ライフサイエンスコーパス: plasma cholesterol

1 ic cholesterol as well as a reduction in the plasma cholesterol.

2 TZ), and assessed reasons for differences in plasma cholesterol.

3 ma glucagon and reduced ( approximately 20%) plasma cholesterol.

4 regulated, indicative of increased uptake of plasma cholesterol.

5 s index, age, sex, smoking status, and total plasma cholesterol.

6 lly with statins to enhance LDLRs and reduce plasma cholesterol.

7 s to the relationship between rs10401969 and plasma cholesterol.

8 with lipid peroxidation (p = 0.004), as was plasma cholesterol.

9 ikely by reducing lipoprotein production and plasma cholesterol.

10 pholipids serving as an ideal transporter of plasma cholesterol.

11 y be a promising new therapy for lowering of plasma cholesterol.

12 erity score is accounted for by variation in plasma cholesterol.

13 lted in hyperglycemia and lower body fat and plasma cholesterol.

14 for atherosclerotic lesions through elevated plasma cholesterol.

15 ing gene expression in liver and lowering of plasma cholesterol.

16 weight gain (11.8 and 5.7 g, respectively), plasma cholesterol (23.1 and 19.6%), and liver triglycer

17 patocyte-derived model had 2-fold more total plasma cholesterol, 4-fold more total plasma triglycerid

18 herogenic profile characterized by decreased plasma cholesterol (63%), cholesteryl ester (63%), free

19 tion, control (nondiabetic) mice had reduced plasma cholesterol (-77%), plaque cholesterol (-53%), an

20 e mice also exhibited a 1.7-fold increase in plasma cholesterol and an atherogenic lipoprotein profil

21 Plasma cholesterol and apoB-containing lipoprotein level

22 ssue-specific effects of the IDOL pathway on plasma cholesterol and atherosclerosis have not been exa

23 nt protein (Clock(Delta19/Delta19)) enhances plasma cholesterol and atherosclerosis in 3 different mo

24 On the chow diet, these mice had similar plasma cholesterol and blood monocyte levels but increas

25 -(R) was found to have beneficial effects on plasma cholesterol and bone metabolism while maintaining

26 KO/L and Tg/L mice exhibited levels of plasma cholesterol and CE accumulation similar to those

27 As designed, total plasma cholesterol and high density lipoprotein concentr

28 directionality of the effect of sortilin on plasma cholesterol and its role in the secretion of hepa

29 Therefore, miR-30c lowers plasma cholesterol and mitigates atherosclerosis by redu

30 cholesterol had comparable effects on total plasma cholesterol and non-high-density lipoprotein chol

31 evated and were accompanied by reductions in plasma cholesterol and normalization of lipoprotein prof

32 Measurements of plasma cholesterol and phospholipids, intestinal absorpt

33 rcholesterolemia, characterized by increased plasma cholesterol and phospholipids, that were distribu

34 with nephrotic syndrome showed a decrease in plasma cholesterol and plasma PCSK9 on remission of thei

35 It produces long-term lowering of plasma cholesterol and prevents atherosclerosis developm

36 of SLOS was negatively correlated with both plasma cholesterol and relative plasma cholesterol, but

37 also been described that dramatically lower plasma cholesterol and restore endothelial function in a

38 dlr (-/-) mice, DKO mice displayed decreased plasma cholesterol and TG levels and reduced atheroscler

39 Their plasma cholesterol and triglyceride levels are both twic

40 Furthermore, the effects of apoE2 on both plasma cholesterol and triglyceride levels are dose depe

41 arameters of bile acid metabolism as well as plasma cholesterol and triglyceride levels in male and f

42 poE4 at doses of (1-2) x 10(9) pfu increased plasma cholesterol and triglyceride levels in normal C57

43 Total plasma cholesterol and triglyceride levels were similar

44 novo SM biosynthesis in apoE-KO mice lowers plasma cholesterol and triglyceride levels, raises HDL c

45 in lipoprotein metabolism by regulating the plasma cholesterol and triglyceride levels.

