ライフサイエンスコーパス: triglyceride

1 95% CI: 0.35, 1.07 per 1 mmol/L increase in triglycerides).

2 of circulating very low-density lipoprotein triglyceride.

3 versus incorporation into newly synthesized triglyceride.

4 tributed to the coexistence of two groups of triglycerides.

5 is decreased in response to palmitic acid or triglycerides.

6 athways that involve hepatic accumulation of triglycerides.

7 esterification was also studied using three triglycerides.

8 ng of the usual post-prandial rise in plasma triglycerides.

9 where they are esterified and accumulated as triglycerides.

10 was dominant in the first stage followed by triglycerides.

11 ting adiponectin, leptin, glycerol and total triglycerides.

12 s for changes in total or HDL cholesterol or triglycerides.

13 advantage in settings of low LDL-C and high triglycerides.

14 d deviations, 95% CI 0.03-0.38) and possibly triglycerides (0.19 standard deviations, 95% CI -0.1-0.4

15 (95% CI: -8.47, -3.53 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0.14, -0.02 mmol/L

16 od pressure (1.24; 1.04-1.48) and high serum triglycerides (1.18; 1.00-1.39), with a trend of increas

17 reduced HDL-cholesterol, 23.33% for elevated triglycerides, 18.95% for raised fasting plasma glucose.

18 interval, -23 to -0.98; P=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0

19 ting versus fasting levels are +26 mg/dl for triglycerides, -8 mg/dl for total cholesterol, -8 mg/dl

20 of proteins provoked a higher hydrolysis in triglycerides, a lower decrease of polyunsaturated chain

21 Fasting triglycerides above the median increased the per-allele

22 sis by inhibiting intestinal cholesterol and triglyceride absorption and promoting macrophage cholest

23 mical, and large variations were observed in triglyceride accumulation and cell proliferation between

24 xygen consumption rate, along with increased triglyceride accumulation and insulin-stimulated glucose

25 or dust or individual SVOCs and assessed for triglyceride accumulation and preadipocyte proliferation

26 11 house dust extracts exhibited significant triglyceride accumulation and/or proliferation at enviro

27 tes were assessed for cell proliferation and triglyceride accumulation following different induction

28 TPs) exhibited near maximal or supra-maximal triglyceride accumulation relative to the rosiglitazone-

29 XR activation and deficiency promote hepatic triglyceride accumulation, a hallmark feature of alcohol

30 tivation of mTORC1 failed to suppress plasma triglycerides after 1 week of glucose feeding.

31 eptin and triglycerides and 2) the aMED with triglycerides (all P-trend </= 0.03).

32 it hypolipidemia and reduced levels of liver triglycerides, along with impaired hepatic lipogenesis.

33 Hepatic triglyceride and ATP content rose by 35% and 16%, respec

34 Increased plasma triglyceride and cholesterol levels are major risk facto

35 sedentary behavior, weight gain, and higher triglyceride and cholesterol levels.

36 ecreased the alcohol-induced increased liver triglyceride and fat droplet accumulation.

37 ever, glucose utilization, glycerol release, triglyceride and glycogen contents, free fatty acid (FFA

38 ined significant for 1) DASH with leptin and triglycerides and 2) the aMED with triglycerides (all P-

39 demonstrated a 17% reduction in circulating triglycerides and a 12% reduction in low-density lipopro

40 igh-and low-density lipoprotein cholesterol, triglycerides and body mass index, and subsequent meta-a

41 We hypothesize that PDX reduces triglycerides and cholesterol by influencing gut microbi

42 arly and the diversion of glucose carbons to triglycerides and cholesterol esters.

43 od intake, adiposity index, fasting insulin, triglycerides and cholesterol levels were all significan

44 arbohydrates, as well as lipoprotein-derived triglycerides and cholesterol, into these thermogenic ce

45 ayed reduced body weight, serum cholesterol, triglycerides and free fatty acids, suggesting altered l

46 a splice variant in APOC3 (rs138326449) with triglycerides and HDL-C.

