161 In skeletal muscle, mirabegron reduced triglycerides, increased the expression of PPARgamma coa

162 delian randomization analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive prot

163 etic effects on whether the phenotype (e.g., triglycerides) is high or low relative to its distributi

164 r LDL cholesterol was reversed, and that for triglycerides largely attenuated.

165 ate to heavy S. mansoni infection with lower triglycerides, LDL-c, and diastolic blood pressure.

166 to diabetic mice reduced total cholesterol, triglycerides, LDL-cholesterol, and the atherogenic inde

167 Bempedoic acid did not significantly modify triglyceride level (MD -1.51%; 95% CI -3.75%, 0.74%; p =

168 deciliter (3.4 mmol per liter) or more and a triglyceride level of 400 mg per deciliter (4.5 mmol per

169 rol level, high VLDL cholesterol level, high triglyceride level, high total cholesterol level, and hi

170 y lipoprotein (VLDL) cholesterol level, high triglyceride level, low high-density lipoprotein (HDL) c

171 cal samples underwent laboratory testing for triglyceride level, total protein level, white blood cel

172 [LDL] cholesterol level, 75.0 mg/dL; median triglycerides level, 240 mg/dL; median HDL-C level, 36 m

173 etes (p = 0.004), while LRRK2-NMC had higher triglyceride levels (p = 0.014).

174 of 12i at 25 mg kg(-1) day(-1) lowered liver triglyceride levels and improved liver markers such as a

175 ), which is associated with very high plasma triglyceride levels and increased risk of life-threateni

176 ow-density lipoprotein (LDL) cholesterol and triglyceride levels and lower high-density lipoprotein c

177 te can rapidly decrease hepatic glycogen and triglyceride levels and renal triglyceride levels in neo

178 n in vivo model of NASH, 10b decreased liver triglyceride levels and showed improvement in fibrosis,

179 g disorder characterized by excessive plasma triglyceride levels for which treatment options are limi

180 function in the fat body affects whole-body triglyceride levels in both sexes, in males, we identify

181 c glycogen and triglyceride levels and renal triglyceride levels in neonatal G6pc -/- mice.

182 ubtracting pre-treatment from post-treatment triglyceride levels necessarily created a greater trigly

183 BMP inhibitor-induced decrease in hepatic triglyceride levels was associated with decreased mRNA e

184 h-density lipoprotein-cholesterol, decreased triglyceride levels, and decreased coronary heart diseas

185 diagnosis, microvascular complications, high triglyceride levels, and tobacco use were additional ind

186 many metabolic traits, including circulating triglyceride levels, glucose tolerance and FGF21 levels.

187 nesis in vivo to increase hepatic and plasma triglyceride levels, showing its role in metabolic adapt

188 blood glucose, glycated hemoglobin (HbA1c), triglyceride levels, triglycerides and glucose (TyG) ind

189 n, GW9662 elevated lipogenesis and increased triglyceride levels.

190 ncreased it in the liver, and lowered plasma triglyceride levels.

191 i mediated knockdown of Alk led to decreased triglyceride levels.

192 F signaling, the CCAP peptide also regulates triglyceride levels.

193 this process through repressing the adipose triglyceride lipase (ATGL) activity in neutrophils in pr

194 Silencing adipose triglyceride lipase (ATGL) in human pseudoislets (shATGL

195 Silencing adipose triglyceride lipase (ATGL) in human pseudoislets with sh

196 The impaired lipolysis in global adipose triglyceride lipase (ATGL) knockout mice reduced free PA

197 bly proline dehydrogenase (POX), and adipose triglyceride lipase (ATGL), as well as markedly reduced

198 ngoing lipolysis in the absence of adipocyte triglyceride lipase (ATGL).

199 Pancreatic triglyceride lipase (PNLIP) increased in adipose tissue

200 ta-oxidation via activation of the conserved triglyceride lipase ATGL-1, triggers a feedback transcri

201 reakdown in both sexes identified a role for triglyceride lipase brummer (bmm) in the regulation of s

202 l chemical sympathectomy and loss of adipose triglyceride lipase protect mice from GDF15-induced weig

203 y increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic ace

204 s index, transaminases, fasting blood sugar, triglyceride, low density lipoprotein level, and lower h

205 As a result, total cholesterol, triglyceride, low-density lipid, high-density lipid, HbA

206 rs: nonsmoker, total cholesterol <=4 mmol/L, triglycerides <=1.7 mmol/L, glycated haemoglobin (HbA1c)

207 ation from body water into glucose), hepatic triglyceride (magnetic resonance spectroscopy), and hepa

208 ial novel risk factor for ovarian cancer and triglycerides may be important particularly in rapidly f

209 se findings suggest that LDL cholesterol and triglycerides may have a causal effect in influencing ca

210 ic acid, a key component of the medium-chain triglyceride (MCT) ketogenic diet.

