ライフサイエンスコーパス: plasma lipid

1 measured fasting and postprandial levels of plasma lipid.

2 inhibition of apoAIV expression might reduce plasma lipids.

3 ontributes to the accumulation of tissue and plasma lipids.

4 the fine mapping of metabolic traits such as plasma lipids.

5 iet recommendations on glycemia, weight, and plasma lipids.

6 < 0.001), independent of diet, exercise, and plasma lipids.

7 MTP targeting is a viable approach to lower plasma lipids.

8 P is a major determinant of daily changes in plasma lipids.

9 tors such as obesity, insulin resistance and plasma lipids.

10 fied species in human red cell membranes and plasma lipids.

11 factor analysis procedures with measures of plasma lipids.

12 ELS149A did not lower and in fact increased plasma lipids.

13 s mouse EL, resulting in increased levels of plasma lipids.

14 ian rhythms controlled by clock genes affect plasma lipids.

15 elopment of atherosclerosis without altering plasma lipids.

16 iation between dietary fat and adiposity and plasma lipids.

17 l hypercholesterolemia, despite no change in plasma lipids.

18 plasma for MPO in promoting peroxidation of plasma lipids.

19 ut of Pcsk9ameliorated the effects of NTS on plasma lipids.

20 expression by MFGM correlated inversely with plasma lipids.

21 liver steatosis in the absence of changes in plasma lipids.

22 overlap between AD, C-reactive protein, and plasma lipids.

23 We investigated plasma lipid 16:1n-7 and FA indexes of elongation and de

24 of diet-induced obesity in humans, even when plasma lipid abnormalities are not present.

25 Elevated triglyceride (TG) is the major plasma lipid abnormality in obese and diabetic patients

26 The authors sought to quantify plasma lipid and glucose testing rates in patients recei

27 et) on active TGF-beta(1) concentrations and plasma lipid and hemostatic risk factors for coronary he

28 ming growth factor beta(1) (TGF-beta(1)) and plasma lipid and hemostatic risk factors for coronary he

29 E3 mice, the APOE2 mice had elevated fasting plasma lipid and insulin levels and displayed prolonged

30 Plasma lipid and lipoprotein changes were similar in stu

31 Plasma lipid and lipoprotein concentrations in chow-fed

32 Before and after the intervention, plasma lipid and lipoprotein subclasses were measured wi

33 Plasma lipid and noncholesterol sterol concentrations we

34 We measured plasma lipids and acylcarnitines using liquid chromatogr

35 Plasma lipids and apolipoproteins and dietary intakes of

36 line, 8 wk, and 16 wk for the measurement of plasma lipids and ARs.

37 Deficiency of TGH in mice lowers plasma lipids and atherogenic lipoproteins without induc

38 vestigate whether the effects of milk fat on plasma lipids and cardiometabolic risk markers are modul

39 5 cluster, and assesses its association with plasma lipids and cardiovascular disease risk.

40 ciation of CETP PTV carrier status with both plasma lipids and CHD.

41 A comprehensive analysis of plasma lipids and eicosanoid metabolites quantified by m

42 ipoprotein lipase (LPL) variant rs13702 with plasma lipids and explored its potential for functionali

43 NRTN was not as effective despite improving plasma lipids and fasting glucose levels.

44 e ADA guidelines were issued, monitoring for plasma lipids and glucose in this population remains low

45 tic plaques as wild-type mice despite higher plasma lipids and glucose levels.

46 o determine the causal link between maternal plasma lipids and infant DNA methylation patterns.

47 in AIV (apoAIV) in the diurnal regulation of plasma lipids and intestinal lipid absorption in mice.

48 Fasting levels of plasma lipids and lipoproteins are reported to improve w

49 ction in sugar intake, on blood pressure and plasma lipids and lipoproteins.

50 and VLDL production in mice that influences plasma lipids and risk for myocardial infarction in huma

51 llumina exome Beadchip to the variability of plasma lipids and stiffness of the common carotid artery

52 ke and drinking patterns are associated with plasma lipids and the risk of MI in Costa Ricans, a popu

53 CD1d, is a therapeutic candidate to decrease plasma lipids and to diminish inflammation.

54 ceride transfer protein is a target to lower plasma lipids and to reduce inflammation in certain immu

55 ount for the high fraction of dimer found in plasma, lipids and proteins "catalyze" dimer formation,

56 100 184 individuals from 46 GLGC studies for plasma lipids, and 22 233 cases and 64 762 controls from

57 relation to biomarkers of glycemic control, plasma lipids, and inflammation markers.