47 ferentially methylated locus associated with triglycerides and high-density lipoprotein cholesterol (

48 arbohydrate diets may preferentially improve triglycerides and high-density lipoprotein cholesterol.

49 ipogenesis (DNL) converts carbohydrates into triglycerides and is known to influence systemic lipid h

50 ficant decrease in plasma total cholesterol, triglycerides and LDL cholesterol comparable to oral ATV

51 Log triglycerides and log adiponectin were not significantly

52 the association of waist circumference with triglycerides and only 1-3% of the association with HDL-

53 CA-diet feeding, with increased cholesterol, triglycerides and phospholipids, in WT, but not TRPC5 KO

54 f esterified fatty acids and sterols, mainly triglycerides and sterol esters, surrounded by a single

55 asured or calculated from total cholesterol, triglycerides, and apoA-I.

56 xcessive accumulation of dermal cholesterol, triglycerides, and ceramides.

57 inhibition also resulted in reduced insulin, triglycerides, and cholesterol levels in plasma.

58 lease and lipid synthesis (particularly FFA, triglycerides, and cholesterol), whereas glycogen produc

59 betes mellitus, history of smoking, elevated triglycerides, and estimated glomerular filtration rate.

60 esterol, HDL cholesterol, total cholesterol, triglycerides, and fasting blood glucose) and identified

61 able increase in insulin resistance, hepatic triglycerides, and gluconeogenesis.

62 ls of hepatic Angptl3 mRNA, Angptl3 protein, triglycerides, and low-density lipoprotein (LDL) cholest

63 r low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD.

64 acids but reduced abundance of diglycerides, triglycerides, and phosphatidylglycerol lipids.

65 matic amino acids, glycoprotein acetyls, and triglycerides, and strong negative associations with hig

66 d cholesterol, creatinine, glucose, insulin, triglycerides, and urea levels.

67 ow-density lipoprotein (LDL) cholesterol and triglycerides] and lower odds of diabetes.

68 rements of serum glucose, total cholesterol, triglycerides, apolipoprotein B (apoB), and apolipoprote

69 -ACBs was also possible when fatty acids and triglycerides are exposed to a non-ionizing, short-wavel

70 at C8-C12 FA (the most common FA found in CO triglycerides) are the best acyl-donors, yielding 80-85%

71 ristic curve 0.806 versus 0.811; P=0.01) and triglycerides (area under the receiver-operating charact

72 reased while plasma glucose, cholesterol and triglycerides, as well as liver glycogen, significantly

73 lyceride content and shorter chain length of triglyceride-associated fatty acids, and these effects b

74 gh-density lipoprotein (HDL) cholesterol, or triglycerides at a genome-wide level of significance, an

75 This tempers triglyceride availabiity for very low density lipoprotei

76 rved among a) liver levels of PERC, TCA, and triglycerides; b) TCA levels in liver and kidney; and c)

77 ide increases manyfold but circulating serum triglyceride barely fluctuates.

78 % confidence interval (CI) 0.87 to 0.97) and triglycerides (beta - 0.08, 95% CI - 0.13 to - 0.03), bu

79 h copy of the Thr allele conferred 42% lower triglycerides (beta=-0.92+/-0.059 SD unit; P=9.6x10(-55)

80 reased Atg2 expression or reduced macrophage triglyceride biosynthesis, normalizes lipid deposition i

81 blood glucose and insulin as well as fasting triglycerides, blood lipoproteins, HbA1c, and body weigh

82 roved dyslipidemia, with reduced circulating triglycerides, but showed differential responses in tota

83 othesized that higher circulating glucose or triglycerides can amplify the FTO impact on BMI.

84 nt of its role as a coactivator of epidermal triglyceride catabolism.

85 ication-58 (CGI-58) are limiting in cellular triglyceride catabolism.

86 DL-CN or LDL-CF) was stratified by LDL-C and triglyceride categories.

87 cose, insulin, insulin-like growth factor I, triglycerides, cholesterol, cortisol, and leptin, were m

88 avorable profile (higher LDL cholesterol and triglycerides).Choline and its metabolites have differen

89 A (mRNA) for effects on plasma lipid levels, triglyceride clearance, liver triglyceride content, insu

90 ibitor of lipoprotein lipase-mediated plasma triglyceride clearance.

