ライフサイエンスコーパス: plasma triglyceride

1 bnormalities in high-density lipoprotein and plasma triglyceride.

2 g was well tolerated, without an increase in plasma triglycerides.

3 disease persisted even after adjustment for plasma triglycerides.

4 lbCre(+) mice did not exhibit any changes in plasma triglycerides.

5 yndecan-1 mutants (Sdc1-/- mice) accumulated plasma triglycerides.

6 ent mice are insulin resistant with elevated plasma triglycerides.

7 blunting of the usual post-prandial rise in plasma triglycerides.

8 t this is associated with elevated levels of plasma triglycerides.

9 ight, insulin resistance, hyperglycemia, and plasma triglycerides.

10 , whereas APOA5 mutation carriers had higher plasma triglycerides.

11 aired hepatic lipid accumulation and reduced plasma triglycerides.

12 (30-52%) and reduced abdominal fat (5%) and plasma triglycerides (25%).

13 tistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LD

14 in GCKR explained 36% of the variability in plasma triglycerides, 7.3% of which was attributable to

15 Plasma triglycerides, a univariate predictor of coronary

16 ivotal role in the regulation of hepatic and plasma triglyceride accumulation, possibly by modulating

17 tive activation of mTORC1 failed to suppress plasma triglycerides after 1 week of glucose feeding.

18 Despite this, these mice had higher plasma triglyceride and apoB levels.

19 olerance, they exhibited marked decreases in plasma triglyceride and apolipoprotein B100 concentratio

20 Mice fed a high-fat diet had a more elevated plasma triglyceride and cholesterol level than those tha

21 ugh these mechanisms, BAT activation reduces plasma triglyceride and cholesterol levels and attenuate

22 Increased plasma triglyceride and cholesterol levels are major ris

23 t a dose of 50 ng/kg significantly increased plasma triglyceride and cholesterol levels by 22 and 31%

24 Ritonavir treatment increased plasma triglyceride and cholesterol levels through incre

25 Plasma triglyceride and cholesterol levels were high in

26 opoietic Dectin-2 or CARD9 did not influence plasma triglyceride and cholesterol levels.

27 n increases energy expenditure and decreases plasma triglyceride and cholesterol levels.

28 8, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride and cholesterol, respectively, in wi

29 iron overload caused a modest (30%) rise in plasma triglyceride and cholesterol.

30 evels with WT controls but greatly increased plasma triglyceride and elevated plasma cholesterol leve

31 se adipocyte-derived hormones with decreased plasma triglyceride and free fatty acid levels may accou

32 owever, these enzymes did not affect fasting plasma triglyceride and free fatty acid levels or trigly

33 s mutant Lrp5 allele are leaner with reduced plasma triglyceride and free fatty acid levels.

34 strong associations with elevated levels of plasma triglyceride and glucose levels.

35 e and endothelial lipase, thereby increasing plasma triglyceride and HDL cholesterol levels in rodent

36 and insulin resistance as well as regulating plasma triglyceride and HDL cholesterol levels.

37 tion within enhancers strongly correlated to plasma triglyceride and HDL-cholesterol, including at CD

38 se, all of which contribute significantly to plasma triglyceride and high-density lipoprotein cholest

39 oglobin desaturations at night showed higher plasma triglyceride and low-density lipoprotein choleste

40 osynthetic genes (lipogenesis) and increased plasma triglyceride and phospholipid levels in both spec

41 PURPOSE OF REVIEW: Elevated plasma triglyceride and reduced HDL concentrations are p

42 These offspring exhibited elevated plasma triglyceride and reduced plasma high density lipo

43 ease by a factor of approximately two in the plasma triglyceride and retinyl fatty acid ester concent

44 and in vivo and leads to decreased levels of plasma triglyceride and total cholesterol in ob/ob mice.

45 Levels of plasma triglyceride and triglyceride accumulation in the

46 ame extent as the DASH diet but also reduced plasma triglyceride and VLDL concentrations without sign

47 l gavage resulted in significant decrease in plasma triglyceride and VLDL within 5h.

48 microarray analyses revealed an increase in plasma triglycerides and altered lipid metabolic pathway

49 unction were associated with lower levels of plasma triglycerides and APOC3.