58 ietary n-3 PUFAs decreased body-weight gain, plasma lipids, and insulin (P < 0.05) and improved gluco

59 ponse was significantly blunted for obesity, plasma lipids, and insulin resistance.

60 sight into the association between TRIB1 and plasma lipids, and liver traits in humans.

61 (MoBa) and included 479 pregnant women with plasma lipids, apoB, and CRP measurements.

62 tero exposure to maternal tobacco smoke with plasma lipids, apolipoprotein B (apoB), and C-reactive p

63 Plasma lipids are maintained within a narrow physiologic

64 Statin-dependent effects on plasma lipids are mediated through the inhibition of HMG

65 of hypercholesterolemia in which changes in plasma lipids are not observed in response to simvastati

66 ent dairy foods may have distinct effects on plasma lipids because of a varying content of MFGM.

67 transfer protein (MTP) is a target to reduce plasma lipids because of its indispensable role in trigl

68 r and factor analysis methods in relation to plasma lipid biomarkers.

69 Gene sets for plasma lipids, blood pressure, and coronary artery disea

70 ve investigated the impact of glucomannan on plasma lipids, body weight, fasting blood glucose (FBG),

71 Both orthologs improved plasma lipids but plasma triglycerides were lower in dMT

72 eficiency failed to initiate peroxidation of plasma lipids, but they did so after supplementation wit

73 ) resulted in the peroxidation of endogenous plasma lipids by catalase-, heme poison-, and ascorbate-

74 ine measurements included blood pressure and plasma lipid, C-reactive protein, and adiponectin levels

75 tors, including blood pressure and levels of plasma lipids, C-reactive protein, and fasting insulin a

76 Fasting plasma lipids, caecal microbiota and gene expression in

77 res were associated with significantly lower plasma lipids, cardiovascular risk, and medication use.

78 om recent genome-wide association studies of plasma lipids (CELSR2/PSRC1/SORT1, MLXIPL, PCSK9, GALNT2

79 local antiatherogenic effects independent of plasma lipid changes.

80 ght, and visceral adipose tissue (VAT) mass; plasma, lipids (cholesterol and triglycerides), liver en

81 on was observed between deposit severity and plasma lipid concentration.

82 relationship between dietary fat intake and plasma lipid concentrations also differed according to P

83 vaccenic acid is the predominant isomer, on plasma lipid concentrations among healthy women.

84 that gene-environment interactions modulate plasma lipid concentrations and potentially CVD risk.

85 , the development of MTP inhibitors to lower plasma lipid concentrations has been hindered by adverse

86 n between recreational physical activity and plasma lipid concentrations in early pregnancy.

87 There was no association with plasma lipid concentrations in either study.

88 he body weight, total fat tissue weight, and plasma lipid concentrations in the mice.

89 Sex and plasma lipid concentrations independently influenced pla

90 Absence of association with plasma lipid concentrations suggests that PPARalpha affe

91 Despite high-dose rosuvastatin lowering plasma lipid concentrations to a greater extent than did

92 Total and individual FFA and plasma lipid concentrations were measured before and aft

93 onal epidemiological studies have associated plasma lipid concentrations with risk for coronary heart

94 vate carboxylase ASO also reduced adiposity, plasma lipid concentrations, and hepatic steatosis in hi

95 To identify genetic variants influencing plasma lipid concentrations, we first used genotype impu

96 in secretion, thereby regulating hepatic and plasma lipid concentrations.

97 ated with sustained reductions in weight and plasma lipid concentrations.

98 p ratio but no significant change in fasting plasma lipid concentrations.

99 .024, 5.09); adjusted by NAFLD severity] and plasma lipid concentrations.

100 Reducing their activities might lower plasma lipid concentrations.

101 the genetic predisposition to elevations in plasma lipids, constructed using single-nucleotide polym

102 To determine if a decrease in plasma lipid content reverses these abnormalities, insul

103 Elevated plasma lipid content, or hyperlipidemia, is a significan

104 Elevated plasma lipids contribute to neurovascular dysfunction in

105 diabetes, although exactly which of the many plasma lipids contribute to this remains unclear.