91 t rate, body temperature, blood glucose, and triglyceride concentration, all of which were regulated

92 ese, and butter induced similar increases in triglyceride concentrations at 4 h (change from baseline

93 Peak postprandial blood triglyceride concentrations did not significantly increa

94 HDL triglyceride concentrations predict post-MI LVEF and ISZ

95 postprandial glucose and higher lactate and triglyceride concentrations.

96 ot result in a substantial increase in blood triglyceride concentrations.

97 e on peak postprandial glucose, insulin, and triglyceride concentrations.The objective of this study

98 cholesterol, as well as reductions in liver triglyceride content and atherosclerosis progression and

99 liver function as demonstrated by increased triglyceride content and dysfunctional expression of enz

100 Fetuses from HF/HS-Veh dams had lower liver triglyceride content and mRNA expression of Srebf1c.

101 e is correspondingly shifted towards lowered triglyceride content and shorter chain length of triglyc

102 It is possible to estimate hepatic triglyceride content by calculating the proton density f

103 cific ablation of either component increases triglyceride content in liver.

104 Purpose To test the hypothesis that hepatic triglyceride content is associated with subclinical vasc

105 A 10-fold increase in hepatic triglyceride content was also associated with an increas

106 us covariates, a 10-fold increase in hepatic triglyceride content was associated with an increased me

107 large population-based cohort study, hepatic triglyceride content was associated with aortic pulse wa

108 s were used to study associations of hepatic triglyceride content with total and regional aortic PWV

109 s, hyperinsulinemic-euglycemic clamps, liver triglyceride content, and liver enzyme expression, was e

110 pectroscopy and MR imaging to assess hepatic triglyceride content, aortic pulse wave velocity (PWV),

111 lipid levels, triglyceride clearance, liver triglyceride content, insulin sensitivity, and atheroscl

112 Despite massive fluctuations in its internal triglyceride content, the liver secretes triglyceride un

113 in association with decreased intracellular triglyceride content.

114 lso observed in UV-C irradiated fatty acids, triglycerides, corn oil, and pork samples.

115 nsity lipoprotein, high-density lipoprotein, triglycerides, cytokines or bile acids were observed.

116 on of energy substrates by the hydrolysis of triglycerides, declines with age.

117 There was a significant decrease in serum triglycerides (decrease of 19%) in the OI group.

118 KO mice were characterized by high levels of triglycerides, diglycerides, fatty acids, ceramides, and

119 fried oil (total polar compounds (TPC), and triglyceride dimers-polymers (TGDP), among others) and e

120 ion and successfully suppressed postprandial triglycerides during an acute meal challenge in humans.

121 acyl chain flux between membrane lipids and triglycerides during nitrogen stress relies primarily on

122 The resulting lack of substrates for triglyceride esterification protects severely hypothyroi

123 -density lipoprotein- and total cholesterol, triglycerides, fasting glucose, body mass index, waist c

124 high-density lipoprotein (HDL) cholesterol, triglycerides, fat mass (FM), systolic and diastolic blo

125 in intestine, Cu depletion, accumulation of triglyceride-filled vesicles in enterocytes, mislocaliza

126 an now be catabolized efficiently to provide triglyceride for lipoprotein assembly and secretion from

127 mental area under the curve (iAUC) of plasma triglycerides.Forty-three healthy subjects were recruite

128 weight, and circulating and tissue levels of triglycerides, free fatty acids (FFA), and leptin?

129 A significant decrease in serum triglycerides (from 103 to 75, 69 and 72 mg/dL), total c

130 n postprandial vascular function, as well as triglyceride, glucose, and insulin responses.