50 Plasma triglycerides and apolipoprotein B-48 concentrati

51 bexarotene significantly (p < 0.01) elevated plasma triglycerides and cholesterol, treatment with MSU

52 tic dyslipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol level

53 ation of the chains based on accumulation of plasma triglycerides and delayed clearance of triglyceri

54 ow that Hs2st(f/f)AlbCre(+) mice accumulated plasma triglycerides and exhibited delayed clearance of

55 in plasma cholesterol or leptin levels, yet plasma triglycerides and fatty acids were decreased.

56 ice were accompanied by partially normalized plasma triglycerides and FFAs, increased plasma lactate,

57 a-inducible protein-10 and I-A(b), and lower plasma triglycerides and glucose.

58 in Genomic Epidemiology consortium, fasting plasma triglycerides and high- and low-density lipoprote

59 small dense LDL (sdLDL) correlate with high plasma triglycerides and low HDL cholesterol levels.

60 lso normalized alcohol-mediated increases in plasma triglycerides and partially reversed decrease in

61 ity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabol

62 Four weeks of dosing resulted in decreased plasma triglycerides and reduced hepatic fat deposition.

63 tration of 8aR dose-dependently reduced both plasma triglycerides and total cholesterol.

64 oprotein lipase, increased fasting levels of plasma triglycerides and very low density lipoprotein ch

65 DO-Me administration reduces total body fat, plasma triglyceride, and free fatty acid levels.

66 total plasma cholesterol, 4-fold more total plasma triglycerides, and 8-fold higher levels of apoB48

67 (e.g., body mass index, waist circumference, plasma triglycerides, and GGT), the independent determin

68 echanisms that are responsible for increased plasma triglycerides, and implications of altered serum

69 vity, reduced visceral adipose mass, reduced plasma triglycerides, and increased HDL-cholesterol).

70 relatives in these families and to evaluate plasma triglyceride as a predictor of death.

71 ted investigations into therapies that lower plasma triglycerides as a means to reduce CVD events.

72 ut mice lacking Apoav had four times as much plasma triglycerides as controls.

73 diated down-regulation, promoting the use of plasma triglycerides as fuel for active muscles.

74 apoAIV(+/+) mice; however, the increases in plasma triglyceride at night were significantly lower in

75 and negatively correlated with the change in plasma triglycerides (beta = -0.051, P = 0.01).

76 -induced Sort1 down-regulation and decreased plasma triglyceride but had no effect on plasma choleste

77 Oral feeding of olive oil further elevated plasma triglycerides, but did not alter plasma cholester

78 A concomitant reduction of plasma triglycerides by 38% (i.p.) and 26% (i.m.) was ob

79 Hydrolysis of plasma triglycerides by LPL can be disrupted by the prot

80 was significantly associated with increased plasma triglycerides, C-reactive protein, interleukin-6,

81 e (LPL) (a protein important for controlling plasma triglyceride catabolism, HDL cholesterol, and oth

82 dependent and apoB-independent pathways, and plasma triglyceride, cholesterol, and phospholipid level

83 t diets had markedly lower fasting levels of plasma triglyceride, cholesterol, and phospholipid than

84 disorder associated with elevated levels of plasma triglyceride, cholesterol, or both.

85 artery disease and characterized by elevated plasma triglycerides, cholesterol, or both.

86 nhibition in Western diet fed mice decreased plasma triglycerides/cholesterol, whereas increasing pla

87 tinyl fatty acid ester absorption as well as plasma triglyceride clearance after oral and intravenous

88 l fat-tolerance test, and a 46% reduction in plasma triglyceride clearance.

89 and inhibitor of lipoprotein lipase-mediated plasma triglyceride clearance.

90 an inhibitor of lipoprotein lipase-mediated plasma triglyceride clearance.

91 a trend (P = 0.069) toward a decrease in the plasma triglyceride concentration after fish-oil supplem

92 Plasma triglyceride concentration has been an inconsiste

93 Plasma triglyceride concentration is a biomarker for cir

94 Elevated plasma triglyceride concentration is a component of the

95 In addition, the plasma triglyceride concentration was greater and the pl

96 They also had a 60% increase in the fasting plasma triglyceride concentration, an increase by a fact

97 Plasma triglyceride concentration, ratio of triglyceride

98 a sample of 264 Caucasian men and women with plasma triglyceride concentrations above the 90th percen

99 ovo lipogenesis, resulting in an increase in plasma triglyceride concentrations and a reduction in pl

100 anges were associated with a 60% increase in plasma triglyceride concentrations and an approximately

101 We also measured plasma triglyceride concentrations and retinyl fatty aci

102 uals with Tangier disease also have elevated plasma triglyceride concentrations and very low HDL, res

103 Increased plasma triglyceride concentrations are an independent ri

104 the changes in the placebo group), and their plasma triglyceride concentrations decreased from 184+/-

105 own to play an important role in determining plasma triglyceride concentrations in humans and mice.