106 Differences in plasma lipids due to diabetes were assessed among the Hi

107 ntrol but may be physiologically relevant to plasma lipids, especially in obese individuals.

108 le preparation protocols for optimized blood plasma lipid extraction and measurement by UPLC-MS lipid

109 h as phospholipids, were determined in human plasma lipid extracts.

110 omannan to better characterize its impact on plasma lipids, FBG, body weight, and BP.

111 We observed a strong association between the plasma lipids gene set and plasma lipid variables, but n

112 examined associations of these variants with plasma lipid, glucose, and insulin concentrations; bodyw

113 y obvious phenotype in terms of body weight, plasma lipids, glucose, and non-esterified fatty acid le

114 on (VO2max), resting blood pressure, fasting plasma lipids, glucose, C-reactive protein, and arterial

115 High levels of plasma lipids have been recognized as a major risk facto

116 he effects on plasma phospholipase activity, plasma lipids, HDL particle size, HDL turnover, and tiss

117 E-deficient mice in vivo without influencing plasma lipids, HDL subpopulations, or cholesterol efflux

118 critical role in lipoprotein metabolism and plasma lipid homeostasis through its high-affinity bindi

119 Despite its importance in plasma lipid homeostasis, the regulation of Lmf1 remains

120 s whereby this protein functions to modulate plasma lipid homeostasis.

121 hibited estrogen agonistic activity on bone, plasma lipids, hot flush, and vagina.

122 similar elevations of plasma apoB and total plasma lipids; however, the lipid cores of the apoB-cont

123 By contrast, plasma lipid hydroperoxide concentrations were similar i

124 First, the plasma lipid hydroperoxide content was reduced significa

125 rdiovascular disease risk factors, including plasma lipids, hypertension, diabetes mellitus, and obes

126 e genome for common variants associated with plasma lipids in >100,000 individuals of European ancest

127 f human cardiac and buccal tissue, RBCs, and plasma lipids in 25 other patients.

128 n the literature to have profound effects on plasma lipids in animal models.

129 f plasma ApoE to wild-type levels normalizes plasma lipids in ApoE KO mice.

130 feeding induced more weight gain and higher plasma lipids in APOE3 compared to APOE4 mice (P < 0.05)

131 ic expression was negatively associated with plasma lipids in humans.

132 holesterol excretion to the bile and reduces plasma lipids in L-Bmal1(-/-)Apoe(-/-) and Apoe(-/-) mic

133 Arglabin reduces inflammation and plasma lipids, increases autophagy, and orients tissue m

134 VSG reduced postprandial levels of plasma lipid, independently of body weight.

135 sis have normal or only modest elevations in plasma lipids, indicating that additional mechanisms con

136 , waist circumference, insulin, glucose, and plasma lipids; infant feeding information was provided b

137 HFD had significantly increased body weight, plasma lipids, insulin, and insulin resistance when comp

138 er a genetic predisposition to elevations in plasma lipids is associated with the presence of MAC.

139 A large fraction of the heritability of plasma lipids is attributable to variants present on the

140 ate [PEFR]) normalized for subject's height, plasma lipid levels (cholesterol, triglycerides, high-de

141 Our data indicate that normalization of plasma lipid levels abolishes progression of atheroscler

142 ments, diabetic retinopathy assessments, and plasma lipid levels all can add to predictive accuracy f

143 w not previously implicated, as modifiers of plasma lipid levels and atherosclerosis, yielding new in

144 iet for 20 or 30 weeks and then analyzed for plasma lipid levels and atherosclerotic lesion formation

145 (PTVs) at the CETP gene were associated with plasma lipid levels and CHD.

146 d reductions in body weight gain (as well as plasma lipid levels and epididymal WAT sizes in HFD-fed

147 pite the observed tissue lipid accumulation, plasma lipid levels and lipoprotein cholesterol distribu

148 ma glycemia, whole body insulin sensitivity, plasma lipid levels and liver steatosis.

149 The use of niacin to improve plasma lipid levels and reduce risk of myocardial infarc

150 patocytes of FGFR4-deficient mice, decreased plasma lipid levels and restored the high-fat diet-induc

151 Plasma lipid levels and the extent and complexity of ath

152 resence of an inactivating mutation and both plasma lipid levels and the risk of coronary heart disea

153 Cellular and plasma lipid levels are tightly controlled by complex ge

154 ects of vertical sleeve gastrectomy (VSG) on plasma lipid levels are weight independent.