131 andial dysmetabolism-an exaggerated spike in triglycerides, glucose, and insulin-increases cardiovasc

132 terol, high-density lipoprotein cholesterol, triglycerides, glucose, fasting insulin) were measured w

133 nuate postprandial metabolic derangements in triglycerides, glucose, or insulin relative to the contr

134 ith the presence of MAC (odds ratio [OR] per triglyceride GRS unit: 1.73; 95% confidence interval [CI

135 lyceride GRS was associated with MAC (OR per triglyceride GRS unit: 1.79; 95% CI: 1.32 to 2.41; p = 0

136 g the MESA Hispanic-Americans cohort (OR per triglyceride GRS unit: 2.04; 95% CI: 1.03 to 4.03; p = 0

137 ta-analysis across all included cohorts, the triglyceride GRS was associated with MAC (OR per triglyc

138 In pooled analyses across all 3 cohorts, a triglyceride GRS was significantly associated with the p

139 asurements of high-density lipoprotein (HDL) triglycerides (HDL-TG) predicted LVEF (beta=1.90 [95% co

140 hemoglobin A1c (HbA1c), insulin resistance, triglycerides, HDL cholesterol (HDL-C), and C-reactive p

141 We assessed changes in HbA1c, triglycerides, HDL cholesterol and BMI in a mixed effect

142 e following components: waist circumference, triglycerides, HDL-c, glucose, and systolic and diastoli

143 etabolic traits such as waist circumference, triglyceride, high-density lipoprotein cholesterol, syst

144 globin, low-density lipoprotein cholesterol, triglycerides, high-sensitivity C-reactive protein, and

145 -containing protein 4) involved in adipocyte triglyceride homeostasis was discovered.

146 ecretion in metabolic pathways, particularly triglyceride homeostasis.

147 on of ATGL enzyme activity similarly reduced triglyceride-hydrolytic activities in wild-type and CGI-

148 No difference in the triglyceride iAUC0-8 h (P-meal = 0.9) was observed betwe

149 the most well-replicated SNP (rs964184) for triglycerides identified by genome-wide association stud

150 The cut-off point of intrahepatic triglyceride (IHTG) content to define nonalcoholic fatty

151 ilipin (PLIN) proteins promote intramuscular triglyceride (IMTG) storage, we investigated the hypothe

152 mbly and allows homeostatic control of serum triglyceride in a fasted state.

153 es, we identified a major linkage signal for triglycerides in 1007 Pima Indians (LOD=9.23; P=3.5x10(-

154 factors except for borderline high and high triglycerides in adolescence were associated with high c

155 C3/APOA5 constitutes a major locus for serum triglycerides in Amerindians, especially the Pimas, and

156 IR leads to accumulation of triglycerides in both muscle tissue and the liver.

157 statistically significant decrease in serum triglycerides in germ-free rats fed a high sugar diet co

158 c steatosis characterized by accumulation of triglycerides in hepatocytes, which leads to hepatocellu

159 MIR122 and then given CL316243, accumulated triglycerides in liver and muscle tissues, and had reduc

160 nalysis of lipids revealed a shift from high triglycerides in mammary gland to high phospholipid leve

161 sitivity best correlated with elevated serum triglycerides in normal-weight participants and with low

162 hese 4 SNPs account for 6.9% of variation in triglycerides in Pimas (and 4.1% in Southwest Amerindian

163 tyrosine and decreased levels of lipids and triglycerides in tumour relative to adjacent healthy tis

164 rences between diets for HDL cholesterol and triglyceride.In comparison with a control diet, the inco

165 on is most visible after fasting, when liver triglyceride increases manyfold but circulating serum tr

166 EC lining the aorta after the peak in plasma triglycerides initiated by a gavage of olive oil in mice

167 used variation of the diet (the medium-chain triglyceride ketogenic diet), have been shown to directl

168 carriers showed significant improvements in triglycerides, LDL- and total cholesterol, insulin, HbA1

169 , and medical-therapy groups, respectively), triglyceride level (-40%, -29%, and -8%), high-density l

170 is in nonobese patients, only elevated serum triglyceride level was independently associated with hig

171 noate (PFNA) were negatively associated with triglyceride levels [percent median change per log10-uni

172 gh-density lipoprotein cholesterol, and high triglyceride levels and hypertension) among normal-weigh

173 an association between genetically predicted triglyceride levels and probability of longevity (OR: 0.