106 epresents an independent risk gene affecting plasma triglyceride concentrations in humans.

107 nucleotide polymorphisms are associated with plasma triglyceride concentrations in the SAFDS.

108 Fasting plasma triglyceride concentrations increased by approxim

109 a human APOAV transgene showed a decrease in plasma triglyceride concentrations to one-third of those

110 Plasma triglyceride concentrations were reduced in male

111 se when mouse apoAII was injected into mice, plasma triglyceride concentrations were significantly in

112 er plasma adiponectin concentrations, higher plasma triglyceride concentrations, and severe disruptio

113 gher in men, were positively associated with plasma triglyceride concentrations, and were negatively

114 ue were significantly associated with higher plasma triglyceride concentrations, low-density lipoprot

115 t risk factor and a key regulatory factor of plasma triglyceride concentrations.

116 on and secretion may explain how HDL affects plasma triglyceride concentrations.

117 3) is required for the maintenance of normal plasma triglyceride concentrations.

118 and its activity alone can directly control plasma triglyceride concentrations.

119 apolipoprotein A5 gene (APOA5) and increased plasma triglyceride concentrations.

120 APOA5 and APOC3 are strongly associated with plasma triglyceride concentrations.

121 diets have repeatedly been shown to increase plasma triglyceride concentrations.

122 Caucasians and is associated with increased plasma triglyceride concentrations.

123 androgen concentrations, blood pressure, and plasma triglyceride concentrations.

124 re similar to those observed on postprandial plasma triglyceride concentrations.

125 The liver, skin, and plasma triglyceride contents are decreased in the neonat

126 resumably leading to reduced local uptake of plasma triglyceride-derived fatty acids and their sparin

127 f AMPK, enhancing LPL activity and uptake of plasma triglyceride-derived fatty acids.

128 holesterol levels were strongly reduced, and plasma triglycerides did not exhibit their normal rise a

129 Plasma triglycerides, fatty acid concentrations, and gly

130 In keeping with that result, plasma triglycerides fell sharply within 10 min after he

131 The Clock gene regulates diurnal plasma triglyceride fluctuation through nuclear receptor

132 The rate of accumulation of plasma triglyceride following Triton WR1339 treatment in

133 8aR also prevented the postprandial rise in plasma triglycerides following a bolus administration of

134 The release of fatty acids from plasma triglycerides for tissue uptake is critically dep

135 e incremental area under the curve (iAUC) of plasma triglycerides.Forty-three healthy subjects were r

136 ions were significantly lower, with elevated plasma triglycerides (>200 mg/dl), and cholesterol (>240

137 hat plays an important role in regulation of plasma triglyceride homeostasis.

138 very low density lipoprotein but maintained plasma triglyceride homeostasis.

139 of lipoprotein lipase (LPL), a key enzyme in plasma triglyceride hydrolysis.

140 rotein lipase (LPL) is the central enzyme in plasma triglyceride hydrolysis.

141 Plasma triglyceride iAUC differed between interventions

142 Plasma triglyceride in apoAIV(-/-) mice showed diurnal v

143 Knockdown of hepatic Sort1 increased plasma triglyceride in mice.

144 ) mice and elevated fasting and postprandial plasma triglycerides in compound Apoe(-)/(-)Ndst1f/fAlbC

145 11 has been hypothesized to be a modifier of plasma triglycerides in FCH.

146 armacological intervention can acutely lower plasma triglycerides in FCS.

147 ndently elevated HDL cholesterol and lowered plasma triglycerides in human apolipoprotein A-I transge

148 protein (LDL) cholesterol and high levels of plasma triglycerides in humans.

149 cting this fusion protein effectively lowers plasma triglycerides in mice and represents a promising

150 hat overexpression of the apoA-V gene lowers plasma triglycerides in mice, these data together sugges

151 ession of lipoprotein lipase (LPL) to reduce plasma triglycerides in mice.

152 among individuals in the lowest quartile of plasma triglycerides in population studies.

153 l as with basal glucose turnover and fasting plasma triglycerides in women.