211 t solid lipids, being blends of medium chain triglyceride (MCT) oil, glyceryl stearate (GS) or hydrog

212 Medium-chain triglycerides (MCT), containing C(8)-C(12) fatty acids,

213 sterol (HDL-cholesterol), total cholesterol, triglycerides, measures of body fatness, markers of infl

214 Of these, ANGPTL5 is suggested to regulate triglyceride metabolism and is increased in obesity and

215 sophila, an established model for studies on triglyceride metabolism, to gain insight into the genes

216 Lipoprotein lipase (LPL) is central to triglyceride metabolism.

217 Using two representative sample types, a triglyceride mixture and dissolved organic matter, this

218 vitamin E acetate, plant oils, medium-chain triglyceride oil, coconut oil, petroleum distillates, an

219 : 0.57-1.27; P = 0.44) reversing and that of triglycerides (OR 1.12; 95% CI: 1.02-1.23; P = 0.01) bec

220 higher trait; 95% CI: 1.49-1.86; P < 0.001), triglycerides (OR 1.34; 95% CI: 1.25-1.44; P < 0.001) an

221 dex, systolic and diastolic blood pressures, triglycerides (p < 0.01), whilst Middle Eastern PCOS wom

222 LRRK2-PD had higher levels of triglycerides (p = 0.015) and higher rates of prediabete

223 plant body mass index (P < 0.001), and serum triglycerides (P = 0.047) independently predicted increa

224 161 in gene ABCG1 associated both with serum triglycerides (P = 5.36 x 10(-9)) and waist circumferenc

225 in and more very-low-density lipoprotein and triglyceride particles in depression.

226 the lipid repertoire, with phospholipids and triglycerides peaking strongly late in the cell cycle.

227 derived factors composed of highly saturated triglycerides, plasmalogens, and acylcarnitines were ass

228 mocysteine, alpha fetal protein cholesterol, triglycerides, prothrombin time.

229 a machine-learning model that predicted both triglyceride (r = 0.47) and glycemic (r = 0.77) response

230 The phospholipid-to-triglyceride ratio was decreased by pasteurization.

231 The work was performed on normo-triglyceride rats over six weeks, suggesting promising e

232 ndrome (MS) (obesity, hypertension, elevated triglycerides, reduced levels of HDL cholesterol and glu

233 tion of risk is explained by cholesterol and triglycerides, respectively, in very low-density lipopro

234 ed SNPs for total cholesterol, LDL, HDL, and triglycerides, respectively.

235 luenced LC and caused selective migration of triglycerides, resulting in higher proportion of unsatur

236 Elevated triglyceride-rich lipoprotein (TRL) and small-dense low-

237 study was to prospectively evaluate whether triglyceride-rich lipoprotein cholesterol (TRL-C) and sm

238 l study, to compare fasting and postprandial triglyceride-rich lipoprotein particle (TRLP) concentrat

239 triglycerides and cholesterol transported in triglyceride-rich lipoproteins (remnant cholesterol) can

240 lammasome and the pathophysiological role of triglyceride-rich lipoproteins containing ApoC3.

241 HBP1 focuses the intravascular hydrolysis of triglyceride-rich lipoproteins on the surface of capilla

242 were found to be potentially attributable to triglyceride's quantile-dependent expressivity, includin

243 bmm largely eliminates the sex difference in triglyceride storage and abolishes the sex difference in

244 Our analysis of triglyceride storage and breakdown in both sexes identif

245 sity or autophagic flux, but it did increase triglyceride storage and disrupt endoplasmic reticulum c

246 s (PAPs) generate diacylglycerol to regulate triglyceride synthesis and cellular signaling.

247 ing glycerolipid metabolism toward increased triglyceride synthesis blocks PNS neuron regeneration, w

248 Fatty acid and triglyceride synthesis increases greatly in response to

249 d mRNA encoding Dgat2, an enzyme integral to triglyceride synthesis.

250 ibit severe hepatomegaly due to glycogen and triglyceride (TG) accumulation in the liver.

251 Using MR, we inferred that higher triglyceride (TG) and LDL cholesterol (LDL-C) levels cau

252 To ensure fetal lipid supply, maternal blood triglyceride (TG) concentrations are robustly elevated d

253 The increase in serum triglyceride (TG) concentrations in response to a meal i

254 drome and insulin resistance, manifests when triglyceride (TG) input in the liver is greater than TG

255 Lowering low-density lipoprotein (LDL-C) and triglyceride (TG) levels form the cornerstone approach o

256 ntial coactivator of ATGL, the rate-limiting triglyceride (TG) lipase in many cell types.