174 Whether reducing triglyceride levels can lower the incidence of clinicall

175 rther analyses revealed that cholesterol and triglyceride levels had decreased by 37% and 60%, respec

176 The reduction of plasma triglyceride levels in Angptl4(-/-) mice and increase fo

177 observed increased liver lipid deposits and triglyceride levels in male LERKO mice, resulting from i

178 rs662799 was robustly associated with higher triglyceride levels in the comparison group (beta = 0.30

179 d 40 to 75 years with fasting lipid data and triglyceride levels of 400 mg/dL or less, without prior

180 Subsequently, 44 human participants (with triglyceride levels of either 90 to 150 mg per deciliter

181 In our study, serum triglyceride levels of P-407 induced mice were elevated

182 ir respective controls but increased hepatic triglyceride levels only in POMC IR KO mice, consistent

183 Genetic predisposition to elevated triglyceride levels was associated with the presence of

184 e, the fasting insulin, glucose, and hepatic triglyceride levels were fully restored to normal levels

185 ing arm (70-84 years), genetically predicted triglyceride levels were not associated with the frailty

186 t evidence to support causal associations of triglyceride levels with longevity and frailty in elderl

187 bservational studies suggest associations of triglyceride levels with longevity and frailty.

188 he interaction effect of fasting glucose and triglyceride levels with rs9939609 in FTO on BMI.

189 BMI, lower HDL cholesterol levels and higher triglyceride levels) and provide evidence that their lin

190 h-density lipoprotein cholesterol levels, in triglyceride levels, and in the ratio of apolipoprotein

191 f mice caused a 8.6-fold elevation in plasma triglyceride levels, but did not alter plasma glucagon l

192 Strategies to reduce triglyceride levels, by increasing MIR122, might be deve

193 normalities, such as hyperglycemia, elevated triglyceride levels, low high-density lipoprotein choles

194 LDL-C (<70 mg/dL), we evaluated accuracy by triglyceride levels.

195 osition of the RBC membranes and with plasma triglyceride levels.

196 s the risk of IHD, probably through reducing triglyceride levels.

197 ior, while conversely showing an increase in triglyceride levels.

198 ele frequency (EAF) 0.006); and rs145556679 (triglycerides levels beta -1.13 (SE 0.17), P=2.53 x 10(-

199 Triglycerides levels showed a significant trend.

200 levels of the key lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone sensitive lipase

201 via activation of cytosolic lipases adipose triglyceride lipase (ATGL) and hormone-sensitive lipase

202 Adipose triglyceride lipase (ATGL) and its coactivator comparati

203 ation and proteasomal degradation of adipose triglyceride lipase (ATGL), a rate limiting enzyme of TA

204 -modulates LD catabolism mediated by adipose triglyceride lipase (ATGL), the key enzyme for intracell

205 , is a highly conserved regulator of adipose triglyceride lipase (ATGL)-mediated lipolysis that plays

206 estine and drives fat loss via the adipocyte triglyceride lipase ATGL-1.

207 corticosterone-infused rats with an adipose triglyceride lipase inhibitor blocked corticosterone-ind

208 ferase 1) and degrade LD via ATGL (adipocyte triglyceride lipase) after FA loading.

209 (VAT) mass; plasma, lipids (cholesterol and triglycerides), liver enzymes, and adipokines; glucose a

210 ore was inversely associated with adiposity, triglycerides, liver enzymes, C-reactive protein, a gene

211 It is unknown whether adding triglyceride-lowering treatment to statin reduces this r

212 pidaemia (LDL cholesterol 3.4-5.7 mmol/L and triglycerides </=4.5 mmol/L) from 45 sites in the USA an

213 association at genome-wide significance for triglycerides mapping to GPC5 (lead SNP rs71427535, p =

214 Orange oil, medium-chain triglyceride (MCT) oil, and WPI were used to make stable

215 BALB/c mice by oral gavage with medium-chain triglycerides (MCTs) plus egg white (EW) and was charact

216 verexpression suggest that changes in plasma triglyceride metabolism do not regulate alpha-cells in t

217 mportant in lipid droplet (LD) formation and triglyceride metabolism.