154 Plasma triglycerides increased transiently after each FO

155 Also, repeated measures of plasma triglycerides indicate that the triglyceride-lowe

156 nse, and to offer a mechanism to explain how plasma triglyceride influences the nature and magnitude

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

158 impaired clearance, whereas the increase in plasma triglycerides is caused mainly by apoE2-impaired

159 Differences in plasma triglyceride, LDL-C, and ApoB levels associated w

160 ere male sex, increased waist circumference, plasma triglycerides, LDL cholesterol, HbA(1c) (A1C), in

161 ipid levels (P <0.003) and 74% higher median plasma triglyceride levels (both P<0.001).

162 (rs3812316, G771C, Gln241His) in MLXIPL with plasma triglyceride levels (combined P = 1.4 x 10(-10)).

163 ealed that four patients displayed increased plasma triglyceride levels after RAPA treatment, which c

164 Nef caused sharp elevations of plasma triglyceride levels and body weight.

165 This was accompanied by increased plasma triglyceride levels and decreased energy expendit

166 apoC-III expression, resulting in increased plasma triglyceride levels and impaired fat tolerance in

167 me (FCS), which is associated with very high plasma triglyceride levels and increased risk of life-th

168 /C3/A4/A5 gene cluster acts as a modifier of plasma triglyceride levels and LDL particle size within

169 66 of the fragment showed no increase in the plasma triglyceride levels and no inhibition of lipolysi

170 the known risk factors for atherosclerosis, plasma triglyceride levels and plasma glucose to insulin

171 r strong evidence of association between low plasma triglyceride levels and protein truncating varian

172 igh amounts of fatty acids, thereby lowering plasma triglyceride levels and reducing obesity.

173 Plasma triglyceride levels are heritable and are correla

174 The findings that plasma triglyceride levels are reduced by Angptl8 deleti

175 cking GPIHBP1 manifest chylomicronemia, with plasma triglyceride levels as high as 5000 mg/dl.

176 eractive EC signaling elicits an increase in plasma triglyceride levels associated with reduced plasm

177 e than wild-type ANGPTL3 in increasing mouse plasma triglyceride levels but not in inhibiting lipopro

178 We found that liver deficiency only reduces plasma triglyceride levels but not other lipid levels.

179 letion of Insig1 leads to higher hepatic and plasma triglyceride levels by inhibiting the processing

180 llustrate this method with an application to plasma triglyceride levels collected on 188 males, ages

181 litating disorder characterized by excessive plasma triglyceride levels for which treatment options a

182 Plasma triglyceride levels have been implicated in ather

183 The reduction of plasma triglyceride levels in Angptl4(-/-) mice and incr

184 We also demonstrate that elevated plasma triglyceride levels in BKS-db mice are associated

185 Hispanics and was associated with increased plasma triglyceride levels in both men and women in each

186 genetic regions that influence variation in plasma triglyceride levels in families that are enriched

187 gnificantly to inter-individual variation in plasma triglyceride levels in humans.

188 ajor locus on chromosome 12p that influences plasma triglyceride levels in Mexican Americans.

189 minal region 17-165 was required to increase plasma triglyceride levels in mice and that a substituti

190 pends on 2-O-and 6-O-sulfation, we evaluated plasma triglyceride levels in mice containing loxP-flank

191 Transient elevation of plasma triglyceride levels in mice treated with a synthe

192 -containing fragment-(207-460) increased the plasma triglyceride levels in mice.

193 plasma cholesterol levels but did not alter plasma triglyceride levels in the E(-)/- mice.

194 19 and is independently associated with high plasma triglyceride levels in three different population

195 re found to be significantly associated with plasma triglyceride levels in two independent studies.

196 tty acid synthesis in HepG2 cells and reduce plasma triglyceride levels in vivo.

197 PGC-1alpha and FXR and results in decreased plasma triglyceride levels in wild-type but not in FXR-n

198 the regulation of basal glucose turnover and plasma triglyceride levels in women, but this gene does

199 ut mice on a chow diet have milky plasma and plasma triglyceride levels of more than 3000 mg/dl.

200 A5*3 haplotype was associated with increased plasma triglyceride levels on all three dietary regimens

201 It is unknown whether lowering plasma triglyceride levels reduces the risk of cardiovas

202 Elevated plasma triglyceride levels represent a risk factor for p

203 ard trend consistent with expression of LPL, plasma triglyceride levels returned to baseline.