46 uate whether sub-RPE deposits correlate with plasma cholesterol and triglyceride levels.

47 ecreased hepatic Sort1 protein and increased plasma cholesterol and triglyceride levels.

48 r degradation in the liver and thus regulate plasma cholesterol and triglyceride levels.

49 ding list of genetic variants that influence plasma cholesterol and triglyceride levels.

50 esions than Ldlr(-/-) controls despite lower plasma cholesterol and triglyceride levels.

51 ablation led to elevated levels of liver and plasma cholesterol and triglycerides and to fatty liver

52 These findings suggest that CCK-increased plasma cholesterol and triglycerides as a result of the

53 ort examined the effect of CCK on increasing plasma cholesterol and triglycerides in mice.

54 it had no effect on PAN-induced increase in plasma cholesterol and triglycerides levels.

55 lipoprotein (LDL) is an important carrier of plasma cholesterol and triglycerides whose concentration

56 rdized criteria, by baseline levels of total plasma cholesterol and triglycerides, low-density lipopr

57 ACAT inhibitor reduced plasma cholesterol and triglycerides, normalized total c

58 mation and cholesterol efflux, together with plasma cholesterol and triglycerides, were unchanged as

59 epatic Pcsk9 showed a 40% to 50% decrease in plasma cholesterol and triglycerides.

60 poB-overexpressing mice, which have elevated plasma cholesterol and triglycerides.

61 ipid disorder characterized by elevations of plasma cholesterol and/or triglyceride in first-degree r

62 by a variable pattern of elevated levels of plasma cholesterol and/or triglycerides.

63 fiber with weight, BMI, waist circumference, plasma cholesterol, and 2-h glucose were observed, sugge

64 ler (NK) cell activity, cytokine production, plasma cholesterol, and HDL cholesterol were measured.

65 a significant reduction in host weight gain, plasma cholesterol, and liver triglycerides, demonstrati

66 /-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.

67 a;LDLR-/- mice exhibited marked increases in plasma cholesterol ( approximately 1,050 mg/dl) and trig

68 R-/- mice manifested a moderate elevation in plasma cholesterol ( approximately 215 mg/dl) and trigly

69 Thus, factors other than plasma cholesterol are additionally involved in determin

70 ary mechanisms by which soluble fiber lowers plasma cholesterol are well known.

71 CLA lowered plasma cholesterol but increased plasma and liver trigly

72 Diabetic mice had similarly reduced plasma cholesterol, but collagen content increased by on

73 ed with both plasma cholesterol and relative plasma cholesterol, but not with 7-dehydrocholesterol, t

74 anti-Apob antisense oligonucleotide reduced plasma cholesterol by approximately 90%.

75 first in class 2-azetidinone that decreases plasma cholesterol by blocking intestinal cholesterol ab

76 suggest that in humans, ezetimibe may reduce plasma cholesterol by inhibiting NPC1L1 function in both

77 HL-WT and HL-S145G reduced plasma cholesterol (by 40 and 57%, respectively), non-hi

78 Plasma cholesterol can be reduced by inhibiting lipoprot

79 SR-BI protein level and an increase in total plasma cholesterol carried in abnormally large HDL parti

80 ( approximately 1.5-1.7-fold increased total plasma cholesterol carried in both normal size and abnor

81 The increase in plasma cholesterol caused by apoE2 is due mostly to impa

82 Plasma cholesterol, cholesterol fractions, and lipoprote

83 hage cholesterol efflux to apoA-I; increased plasma cholesterol, cholesteryl esters (CEs), free chole

84 ion in lesion size and no reduction in total plasma cholesterol compared with alphaalphaee mice witho

85 The reduced plasma cholesterol concentration is unlikely to be attri

86 A gradual decrease in plasma cholesterol concentration occurred during surgery

87 site; age at diagnosis; body mass index; and plasma cholesterol concentration.