155 Plasma lipid levels as well as coronary artery disease (

156 Plasma lipid levels between animals of various PTL genot

157 lectively, these data indicate that reducing plasma lipid levels by genetic inactivation of the mttp

158 New genes regulating plasma lipid levels can be found in mice and then tested

159 These findings suggest that plasma lipid levels can influence cognition and synaptic

160 Despite enhanced weight gain and plasma lipid levels compared with Apoe(-/-) controls, Ep

161 the pathways targeted by the CNS to control plasma lipid levels could offer alternative targets to c

162 ffects of these rare in European variants on plasma lipid levels in 828 Hutterites and applied a Baye

163 es may have therapeutic benefits in lowering plasma lipid levels in diabetes and obesity by triggerin

164 patic apolipoprotein B secretion and reduces plasma lipid levels in mice, and its hepatic expression

165 espite similar total lesion area and similar plasma lipid levels in the two groups of mice.

166 eemed to have modestly beneficial effects on plasma lipid levels in this sample of persons with relat

167 e cholesterol transport and slightly reduced plasma lipid levels in vivo.

168 -6 polyunsaturated fatty acids (PUFAs) lower plasma lipid levels is incompletely understood.

169 herosclerotic lesions at the aortic root and plasma lipid levels of 234 female F2 mice were analyzed

170 cantly in atherosclerosis susceptibility and plasma lipid levels on the apolipoprotein E-deficient (a

171 pcat3 deficiency has a much bigger effect on plasma lipid levels than that of liver deficiency.

172 Apolipoprotein E (ApoE) regulates plasma lipid levels via modulation of lipolysis and serv

173 rosclerotic burden in the large vessels, and plasma lipid levels were analyzed.

174 High-risk plasma lipid levels were defined according to the Nation

175 Although plasma lipid levels were more strongly associated with a

176 Plasma lipid levels were not changed in G2A(-/-)ApoE(-/-

177 Plasma lipid levels were then reduced.

178 y was to determine whether reducing elevated plasma lipid levels with a "genetic switch" in Reversa m

179 ion of hepatic Ces3/Tgh expression decreases plasma lipid levels without causing severe hepatic steat

180 organ modulating lipoprotein metabolism and plasma lipid levels) uptake studies to establish the imp

181 rospective study (with up to six measures of plasma lipid levels) were genotyped for 20 LPL tagging (

182 tection from obesity on a high-fat diet, low plasma lipid levels, and a neuromuscular abnormality (hi

183 entrations, adverse events, CD4 cell counts, plasma lipid levels, and HIV-1 RNA levels in seminal pla

184 his analysis supports that PTP-1beta affects plasma lipid levels, and may lead to obesity and hyperte

185 res included changes in waist circumference, plasma lipid levels, and other cardiometabolic risk fact

186 nicity, sex, apoE genotypes, CHD end points, plasma lipid levels, and other CHD risk factors was deve

187 d in Tm6sf2-deficient mice including reduced plasma lipid levels, diminished hepatic triglycerides se

188 There were no significant differences in plasma lipid levels, lipoprotein distributions, and HDL

189 No significant alterations in plasma lipid levels, liver lipid content and distributio

190 ngeable apolipoprotein family that modulates plasma lipid levels, recombinant human apolipoprotein (a

191 Angptl3 messenger RNA (mRNA) for effects on plasma lipid levels, triglyceride clearance, liver trigl

192 hat ApoE knock-out mice have highly elevated plasma lipid levels, which may independently affect brai

193 ocrine control of cholesterol metabolism and plasma lipid levels.

194 le metabolic improvements, including reduced plasma lipid levels.

195 abolished rhythmicity in MTP expression and plasma lipid levels.

196 the purpose of finding new genes regulating plasma lipid levels.

197 in macrophages in the absence of changes in plasma lipid levels.

198 Regression was independent of plasma lipid levels.

199 ave the unexpected side effect of increasing plasma lipid levels.

200 with its proposed role in the modulation of plasma lipid levels.

201 no significant changes in CD4 cell counts or plasma lipid levels; and no detectable HIV-1 RNA in semi

202 temic cholesterol metabolism and circulating plasma lipids levels.