204 s also a unexpected further reduction of the plasma triglyceride levels that is associated with incre

205 ipid contents, and inhibited the increase of plasma triglyceride levels upon oral oil administration

206 Failure to defend the lower limit of plasma triglyceride levels was associated with impaired

207 - mice (28.2 3.3 mmol/L vs 27.0 3.1 mmol/L), plasma triglyceride levels were lower in CTGF+/- mice th

208 Unexpectedly, plasma triglyceride levels were robustly elevated upon h

209 Plasma triglyceride levels were significantly higher, an

210 iant (which has been associated with reduced plasma triglyceride levels) and other inactivating mutat

211 te that APOAV is an important determinant of plasma triglyceride levels, a major risk factor for coro

212 benefits ascribed to them, including reduced plasma triglyceride levels, amelioration of atherosclero

213 ered hepatic triglyceride secretion rate and plasma triglyceride levels, and improved plasma lipoprot

214 n, adipose Grp78-knockout mice showed normal plasma triglyceride levels, and plasma glucose and insul

215 liver of mice caused a 8.6-fold elevation in plasma triglyceride levels, but did not alter plasma glu

216 ression of ANGPTL8 in livers of mice doubles plasma triglyceride levels, but does not alter beta cell

217 By lowering plasma triglyceride levels, pravastatin therapy may favo

218 lipogenesis in vivo to increase hepatic and plasma triglyceride levels, showing its role in metaboli

219 In humans, apoE plasma levels correlate with plasma triglyceride levels, suggesting that excess apoE

220 triglyceridemia and 333 controls with normal plasma triglyceride levels, we investigated these issues

221 activity and decreases its ability to raise plasma triglyceride levels.

222 ion, augmented VLDL production, and elevated plasma triglyceride levels.

223 ce and insulin sensitivity, but have reduced plasma triglyceride levels.

224 isms have noted a strong effect of apoA-V on plasma triglyceride levels.

225 hree-fold more common in the group with high plasma triglyceride levels.

226 f the LXR target gene SREBP-1c and increases plasma triglyceride levels.

227 id composition of the RBC membranes and with plasma triglyceride levels.

228 high apoE plasma levels correlate with high plasma triglyceride levels.

229 d 11beta-HSD-1(-/-) mice have markedly lower plasma triglyceride levels.

230 suggesting that excess apoE may also affect plasma triglyceride levels.

231 nals plays a significant role in determining plasma triglyceride levels.

232 tine, increased it in the liver, and lowered plasma triglyceride levels.

233 ymorphic variant in ANGPTL4 results in lower plasma triglyceride levels.

234 oprotein C-III (APOC3) is a key regulator of plasma triglyceride levels.

235 ion, improved glucose tolerance, and lowered plasma triglyceride levels.

236 protein C3 (APOC3) was associated with lower plasma triglyceride levels.

237 ggregate within a gene, were associated with plasma triglyceride levels.

238 bypassing the local loop, without increasing plasma triglyceride levels.

239 ecreased HDL-CE, apoA-I, and apoA-II levels; plasma triglycerides, low density lipoprotein (LDL) chol

240 nfluenced plasma AR concentrations, although plasma triglycerides may explain higher concentrations i

241 gptl4 overexpression suggest that changes in plasma triglyceride metabolism do not regulate alpha-cel

242 e protein 4 (Angptl4), a potent regulator of plasma triglyceride metabolism, binds to lipoprotein lip

243 oprotein apoC-III plays an important role in plasma triglyceride metabolism.

244 ein CIII (apoCIII) is a major determinant of plasma triglyceride metabolism.

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

246 ielded the strongest evidence for linkage of plasma triglycerides near marker D12S391 on chromosome 1

247 After 12 wk of intervention, plasma triglyceride, NEFA, and glucose concentrations we

248 her in the trans10, cis12-CLA group, whereas plasma triglyceride, NEFA, glucose, and insulin concentr

249 stable for the next 3 weeks, whereas neither plasma triglyceride, non-esterified fatty acid, or islet

250 gs improve cardiovascular health by lowering plasma triglycerides, normalize low density lipoprotein

251 ipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.

252 ock markers (plasma melatonin and cortisol), plasma triglycerides, or clock gene expression in whole

253 tly reduced food intake (p < 0.001), fasting plasma triglyceride (p < 0.001) and total cholesterol (p

254 measures of coronary heart disease risk than plasma triglycerides perhaps because their known metabol

255 was significant forearm uptake of both whole plasma triglyceride (presumed to represent primarily VLD

256 h fasting insulin (r = -0.39, P = 0.042) and plasma triglyceride (r = -0.61, P < 0.001).