88 stinal deletions of Mttp and Abca1 decreased plasma cholesterol concentrations by 45 and 24%, respect

89 After the low-fiber meal, plasma cholesterol concentrations did not change signifi

90 When all groups were combined (n = 234), plasma cholesterol concentrations had a weak positive co

91 Biliary and plasma cholesterol concentrations in these animals were

92 typically rises and the desired reduction in plasma cholesterol concentrations is frequently accompan

93 sterol or LDL cholesterol in volunteers with plasma cholesterol concentrations representative of a mi

94 Corrected for differences in plasma cholesterol concentrations, aortic cholesterol co

95 Some treatments reduced plasma cholesterol concentrations, but none altered the

96 was associated with up to a 60% reduction in plasma cholesterol concentrations.

97 ngly accepted as a dietary strategy to lower plasma cholesterol concentrations.

98 iency or Pio administration had no effect on plasma cholesterol concentrations.

99 of the correlation between atherosclerosis, plasma cholesterol content, inflammation, and alpha1-AT

100 ase endogenous apoB-containing lipoproteins, plasma cholesterol decreased 33% (hHLTg+/0) and 75% (hHL

101 hHLTg+/0 mice and the apoE-/-,hHLTg+/0 mice, plasma cholesterol decreased by 50%.

102 Fasting plasma cholesterol decreased significantly after a PUFA-

103 One hour after injection, the plasma cholesterol efflux-promoting capacity was nearly

104 e process associated with elevated levels of plasma cholesterol, especially low-density lipoproteins.

105 The plasma cholesterol esterification enzyme lecithin:choles

106 cithincholesterol acyltransferase, the major plasma cholesterol esterification enzyme, which increase

107 iation of baseline fatty acid composition in plasma cholesterol esters with 6-year incidence of hyper

108 lipid compartments, including phospholipids, plasma, cholesterol esters, and adipose tissue.

109 rance of (125)I-labeled LDL from plasma, but plasma cholesterol fell, suggesting that LDL production

110 est a novel mechanism by which to manipulate plasma cholesterol flux.

111 ficacy, clinically relevant side effects, or plasma cholesterol fractions.

112 Plasma cholesterol (from 151 +/- 29 mg/dl to 190 +/- 33

113 No differences were found in plasma cholesterol, glucose, or insulin levels between r

114 studies of patients using statins to reduce plasma cholesterol have suggested that statins may be us

115 iet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol

116 significant associations with known loci of plasma cholesterol, high-density lipoprotein, low-densit

117 However, its role in plasma cholesterol homeostasis and atherosclerosis has n

118 oprotein receptor (LDLR) plays a key role in plasma cholesterol homeostasis by binding and internaliz

119 t, plasma apolipoprotein E maintains overall plasma cholesterol homeostasis by facilitating efficient

120 DL receptor protein expression, and restored plasma cholesterol homeostasis in mice lacking a functio

121 tein receptor (LDLR) family and functions in plasma cholesterol homeostasis.

122 ikely interferes with its role in regulating plasma cholesterol homeostasis.

123 at least in part, through the regulation of plasma cholesterol homeostasis.

124 Both ezetimibe and the glucuronide lower plasma cholesterol; however, the glucuronide exhibits gr

125 e levels of hepatic and plasma TG as well as plasma cholesterol in a CES1-dependent manner.

126 onsequently an approximately 70% increase in plasma cholesterol in abnormally large high density lipo

127 The increased plasma cholesterol in CCK-treated mice was distributed i

128 Finally, analysis of plasma cholesterol in Egr1(-/-) mice indicated a signifi

129 al. and has been demonstrated to lower total plasma cholesterol in man.

130 sed plasma triglyceride but had no effect on plasma cholesterol in mice.