218 Our results suggest that elevated plasma triglycerides might be partially responsible for increas

219 ly, elevated HDL components, i.e., small HDL triglycerides, might have a causal role of elevating glu

220 iz., triglyceride polymers, dimers, oxidized triglyceride monomers, diglycerides and free fatty acids

221 extremely large very-low-density lipoprotein triglycerides (odds ratio [OR] = 4.86 per 1 standard dev

222 With triglycerides of 200 to 399 mg/dL in nonfasting patients

223 kers (plasma melatonin and cortisol), plasma triglycerides, or clock gene expression in whole blood.

224 out affecting circulating total cholesterol, triglycerides, or glycerol levels.

225 Placental triglyceride oscillations in the third trimester of huma

226 sting hypoglycaemia and hepatic glycogen and triglyceride overaccumulation.

227 uced food intake (p < 0.001), fasting plasma triglyceride (p < 0.001) and total cholesterol (p < 0.05

228 carriers showed significant improvements in triglycerides (p = 0.01), insulin and HOMA-IR (p-values

229 t baseline predicted lower concentrations of triglycerides (P = 0.021) and homeostatic model assessme

230 Diurnal triglyceride patterns were disrupted in human placentas

231 l polar compounds, polymeric compounds viz., triglyceride polymers, dimers, oxidized triglyceride mon

232 r HOMA-IR (3.7 vs. 1.9, p < 0.0001) and high triglycerides (prevalence risk ratio 14.3/5.8, 2.5, p =

233 Hepatic glucose and triglyceride production rates of Adipoq(-/-) dams were s

234 In this triglyceride range, 73% of fasting and 81% of nonfasting

235 s and the following traits: BMI, WC, FM, and triglycerides (range: alpha-carotene = -0.19 to -0.12; b

236 erol (TC), LDL cholesterol, HDL cholesterol, triglycerides, ratio of TC to HDL cholesterol (TC:HDL),

237 for all doses vs. placebo) and in levels of triglycerides (reductions of 33.2 to 63.1%), LDL cholest

238 However, at 2 h, the triglyceride response caused by the cream cheese (change

239 At 6 h, the triglyceride response induced by cream cheese was signif

240 We show that kinesin motors are recruited to triglyceride-rich lipid droplets (LDs) in the liver by t

241 ntified rare coding variants in genes in the triglyceride-rich lipoprotein (TRL) clearance pathway th

242 ntly in liver and small intestine, sites for triglyceride-rich lipoprotein biogenesis and export.

243 Triglyceride-rich lipoprotein fractions of plasma were i

244 type (APOE3/3 common genotype, or APOE3/E4), triglyceride-rich lipoproteins (TRLs) were isolated at f

245 of both hepatically and intestinally derived triglyceride-rich lipoproteins.

246 sterol, HDL cholesterol, TC:HDL cholesterol, triglycerides, SBP, and DBP; calculated overall effect s

247 How the liver controls triglyceride secretion is unknown, but is fundamentally

248 uced plasma lipid levels, diminished hepatic triglycerides secretion and increased hepatosteatosis.

249 fat weight [SMD=0.67 (95% CI: 0.53, 0.81)], triglycerides [SMD=0.97 (95% CI: 0.53, 1.40)], and FFA [

250 , specifically decreased hepatic 18:2 FA and triglyceride species and a shift in 18:2 FA use for oxid

251 lism was further dysregulated with increased triglyceride species and a subsequent decrease in phosph

252 bited significantly lower postprandial serum triglycerides, suggestive of a role for TM6SF2 in the sm

253 To better understand the metabolism of triglyceride synthesis in algae, we examined their metab

254 enhanced lipolysis and not caused by reduced triglyceride synthesis or fatty acid uptake.

255 e expression of all genes involved in FA and triglyceride synthesis that are normally regulated by SR

256 ed human Agpat1 and Dgat1 mRNAs, involved in triglyceride synthesis, as targets of MIR122.

257 e, reducing mRNA levels of genes involved in triglyceride synthesis.

258 IR122 expression and the effect of MIR122 on triglyceride synthesis.

259 tors and enzymes that mediate fatty acid and triglyceride synthesis.