257 C with fenofibrate treatment correlated with plasma triglyceride reduction (LDLIII r(2) = 67%, P: < 0

258 e peritoneum or quadriceps muscle results in plasma triglyceride reduction in mice.

259 le physiologic factors that may mitigate the plasma triglyceride response, underlying metabolic mecha

260 n-3 PUFA consumption lowers plasma triglycerides, resting heart rate, and blood pres

261 In mice, CCl(4) decreased plasma triglyceride-rich lipoproteins, increased cellula

262 t an oral fat load test, with measurement of plasma triglyceride-rich lipoproteins, oxidized low-dens

263 he concentration of large VLDL, but as basal plasma triglyceride rises there is an increasing tendenc

264 patic triglyceride concentrations and higher plasma triglycerides secondary to increased hepatic secr

265 the strong association of this variant with plasma triglycerides, supporting the value of sensitive

266 essfully be applied to detect differences in plasma triglyceride synthesis in lean and high-fat diet

267 mer distribution analysis (MIDA) to quantify plasma triglyceride synthesis is specifically highlighte

268 inor alleles associated with lower levels of plasma triglyceride (TG) and LDL cholesterol (LDL-C), hi

269 ied a locus on chromosome 19 associated with plasma triglyceride (TG) concentration and nonalcoholic

270 -carbohydrate (LF/HC) diets commonly elevate plasma triglyceride (TG) concentrations, but the kinetic

271 llele frequency ~0.25% (UK)) associated with plasma triglyceride (TG) levels (-1.43 s.d. (s.e.=0.27 p

272 were noted to be positively associated with plasma triglyceride (TG) levels and influenced by a VII

273 Some studies show that plasma triglyceride (TG) levels are a significant indepe

274 Sulf2 ASO lowered the random, nonfasting plasma triglyceride (TG) levels by 50%, achieving nondia

275 de scan for susceptibility genes influencing plasma triglyceride (TG) levels in a Mexican American po

276 tently shown association with differences in plasma triglyceride (TG) levels.

277 ymorphisms (SNPs) of 10 loci that affect the plasma triglyceride (TG) response to an omega-3 (n-3) fa

278 supporting the roles of small, dense LDL and plasma triglyceride (TG), both features of the atherogen

279 all, dense LDL particles, elevated levels of plasma triglycerides (TG), and low levels of HDL charact

280 ght and composition, blood pressure (BP) and plasma triglycerides (TG).

281 e effect of brief oral lipid stimulations on plasma triglyceride [(TG)pl] concentrations was analyzed

282 risk factor for cardiovascular disease, and plasma triglycerides (TGs) correlate strongly with plasm

283 n hepatic lipid contents, but an increase in plasma triglycerides (TGs).

284 A5 gene (APOA5) variation is associated with plasma triglycerides (TGs).

285 digm was able to counteract the elevation in plasma triglycerides that is a side effect of LXR agonis

286 l of human apo E had a 35% decrease in total plasma triglycerides that was due to a reduction in VLDL

287 o evidence that APOC3 increases the level of plasma triglycerides through an LPL-independent mechanis

288 yielded significant evidence for linkage of plasma triglycerides to a genetic location between marke

289 oprotein lipase (LPL)-mediated hydrolysis of plasma triglycerides to FFAs.

290 Plasma triglyceride, total cholesterol, and high density

291 Body mass index (BMI), waist-to-hip ratio, plasma triglyceride (TRG), total cholesterol, low-densit

292 Plasma triglyceride values were transformed, and a varia

293 ant effects of sex and BMI, heritability for plasma triglycerides was estimated as 46 +/- 7% (P < 0.0

294 Both orthologs improved plasma lipids but plasma triglycerides were lower in dMTP mice due to lowe

295 Plasma triglycerides were reduced by diet (from 135 +/-

296 CKR variants were positively correlated with plasma triglycerides, whereas minor alleles of ADIPOR2,

297 iminated the detrimental effect of increased plasma triglycerides, while the beneficial effect of inc

298 diet interaction (P = 0.033) was evident for plasma triglycerides, with 17% and 30% decreases in APOE

299 low density lipoprotein cholesterol and with plasma triglycerides (women only for popliteal) (p < 0.0

300 atty acids in plasma and tissues and reduced plasma triglyceride, yet had little impact on low-densit