131 bsorption in the intestine, thereby reducing plasma cholesterol in preclinical models of hypercholest

132 Ezetimibe effectively reduces plasma cholesterol in several species including human, m

133 ma cholesterol levels, but nearly all of the plasma cholesterol in the former animals is packaged in

134 ipoprotein size, suggests that the increased plasma cholesterol in the mutants was due to decreased s

135 Plasma cholesterol increased in all cholesterol-fed pigs

136 id pool size, fecal bile acid excretion, and plasma cholesterol independently of Cyp7a1 activity.

137 ption reversed the increase in total and LDL plasma cholesterol induced by the HFD feeding in both HF

138 LDLR) is the primary mechanism for uptake of plasma cholesterol into cells and serves as a prototype

139 ) is the primary mechanism for the uptake of plasma cholesterol into cells and serves as a prototype

140 d in VLDL particles, whereas, in the latter, plasma cholesterol is found in smaller LDL particles.

141 After the 3-d high-fat diet, plasma cholesterol, LDL cholesterol, and HDL cholesterol

142 t effect of the rTFA diet was found on total plasma cholesterol, LDL cholesterol, apolipoprotein B, a

143 gnificant difference was observed in fasting plasma cholesterol, LDL cholesterol, glucose, or insulin

144 individual SNPs showed association to total plasma cholesterol, LDL-cholesterol and VLDL-cholesterol

145 mines the effect of cholecystokinin (CCK) on plasma cholesterol level and intestinal cholesterol abso

146 ne was lower in the CEL transgenic mice, but plasma cholesterol level and lipoprotein profile were si

147 ave been attributed to its ability to reduce plasma cholesterol level and to limit foam cell formatio

148 Wild-type mice doubled their plasma cholesterol level following a high cholesterol di

149 intestinal cholesterol absorption and total plasma cholesterol level has renewed interest in the abs

150 es, in pentobarbital clearance, and in total plasma cholesterol level.

151 breast-fed girl with xanthomas and very high plasma cholesterol levels (1023 mg/dl).

152 ce of circulating lipoproteins and decreased plasma cholesterol levels (46 mg/dl in Pcsk9(-/-) mice v

153 apo A-I mimetic peptide 18A not only reduced plasma cholesterol levels (baseline, 562+/-29.0 mg/dL ve

154 y lipoprotein receptor levels, and decreased plasma cholesterol levels (by 35-40%).

155 p1 overexpression in CD1 male mice increased plasma cholesterol levels 20-50%.

156 her, these results imply that an increase in plasma cholesterol levels accelerates the development of

157 otic apolipoprotein E-deficient mice reduced plasma cholesterol levels and aortic CD36 expression and

158 there may be a relationship between abnormal plasma cholesterol levels and breast cancer risk.

159 in apoE-deficient mice (apoE(-/-)) corrected plasma cholesterol levels and did not cause hypertriglyc

160 injured arteries showed striking effects of plasma cholesterol levels and drug treatment on neointim

161 tivity of the receptor lead to elevations in plasma cholesterol levels and early-onset coronary ather

162 Clock activity is crucial in maintaining low plasma cholesterol levels and in reducing atherogenesis

163 injection of [Thr(28),Nle(31)]CCK increased plasma cholesterol levels and intestinal cholesterol abs

164 Her parents had normal plasma cholesterol levels and reported no family history

165 Here we show that the total plasma cholesterol levels and size distribution of lipop

166 9) has emerged as an important regulator of plasma cholesterol levels and therapeutic target.

167 PS-DHA-treated mice had significantly lower plasma cholesterol levels and three times smaller athero

168 High plasma cholesterol levels are a major risk factor for at

169 Increased total plasma cholesterol levels are also seen in hepatic COMMD

170 It has been shown in animal models that plasma cholesterol levels are considerably lowered by sp

171 cate that atherosclerosis susceptibility and plasma cholesterol levels are controlled by separate gen

172 mice infected with Pcsk9-Ad had no change in plasma cholesterol levels as compared with knockout mice

173 There were no differences in total plasma cholesterol levels between groups.

174 poAI genotypes despite robust differences in plasma cholesterol levels between the groups.