257 on failure in the CNS by favorably producing triglyceride (TG) storage lipids rather than phospholipi

258 ever, expression of gene modules involved in triglyceride (TG) synthesis and adipogenesis decreased,

259 Reactive oxygen species (ROS), cellular triglyceride (TG), and glucose and B-hydroxybutyrate (BH

260 Serum triglyceride (TG), total cholesterol (TC), high-density

261 -density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with in

262 essential for the assembly and secretion of triglyceride (TG)-rich, apoB-containing lipoproteins.

263 M1 PUFA containing triglycerides (TG) and phospholipids were correlated wit

264 density lipoprotein cholesterol (HDL-c) and triglycerides (TG) from two independent GWAS datasets.

265 density lipoprotein cholesterol (HDL-C), and triglycerides (TG) were evaluated preconception and thro

266 are associated with total cholesterol (TC), triglycerides (TG), and lipoprotein concentrations is un

267 istically significant age-related changes in triglycerides (TG), diglycerides (DG), phosphatidylcholi

268 28-0.59), which included ceramides (Cer) and triglycerides (TG).

269 erol [LDL-C; 61 studies; 86,854 people], and triglycerides [TG; 84 studies; 121,009 people]) levels a

270 (LDL) >130 mg/dL, 2,756 subjects (7.0%); and triglycerides (TGs) >150 mg/dL, 2,881 subjects (7.3%).

271 with shRNA targeting ATGL (shATGL) increased triglycerides (TGs) and the number and size of LDs, indi

272 Luteal tissue was enriched in triglycerides (TGs) compared to other tissues, except fo

273 ic pathway responsible for the catabolism of triglycerides (TGs) that is complemented by lipophagy as

274 ation, glucose and insulin, cholesterol, and triglycerides (TGs), and further measured blood pressure

275 maging adipocyte cell membranes, hydrolyzing triglycerides (TGs), or inducing apoptosis.

276 ther melanizing or nonmelanizing conditions; triglycerides (TGs), sterol esters (SEs), and polyisopre

277 and high-density lipoproteins [LDL and HDL], triglycerides [TGs], and glycated haemoglobin [HbA1c]).

278 oprotein, HDL; low-density lipoprotein, LDL; triglycerides, TGs) with risk for BC using Mendelian ran

279 is over-accumulation of hepatic glycogen and triglycerides that can lead to steatohepatitis and a ris

280 lar health by lowering blood cholesterol and triglycerides, the lipoMSN is used to deliver a combinat

281 aroglitazar had lower weight, lower HOMA-IR, triglycerides, total cholesterol, and ALT.

282 An intracellular chaperone, microsomal triglyceride transfer protein (MTP), is required for the

283 Microsomal triglyceride transfer protein (MTTP) is an endoplasmic r

284 al (CI), 0.04-0.47, P value = 1.72 x 10-28), triglycerides (TRG) (beta -0.23, 95% CI, -0.30, -0.15, P

285 ol, LDL, high-density lipoprotein [HDL], and triglycerides) using independent genomewide significant

286 rate, blood pressure), metabolic (HOMA(ir), triglycerides, waist circumference), and immune (white b

287 deviation increase in genetically-predicted triglycerides was 1.18 (95% CI 1.09-1.27; p = 2 x 10(-5)

288 olesterol 1.45 (0.38) mmol/L, and the median triglycerides was 1.50 (IQR = 1.11) mmol/L.

289 Total cholesterol, LDL, HDL, and triglyceride were evaluated at 3 months (n = 262) and 18

290 /-3.6 years, 294 (29%) were female, and mean triglycerides were 111.4+/-61.9 mg/dL.

291 creased levels of apoB, LDL cholesterol, and triglycerides were associated with higher risk of any is

292 age-matched controls, the levels of whole SN triglycerides were correlated with inflammation-attenuat

293 ride changes could not move in parallel when triglycerides were decreased pharmacologically, so that

294 .55 mmol/L, p < 0.001) were increased, while triglycerides were decreased, after surgery (1.62 vs. 1.

295 , systolic and diastolic blood pressure, and triglycerides were higher in the UK cohort whilst testos

296 while factors composed of highly unsaturated triglycerides were linked to healthy AHEI components.

297 Triglycerides were significantly higher in HH group.

298 d egg yolk malondialdehyde, cholesterol, and triglyceride, while increased glutathione peroxidase.

299 81 g; 95% CI: 0.11 to 1.51 g; p = 0.023) and triglycerides with higher LV mass (beta = 1.37 g; 95% CI

300 n the level of 18:1n-9, suggesting that only triglycerides with neosynthesized monoenes are marked ou