ライフサイエンスコーパス: plasma lipid

1 measured fasting and postprandial levels of plasma lipid.

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

3 inhibition of apoAIV expression might reduce plasma lipids.

4 2 diabetes, body mass index, and four major plasma lipids.

5 ontributes to the accumulation of tissue and plasma lipids.

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

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

8 < 0.001), independent of diet, exercise, and plasma lipids.

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

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

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

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

13 factor analysis procedures with measures of plasma lipids.

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

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

16 ian rhythms controlled by clock genes affect plasma lipids.

17 t-to-height ratio (WtHR), blood pressure and plasma lipids.

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

19 expression by MFGM correlated inversely with plasma lipids.

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

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

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

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

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

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

26 Plasma lipid and lipoprotein changes were similar in stu

27 Plasma lipid and lipoprotein concentrations in chow-fed

28 sociated with similar patterns of changes in plasma lipid and lipoprotein levels and with similar eff

29 LDL-C <70 mg/dl and percent change in other plasma lipid and lipoprotein levels.

30 Plasma lipid and noncholesterol sterol concentrations we

31 We measured plasma lipids and acylcarnitines using liquid chromatogr

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

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

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

35 5 cluster, and assesses its association with plasma lipids and cardiovascular disease risk.

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

37 worldwide display mildly elevated levels of plasma lipids and cholesterol linked to diet and life-st

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 100 184 individuals from 46 GLGC studies for plasma lipids, and 22 233 cases and 64 762 controls from

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

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

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

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

57 to western diet induced obesity, changes in plasma lipids, and reduced aortic atherosclerosis.

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

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

60 Plasma lipids are maintained within a narrow physiologic

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

62 lying the observed genetic associations with plasma lipids at 6p21 in human.

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

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

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

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

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

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

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

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

71 Fasting plasma lipids, caecal microbiota and gene expression in

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

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

74 local antiatherogenic effects independent of plasma lipid changes.

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

76 it to the data when considering all maternal plasma lipid classes but not when based only on non-este

77 ted a good fit to the data when all maternal plasma lipid classes were included but not with modellin

78 tic TG secretion and contributed to impaired plasma lipid clearance following an oral lipid gavage.

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

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

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

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

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

84 Sex and plasma lipid concentrations independently influenced pla

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

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

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

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

89 FADS variants have been associated with plasma lipid concentrations, risk of cardiovascular dise

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

91 Reducing their activities might lower plasma lipid concentrations.

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

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

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

95 .024, 5.09); adjusted by NAFLD severity] and plasma lipid concentrations.

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

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

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

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

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

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

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

103 y LA intake on the fatty acid composition of plasma lipids, fasting glucose, and high-sensitivity C-r

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

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

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

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

108 This study demonstrates that plasma lipids have the potential to improve the detectio

109 Plasma lipids, hemoglobin A1C, body composition, the ora

110 ystolic, diastolic, and mean blood pressure; plasma lipids; high-sensitivity C-reactive protein; meta

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

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

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

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

115 By contrast, plasma lipid hydroperoxide concentrations were similar i

116 First, the plasma lipid hydroperoxide content was reduced significa

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

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

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

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

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

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

123 ective was to estimate its average effect on plasma lipids in humans and its safety profile.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 lic risk through associations to circulating plasma lipid levels and identify lipid-associated CpGs w

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

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

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

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

145 Plasma lipid levels and the extent and complexity of ath

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

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

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

149 Plasma lipid levels as well as coronary artery disease (

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

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

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

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

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

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

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

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

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

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

160 -6 polyunsaturated fatty acids (PUFAs) lower plasma lipid levels is incompletely understood.

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

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

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

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

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

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

167 Although plasma lipid levels were more strongly associated with a

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

169 Plasma lipid levels were then reduced.

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

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

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

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

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

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

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

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

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

179 Alcohol intake influences plasma lipid levels, and such effects may be moderated b

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

181 he associations of these genetic scores with plasma lipid levels, lipoprotein levels, and the risk of

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

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

184 cated many susceptible genes associated with plasma lipid levels, their physiological and molecular f

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

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

187 ocrine control of cholesterol metabolism and plasma lipid levels.

188 le metabolic improvements, including reduced plasma lipid levels.

189 abolished rhythmicity in MTP expression and plasma lipid levels.

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

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

192 Regression was independent of plasma lipid levels.

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

194 iver-specific overexpression of TRIB1 lowers plasma lipid levels.

195 ated MTP regulation in the intestine affects plasma lipid levels.

196 umption interactions associated with fasting plasma lipid levels.

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

198 temic cholesterol metabolism and circulating plasma lipids levels.

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

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

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

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

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

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

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

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

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

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

209 lipoprotein E (apoE) is the key regulator of plasma lipids, mediating altered functionalities in lipo

210 of plasma fasting glucose, serum hsCRP, and plasma lipid mediators (eicosanoids and related analogs)

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

212 Plasma lipid metabolites were studied through the determ

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

214 lipids associated with AF or future AF from plasma lipids (n = 316) measured from participants in th

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

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

217 45% kcal %fat) diet to explore the impact of plasma lipids on the development of neuropathy.

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

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

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

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

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

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

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

225 Plasma lipid panel and norepinephrine level were also me

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

227 f approximately 100 genetic loci determining plasma lipid parameters.

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

229 anion scavenging ability, linoleic acid and plasma lipid peroxidation ability.

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

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

232 ously reported GWAS variants associated with plasma lipid phenotypes.

233 1, a monoclonal antibody specific for native plasma lipid-poor (prebeta1) HDL.

234 Plasma lipid profile and homocysteine levels, blood pres

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 -deficient mice also had altered hepatic and plasma lipid profiles.

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

257 Plasma lipids, renal function, and key lipid regulatory

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

259 iations between PFAA and body fat% (BF%) and plasma lipids SDS at 3 months and 18 months of age were

260 These include the identification of plasma lipid signatures that predict pathological lipid

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

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

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

264 Median heritability of the plasma lipid species was 0.37.

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

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

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

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

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

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

271 this study was to assess if the addition of plasma lipids to traditional risk factors could improve

272 hip between genetic variants associated with plasma lipid traits (high-density lipoprotein, HDL; low-

273 re genome-wide significantly associated with plasma lipid traits and coronary artery disease (CAD), b

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

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

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

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

278 re used to construct genetic instruments for plasma lipid traits.

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

280 ked genetically as well as epigenetically to plasma lipid traits.

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

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

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

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

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

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

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

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

289 The intensities of 94 out of 195 plasma lipids were altered by the repeated administratio

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