203 ulatum G4 or Bifidobacterium longum BB536 on plasma lipids, lipid peroxidation and the faecal excreti

204 response variables were body weight; fasting plasma lipid, lipoprotein, glucose, glycated hemoglobin

205 ge servings of either oat or wheat cereal on plasma lipids, lipoprotein subclasses, lipoprotein parti

206 Plasma lipids; lipoproteins; apolipoprotein (apo) B, A-I

207 optimal FGF21 analog reduced blood glucose, plasma lipids, liver triglycerides, and plasma glucagon

208 between childbearing and changes in fasting plasma lipids (low density lipoprotein, HDL, and total c

209 lerosis regression occurs in these mice upon plasma lipid lowering induced by a change in diet and th

210 of lipids from atherosclerotic lesions upon plasma lipid lowering without significantly affecting th

211 mpact vascular function independent of their plasma lipid-lowering action.

212 imed to improve the oral bioavailability and plasma lipid-lowering effect of probucol (PB) by constru

213 er increase liver steatosis despite lowering plasma lipids, mainly due to reduced hepatic lipogenesis

214 factor 1 (Lmf1) is a critical determinant of plasma lipid metabolism, as demonstrated by severe hyper

215 Plasma lipid metabolites were studied through the determ

216 vegan diet appeared to improve glycemia and plasma lipids more than did conventional diabetes diet r

217 ng design was used to examine the effects on plasma lipids of 3 diets that differed in total fat: the

218 e are limited data about dietary intakes and plasma lipids of elderly US Hispanics.

219 s (NAPEs) are a relatively abundant group of plasma lipids of unknown physiological significance.

220 45% kcal %fat) diet to explore the impact of plasma lipids on the development of neuropathy.

221 ta was decreased by 50% to 80%, unrelated to plasma lipid or IL-10 levels.

222 were overweight or obese but did not improve plasma lipids or glucose and decreased HDL more than in

223 This occurred without affecting plasma lipids or glucose, suggesting independence from c

224 s without causing unfavorable alterations in plasma lipids or glycemic control.

225 emic insulin sensitivity, glucose tolerance, plasma lipid, or blood pressure.

226 fish-oil supplementation on blood pressure, plasma lipids, or plasma glucose, although there was a t

227 nificant increase in the lag phase preceding plasma lipid oxidation.

228 used 185 common variants recently mapped for plasma lipids (P < 5 x 10(-8) for each) to examine the r

229 We evaluated the usefulness of multiple plasma lipid parameters in predicting coronary heart dis

230 f approximately 100 genetic loci determining plasma lipid parameters.

231 te that ANGPTL4 is an important regulator of plasma lipid partitioning during sustained cold.

232 , injection of LPS causes significantly less plasma lipid peroxidation in IRAK-1(-/-) mice compared w

233 ; 103 +/- 9 versus 73 +/- 6 mmHg; P < 0.01), plasma lipid peroxides (2.6 +/- 0.3 versus 2.0 +/- 0.3 n

234 ain only a fraction of the total variance in plasma lipid phenotypes and CAD.

235 ously reported GWAS variants associated with plasma lipid phenotypes.

236 1, a monoclonal antibody specific for native plasma lipid-poor (prebeta1) HDL.

237 Plasma lipid profile and homocysteine levels, blood pres

238 Beneficial effects on the plasma lipid profile and LDL oxidation rates have also b

239 Body weight, adipocyte size, and plasma lipid profile were not affected by isoflavone sup

240 The plasma lipid profile, activity of liver enzymes, and oxi

241 onds to lower blood glucose levels, improved plasma lipid profile, and increased sensitivity to insul

242 As expected from the pro-atherogenic plasma lipid profile, aortic atherosclerosis was increas

243 TLR3 deficiency also modified the plasma lipid profile, decreasing VLDL levels due to decr

244 G5/G8 in only the liver had no effect on the plasma lipid profile, including cholesterol, HDL-C, and

245 oE-KO and LCAT-Tg mice, without changing the plasma lipid profile, lipoprotein lipid composition, or

246 nts in glucose homeostasis, fatty liver, and plasma lipid profile.

247 esistance, leptin resistance, and changes in plasma lipid profile.

