ライフサイエンスコーパス: plasma triglyceride

1 bnormalities in high-density lipoprotein and plasma triglyceride.

2 disease persisted even after adjustment for plasma triglycerides.

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

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

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

6 ent mice are insulin resistant with elevated plasma triglycerides.

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

8 , whereas APOA5 mutation carriers had higher plasma triglycerides.

9 sterol, nor any consistent associations with plasma triglycerides.

10 blunting of the usual post-prandial rise in 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 Mice fed a high-fat diet had a more elevated plasma triglyceride and cholesterol level than those tha

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

21 Increased plasma triglyceride and cholesterol levels are major ris

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

23 Ritonavir treatment increased plasma triglyceride and cholesterol levels through incre

24 Plasma triglyceride and cholesterol levels were high in

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

26 8, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride and cholesterol, respectively, in wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 Levels of plasma triglyceride and triglyceride accumulation in the

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

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

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

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

48 Plasma triglycerides and apolipoprotein B-48 concentrati

49 lude 1) that TNF-alpha functions to regulate plasma triglycerides and body adiposity and 2) that alth

50 The postabsorptive concentrations of plasma triglycerides and common polymorphisms of apolipo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 Plasma triglyceride concentration has been an inconsiste

89 Plasma triglyceride concentration is a biomarker for cir

90 Elevated plasma triglyceride concentration is a component of the

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

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

93 Plasma triglyceride concentration, ratio of triglyceride

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

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

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

97 We also measured plasma triglyceride concentrations and retinyl fatty aci

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

99 Increased plasma triglyceride concentrations are an independent ri

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

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

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

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

104 Fasting plasma triglyceride concentrations increased by approxim

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

106 Plasma triglyceride concentrations were reduced in male

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

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

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

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

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

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

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

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

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

116 Caucasians and is associated with increased plasma triglyceride concentrations.

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

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

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

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

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

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

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

124 Plasma triglycerides did not vary with minor illness.

125 Plasma triglycerides, fatty acid concentrations, and gly

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

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

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

129 8aR also prevented the postprandial rise in plasma triglycerides following a bolus administration of

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

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

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

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

134 very low density lipoprotein but maintained plasma triglyceride homeostasis.

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

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

137 Plasma triglyceride iAUC differed between interventions

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

139 Knockdown of hepatic Sort1 increased plasma triglyceride in mice.

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

141 11 has been hypothesized to be a modifier of plasma triglycerides in FCH.

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

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

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

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

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

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

148 Plasma triglycerides increased transiently after each FO

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

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

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

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

153 fferences in total cholesterol (women only), plasma triglycerides, LDL cholesterol, apolipoprotein B

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

155 Donor age (P < 0.006) and average fasting plasma triglyceride level (P < 0.009) were significantly

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

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

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

159 ivariate correlates of TxCAD, higher fasting plasma triglyceride levels and body weight are the only

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

161 istently and strongly associated with raised plasma triglyceride levels and coronary artery disease.

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

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

164 66 of the fragment showed no increase in the plasma triglyceride levels and no inhibition of lipolysi

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

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

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

168 Plasma triglyceride levels are heritable and are correla

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

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

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

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

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

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

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

176 Plasma triglyceride levels have been implicated in ather

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

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

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

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

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

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

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

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

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

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

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

188 19 and is independently associated with high plasma triglyceride levels in three different population

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

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

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

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

193 In contrast, plasma triglyceride levels increased (mostly in very low

194 (4) Fatty liver from birth and elevated plasma triglyceride levels later in life.

195 nd observed severe hypertriglyceridemia with plasma triglyceride levels of 4,521+/-6, 394 mg/dl vs. 4

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

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

198 Elevated plasma triglyceride levels represent a risk factor for p

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

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

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

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

203 LPL knock-out background (LPL1) background, plasma triglyceride levels were lowered 22 and 33% in th

204 Unexpectedly, plasma triglyceride levels were robustly elevated upon h

205 Plasma triglyceride levels were significantly higher, an

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

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

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

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

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

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

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

213 These transgenic animals had 3-fold higher plasma triglyceride levels, higher very low density lipo

214 By lowering plasma triglyceride levels, pravastatin therapy may favo

215 apoE2 levels also correlated positively with plasma triglyceride levels, suggesting impaired lipolysi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 ice exhibited significantly higher levels of plasma triglycerides (P < 0.05), total cholesterol (P <

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

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

253 jor enzyme responsible for the hydrolysis of plasma triglycerides, promotes binding and catabolism of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 Plasma triglyceride, total cholesterol, and high density

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

289 Plasma triglyceride values were transformed, and a varia

290 The elevated plasma triglyceride was accounted for mainly by a 97% in

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

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

293 Compared with pre-Rx levels, plasma triglycerides were not significantly changed by e

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

295 In addition, plasma triglycerides were significantly higher (212% of

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