ライフサイエンスコーパス: plasma cholesterol

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

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

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

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

5 regulated, indicative of increased uptake of plasma cholesterol.

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

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

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

9 pholipids serving as an ideal transporter of plasma cholesterol.

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

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

12 s by 60% in en face aortas, without changing plasma cholesterol.

13 s to the relationship between rs10401969 and plasma cholesterol.

14 ikely by reducing lipoprotein production and plasma cholesterol.

15 mal chow diet, resulting in mildly increased plasma cholesterol.

16 s for hypertension including body weight and plasma cholesterol.

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

18 for atherosclerotic lesions through elevated plasma cholesterol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 Measurements of plasma cholesterol and phospholipids, intestinal absorpt

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

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

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

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

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

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

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

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

42 Total plasma cholesterol and triglyceride levels were similar

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

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

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

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

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

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

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

50 TRIB1 is a GWAS locus associated with plasma cholesterol and triglycerides (TG) 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 poB-overexpressing mice, which have elevated plasma cholesterol and triglycerides.

60 epatic Pcsk9 showed a 40% to 50% decrease in 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 hage cholesterol efflux to apoA-I; increased plasma cholesterol, cholesteryl esters (CEs), free chole

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

84 The reduced plasma cholesterol concentration is unlikely to be attri

85 A gradual decrease in plasma cholesterol concentration occurred during surgery

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

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

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

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

90 Biliary and plasma cholesterol concentrations in these animals were

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

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

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

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

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

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

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

98 Fasting plasma cholesterol decreased significantly after a PUFA-

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

100 teristics: HDL cholesterol concentration (in plasma); cholesterol efflux capacity; antioxidant abilit

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

102 The plasma cholesterol esterification enzyme lecithin:choles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Plasma cholesterol increased in all cholesterol-fed pigs

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 ion could be an effective strategy to reduce plasma cholesterol levels and atherosclerosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 Plasma cholesterol levels fell sharply, and microscopic

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

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

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

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

185 Cholesterol feeding elevated plasma cholesterol levels in both strains.

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

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

188 Despite similar total plasma cholesterol levels in response to hypercholestero

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

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

191 Plasma cholesterol levels increased in the following ord

192 Control of plasma cholesterol levels is a major therapeutic strateg

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

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

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

196 Ilrun and found they had significantly lower plasma cholesterol levels resulting from reduced liver l

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

198 Remarkably, GPR146 deficiency reduces plasma cholesterol levels substantially in both wild-typ

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

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

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

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

203 Reductions in plasma cholesterol levels were significantly correlated

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

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

206 Plasma cholesterol levels were strongly reduced, and pla

207 Plasma cholesterol levels were the same in all groups.

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

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

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

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

212 G member 8 (Abcg5/8), decreased hepatic and plasma cholesterol levels, and increased biliary and fec

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

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

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

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

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

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

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

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

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

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

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

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

225 guat treatment lowered hepatic steatosis and plasma cholesterol levels.

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

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

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

229 es with a heterozygous mutation and measured plasma cholesterol levels.

230 independent of their suppressive actions on plasma cholesterol levels.

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

232 rong candidate susceptibility gene for total plasma cholesterol levels.

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

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

235 y increased plasma triglyceride and elevated plasma cholesterol levels.

236 herosclerosis independent of their effect on plasma cholesterol levels.

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

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

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

240 lved in cholesterol biosynthesis and reduces plasma cholesterol levels.

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

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

243 ietary sources that might effectively reduce plasma cholesterol levels.

244 cholesterol intake produce modest changes in plasma cholesterol levels.

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

246 ced atherosclerotic lesions without reducing plasma cholesterol levels.

247 5% to 1% of normal levels but did not affect plasma cholesterol levels.

248 ining a quantitative trait locus influencing plasma cholesterol levels.

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

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

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

252 red to the vehicle control without affecting plasma cholesterol levels.

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

254 Plasma cholesterol lowering is beneficial in patients wi

255 levated cardiovascular disease risk, despite plasma cholesterol lowering.

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

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

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

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

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

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

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

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

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

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

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

267 epatic Gcgr (glucagon receptor) signaling in plasma cholesterol regulation and identify its underlyin

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

269 However, the capacity of LDL to act as a plasma cholesterol reservoir and its potential impact in

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

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

272 (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

273 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

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

275 lerated atherogenesis without an increase in plasma cholesterol, seen in traditional models of diabet

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

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

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

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

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

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

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

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

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

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

286 In the remaining mice, plasma cholesterol was lowered by switching to chow diet

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.