260 ucose, high-density lipoprotein-cholesterol, triglycerides, systolic blood pressure and the incidence

261 th marked increases in both liver and muscle triglyceride (TAG) and diacylglycerol (DAG) content, whi

262 ecrease of genes involved in cholesterol and triglyceride (TAG) metabolism, concomitantly with lower

263 Synthesis and secretion of hepatic triglycerides (TAG) associated with very-low-density lip

264 g) for TC, LDL cholesterol, HDL cholesterol, triglycerides, TC:HDL cholesterol, SBP, and DBP, respect

265 he mechanism responsible for accumulation of triglyceride (TG) and PNPLA3 in hepatic lipid droplets (

266 ssess the association, if any, between serum triglyceride (TG) levels and gemfibrozil consumption wit

267 Elevated triglyceride (TG) levels are well-correlated with the ri

268 C3 encodes apoC-III, a critical inhibitor of triglyceride (TG) lipolysis and remnant TRL clearance.

269 %CI 1.45-1.69, P = 3.84 x 10(-31)) and serum triglycerides (TG) (beta = 0.067, P = 4.5 x 10(-21)).

270 illustrate the use of MARV with analysis of triglycerides (TG), fasting insulin (FI) and waist-to-hi

271 density lipoprotein cholesterol (LDL-C), and triglycerides (TG).

272 reduction was associated with a decrease in triglycerides (TGs) (beta = 0.090; 95% CI: 0.026, 0.154;

273 h overexposure of lean organs to circulating triglycerides (TGs) and nonesterified fatty acids (NEFAs

274 Triglycerides (TGs) are the major transporters of dietar

275 pression correlates with steatosis and serum triglycerides (TGs) in humans.

276 nd region-specific z-scores for cholesterol, triglycerides (TGs), high-density (HDL-C), and low-densi

277 Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholestero

278 nd DARS for total cholesterol, and TRIB1 for triglycerides) that were causal mediators for the corres

279 (HbA1c), fasting blood glucose, insulin, and triglycerides.The objective of this study was to review

280 pproach to derive patient-specific ratios of triglycerides to very low-density lipoprotein cholestero

281 used for metabolic traits (fasting insulin, triglyceride, total cholesterol, low-density lipoprotein

282 iations with first-trimester serum levels of triglycerides, total cholesterol, and C-reactive protein

283 y, body fat percentage, waist circumference, triglycerides, total cholesterol, and C-reactive protein

284 Here we demonstrate that microsomal triglyceride transfer protein (MTP), a protein involved

285 1A1, and catalase, as well as the microsomal triglyceride transfer protein, involved in regulating li

286 xpression of Mttp and its product microsomal triglyceride transfer protein.

287 obesity, self-rated health, smoking status, triglycerides, type 2 diabetes, waist-hip ratio, attenti

288 ein, HbA1c, height, obesity, smoking status, triglycerides, type 2 diabetes, waist-hip ratio, childho

289 nal triglyceride content, the liver secretes triglyceride under tight homeostatic control.

290 High-density lipoprotein and triglyceride values rapidly equalized among participants

291 DL)-lipoproteins, VLDL-cholesterol (C), VLDL-triglycerides, VLDL-diameter, branched/aromatic amino ac

292 The metabolic origin of stress-induced triglyceride was found to be a continuous 8:2 ratio betw

293 No causal effect of LDL-cholesterol or triglycerides was found.

294 rage of oxidized LDL, cholesteryl esters and triglycerides were abolished in Hilpda cKO macrophages,

295 Plasma concentrations of triglycerides were measured immediately before the meal

296 volume of an adipocyte decreases by loss of triglycerides, which creates stress between the cell con

297 n effect between fasting glucose and fasting triglycerides with rs9939609 on BMI (p = 0.0005 and p =

298 ne the associations of genetically predicted triglycerides with two ageing phenotypes - longevity ( >

299 ity programmed increased adiposity and liver triglycerides, with decreased glucose tolerance, liver N

300 igh blood pressure, fasting blood sugar, and triglycerides, with marginal significance.