175 apoE4-202 resulted in a 90% reduction in the plasma cholesterol levels but did not alter plasma trigl

176 that suppression of endogenous miR-29 lowers plasma cholesterol levels by ~40%, commensurate with the

177 In vivo studies have also indicated that plasma cholesterol levels can regulate tumor growth in m

178 pectedly, SM22alpha-TFPI/apoE(-/-) had lower plasma cholesterol levels compared to apoE(-/-) mice.

179 nimals bearing tumors presented with reduced plasma cholesterol levels compared with animals fed a co

180 HL activity increased by 25- and 50-fold and plasma cholesterol levels decreased by 80% and 85%, resp

181 er an additional 14 weeks on a low-fat diet, plasma cholesterol levels decreased from 21.0 +/- 2.6 to

182 asma concentration, lack of correlation with plasma cholesterol levels despite its association with H

183 tein AI-null mice that have markedly reduced plasma cholesterol levels due to a virtual absence of hi

184 es, transgenic rabbits had a 70% increase in plasma cholesterol levels due to an accumulation of LDL

185 Mice deficient in PDZK1 have elevated plasma cholesterol levels due to the virtually complete

186 Plasma cholesterol levels fell sharply, and microscopic

187 mice fed a chow diet, Cre induction reduced plasma cholesterol levels from 233.9+/-46.0 to 37.2+/-6.

188 n active payload resulting in a reduction of plasma cholesterol levels if siRNA was formulated into d

189 The sterol LY295427 reduces plasma cholesterol levels in animals by increasing the e

190 o, systemic administration of TFPIct reduced plasma cholesterol levels in apoE(-/-) mice.

191 isoprostane generation, but had no effect on plasma cholesterol levels in apoE-/- mice.

192 Cholesterol feeding elevated plasma cholesterol levels in both strains.

193 ated plasma triglycerides, but did not alter plasma cholesterol levels in CCK-treated mice.

194 with the extract also significantly reduced plasma cholesterol levels in ob/ob mice.

195 Despite similar total plasma cholesterol levels in response to hypercholestero

196 on sequence variations have large effects on plasma cholesterol levels in selected populations.

197 rol and STZ-induced diabetic animals reduced plasma cholesterol levels in STZ-induced diabetic mice,

198 Plasma cholesterol levels increased in the following ord

199 Control of plasma cholesterol levels is a major therapeutic strateg

200 STZ-induced diabetic Ldlr(-/-) mice had plasma cholesterol levels more than double those of nond

201 When macrophage apoE was present, plasma cholesterol levels normalized, and ACAT1 deficien

202 y 53% with a corresponding increase in total plasma cholesterol levels of 50-70% in SR-BI att mice, a

203 c diabetic and nondiabetic mice with similar plasma cholesterol levels show a similar extent of ather

204 ntly, SR-BI/ApoE double null mice have lower plasma cholesterol levels than ApoE null mice, suggestin

205 receptor (LDLR) is a critical determinant of plasma cholesterol levels that internalizes lipoprotein

206 cancer drug, can induce NASH and changes in plasma cholesterol levels through mechanisms that are un

207 It was observed that plasma cholesterol levels were reduced during tumor deve

208 Reductions in plasma cholesterol levels were significantly correlated

209 Both VLDL particle size and plasma cholesterol levels were significantly reduced in

210 Pre-pregnancy plasma cholesterol levels were similar between wild-type

211 Plasma cholesterol levels were strongly reduced, and pla

212 Plasma cholesterol levels were the same in all groups.

213 to 4-fold increased plasma PON1 levels, but plasma cholesterol levels were unchanged.

214 The association of high plasma cholesterol levels with the development of athero

215 pears difficult, changes sufficient to lower plasma cholesterol levels would retard the progression o

216 e expression, and function (normalization of plasma cholesterol levels).