248 ferric reducing ability of plasma assay, and plasma lipid profile.

249 rated and polyunsaturated fatty acids on the plasma lipid profile.

250 y brain ApoE loss in the context of a normal plasma lipid profile.

251 ue, although no changes were observed in the plasma lipid profile.

252 DL receptor, and LCAT deficiencies; improves plasma lipid profile; and ameliorates proteinuria in nep

253 Additionally, plasma lipid profiles also displayed an increase in palm

254 livers of mutant animals, as well as altered plasma lipid profiles and inflammatory parameters.

255 rosclerotic plaque size without altering the plasma lipid profiles in apolipoprotein E-deficient mice

256 body weight) for an additional 4 wk improved plasma lipid profiles in both APOE3 and APOE4 mice.

257 with LXR agonist had differential effects on plasma lipid profiles in LDLR(-/-) and apoE(-/-) mice.

258 were associated modest favorable effects on plasma lipid profiles, but a small rise in fasting plasm

259 in liver would not be expected to modify the plasma lipid profiles.

260 y whole grains have been reported to improve plasma lipid profiles.

261 ase risk in part because of their effects on plasma lipid profiles.

262 vation and atherosclerosis in the absence of plasma lipid reduction.

263 Plasma lipids, renal function, and key lipid regulatory

264 ovascular disease, individual variability in plasma lipid responses exists.

265 Plasma lipid species (310) were measured by a targeted l

266 Our results imply that: a) not all plasma lipid species are genetically informative for T2D

267 risk factors, demonstrates the potential of plasma lipid species as biomarkers for cardiovascular ri

268 Median heritability of the plasma lipid species was 0.37.

269 le enabling a broad coverage and recovery of plasma lipid species.

270 Patients were characterized regarding plasma lipid status, lipid-lowering drug treatment, and

271 tocopherol absorbed was not dependent on the plasma lipid status.

272 t/high-cholesterol diet on body composition, plasma lipids, systemic and tissue-specific insulin sens

273 identify several novel loci associated with plasma lipids that are also associated with CAD.

274 The response of plasma lipids to dietary fat manipulation is highly hete

275 enes have been identified as associated with plasma lipid traits by GWAS, though only relatively few

276 cts with the genetic factors associated with plasma lipid traits remains poorly understood.

277 B1 are significantly associated with several plasma lipid traits, circulating liver enzymes, and the

278 ly 100 genomic loci that are associated with plasma lipid traits, two-thirds of which had never been

279 alidation of novel GWAS loci associated with plasma lipid traits.

280 These studies show that MTP expression and plasma lipid undergo diurnal regulation and exhibit peak

281 lesteryl ester hydroperoxides are present in plasma, lipid uptake by monocytes in circulation may con

282 ation between the plasma lipids gene set and plasma lipid variables, but none of the 3 genome-wide as

283 reportedly bind to intracellular membranes, plasma lipid vesicles, and artificial lipid bilayers wit

284 ontrol) administration and the FA profile of plasma lipids was determined.

285 No effect on plasma lipids was observed.

286 To bypass the effect of ApoE loss on plasma lipids, we generated a novel mouse model that exp

287 increases the DHA content of their infants' plasma lipids, we hypothesized that it might also improv

288 mechanisms that modulate the distribution of plasma lipids, we performed lipid profiling during oral

289 Changes in plasma lipids were also evaluated at these time points.

290 n of 28 h, blood was collected every 4 h and plasma lipids were analyzed by HPLC/MS.

291 Glycated hemoglobin (Hb A(1c)) and plasma lipids were assessed at weeks 0, 11, 22, 35, 48,

292 Plasma lipids were associated with common variants locat

293 increased the degree of adiposity; however, plasma lipids were elevated only in the Western diet-fed

294 tatistical analyses, we report 51 individual plasma lipids were significantly associated with obesity

295 between cereal fiber and anthropometrics and plasma lipids were similar.

296 PCSK9 and plasma lipids were studied in nephrotic syndrome patient

297 ified in genome-wide association studies for plasma lipids, were associated with aortic valve disease

298 associated with coronary artery disease and plasma lipids, whereas some exhibited coaggregation betw

299 As expected, the control diet increased plasma lipids, whereas the MFGM diet did not [total chol

300 sma, does not accumulate in LDL but protects plasma lipids, which are extracted together with hydroxy