217 estinal cholesterol absorption contribute to plasma cholesterol levels, a risk factor for coronary he

218 cient mice with apoE2-202 did not affect the plasma cholesterol levels, and also did not induce hyper

219 Diabetes had no effect on plasma cholesterol levels, but diabetic/hyperlipemic (D-

220 LDLR:(-/-)APOB:(100/100)) have similar total plasma cholesterol levels, but nearly all of the plasma

221 rosclerosis, deletion of Sort1 did not alter plasma cholesterol levels, but reduced the development o

222 - mice exhibited a marked reduction in total plasma cholesterol levels, compared with those in Mttp+/

223 ia (FHbeta), a syndrome characterized by low plasma cholesterol levels, is caused by mutations in the

224 Consistent with plasma cholesterol levels, liver expression of HMG-CoA r

225 (ABCA1-Tg) mice had significantly increased plasma cholesterol levels, mostly because of a 2.8-fold

226 Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller l

227 ar as PCSK9 inhibition induces a decrease in plasma cholesterol levels, understanding the nature of t

228 sis in the setting of elevated physiological plasma cholesterol levels, we deleted the MCP-1 gene in

229 that the liver is the primary determinant of plasma cholesterol levels, we sought to examine the cons

230 understand why these mutations result in low plasma cholesterol levels, we used gene targeting in mou

231 type mice, Ces1/Ces1g (-/-) mice had reduced plasma cholesterol levels.

232 d) and the aorta (1.6-fold), despite reduced plasma cholesterol levels.

233 esion size or number, vascular cytokines, or plasma cholesterol levels.

234 sin/kexin type 9 (PCSK9) as a determinant of plasma cholesterol levels.

235 independent of their suppressive actions on plasma cholesterol levels.

236 rong candidate susceptibility gene for total plasma cholesterol levels.

237 e of coronary heart disease independently of plasma cholesterol levels.

238 LDL, resulting in a significant increase in plasma cholesterol levels.

239 y increased plasma triglyceride and elevated plasma cholesterol levels.

240 herosclerosis independent of their effect on plasma cholesterol levels.

241 s 2-fold (P<0.05) without further increasing plasma cholesterol levels.

242 riched in cholic acid, and a 13% decrease in plasma cholesterol levels.

243 ongenital diarrhea, steatorrhea, and reduced plasma cholesterol levels.

244 SR-BI protein in liver, with no reduction in plasma cholesterol levels.

245 ion, and one of the risk factors is elevated plasma cholesterol levels.

246 ietary sources that might effectively reduce plasma cholesterol levels.

247 cholesterol intake produce modest changes in plasma cholesterol levels.

248 ced atherosclerotic lesions without reducing plasma cholesterol levels.

249 5% to 1% of normal levels but did not affect plasma cholesterol levels.

250 ining a quantitative trait locus influencing plasma cholesterol levels.

251 rugs commonly used for the treatment of high plasma cholesterol levels.

252 lved in cholesterol biosynthesis and reduces plasma cholesterol levels.

253 aceuticals as effective in the regulation of plasma cholesterol levels.

254 own of hepatic CES1 increased hepatic TG and plasma cholesterol levels.

255 the oral cavity and the gut correlated with plasma cholesterol levels.

256 Saponins have plasma cholesterol lowering effect in humans and are imp

257 Plasma cholesterol lowering is beneficial in patients wi

258 levated cardiovascular disease risk, despite plasma cholesterol lowering.

259 se was associated with a 30%-60% increase in plasma cholesterol, mainly because of the accumulation o

260 esis genes would be affected by miR-122, and plasma cholesterol measurements showed reduced levels in

261 However, the precise role of BAT in plasma cholesterol metabolism and atherosclerosis develo

262 hypercholesterolemic diets Chol 1 (yielding plasma cholesterol of 153 mg/dL) or Chol 2 (yielding 359

263 Increased plasma cholesterol of Tcf1-/- mice resides predominantly

264 stigate the effect of genetic alterations in plasma cholesterol on Abeta pathology, we crossed the PD

265 There was no effect of HJ6.3 on total plasma cholesterol or cerebral amyloid angiopathy.

266 food consumption or diet-induced changes in plasma cholesterol or leptin levels, yet plasma triglyce

267 ne of the treatments affected body weight or plasma cholesterol or triglycerides levels.

268 Plasma cholesterol (P < 0.001), histological hepatic fib

269 ere comparable with controls in body weight, plasma cholesterol, plasma high-density lipoprotein chol

270 However, the proportion of plasma cholesterol present in VLDL remained unchanged, w

271 xin type 9 (PCSK9) is an important factor in plasma cholesterol regulation through modulation of low

272 bile acid synthesis, has been implicated in plasma cholesterol responsiveness.

273 gulation of Cyp7a1 is a major determinant of plasma cholesterol responsiveness.

274 (0.65-1) mmol/liter (P=0.037), and the mean plasma cholesterol rose from 5.2 (3.4-6.8) to 5.5 (3.8-7

275 ar, P<0.0001), male sex (RR=2.76, P=0.0002), plasma cholesterol (RR=1.02 per 1 mg/dL, P<0.0001), dura

276 ear, P<0.0001), male sex (RR=1.98, P=0.009), plasma cholesterol (RR=1.02/mg per dL, P<0.0001), hypert

277 tosterol-supplemented margarine lowers total plasma cholesterol (TC) and LDL-cholesterol concentratio

278 jection of HD-Ad-mVLDLR led to a lowering of plasma cholesterol that lasted >/=6 months.

279 hed for age and smoking, with adjustment for plasma cholesterol, the relative risks (RRs) and 95% CIs

280 rodents promotes the biliary elimination of plasma cholesterol, this study was designed to elucidate

281 s suggest that overexpression of TFPI lowers plasma cholesterol through the interaction of its carbox

282 mice showed a 6- to 7-fold increase in total plasma cholesterol (TPC) compared to their chow-fed mice

283 In comparison to LDLr-/- mice, the total plasma cholesterol (TPC) of ACAT2-/- LCAT-/- LDLr-/- mic

284 heavy proteinuria; hypoalbuminemia; elevated plasma cholesterol, triglyceride, LDL, VLDL, and total c

285 The deficiency in iNOS had no effect on plasma cholesterol, triglyceride, or nitrate levels.

286 en variably reported to reduce or not affect plasma cholesterol values.

287 e in that the ratio of unesterified to total plasma cholesterol was normal, females were fertile, and

288 Within 2 days after apoE complementation, plasma cholesterol was normalized to wild-type levels, a

289 was increased in ApoE(-/-) plasma, and total plasma cholesterol was reduced in EIIIA(-/-)ApoE(-/-) mi

290 Plasma cholesterol was significantly reduced in this gro

291 rol levels in STZ-induced diabetic mice, but plasma cholesterol was still markedly elevated compared

292 d a 310% increase in circulating FFAs; total plasma cholesterol was unaffected.

293 Total plasma cholesterol was unaltered by diabetes or treatmen

294 iets or cholesterol-lowering drugs to modify plasma cholesterol, we observed no differences in Abeta

295 y fibres have diverse mechanisms in reducing plasma cholesterol, which could be useful for treating h

296 Other than plasma cholesterol, which was reduced in VHF and PHF rat

297 miR-30c mimic caused sustained reductions in plasma cholesterol with no obvious side effects.

298 ever, these animals exhibit markedly reduced plasma cholesterol, with mutations in Apoe and Ldlr epis

299 peptide resulted in a 30% reduction in total plasma cholesterol within 3-30 min, which reflected a 40

300 Os) for 6 weeks decreased VLDL secretion and plasma cholesterol without causing steatosis.