ライフサイエンスコーパス: very-low-density lipoprotein

1 oxidation and export (as triglyceride within very low-density lipoprotein).

2 without significant changes in plasma TG or very low density lipoprotein.

3 ype EL, whereas LPL only mediated binding of very low density lipoprotein.

4 structural diversity in olive oil and human very-low density lipoprotein.

5 ch was due to a decrease in the secretion of very low density lipoproteins.

6 creased hepatic secretion of TG into nascent very low density lipoproteins.

7 t dictates the synthesis of chylomicrons and very low density lipoproteins.

8 poC-III and apoC-IV levels were decreased in very low-density lipoproteins.

9 suggesting that it arises from lipolysis of very-low-density lipoproteins.

10 Indeed, LpL mediated hydrolysis of very-low-density lipoprotein activated PPARalpha in card

11 pairment in their catabolism of remnants and very low-density lipoprotein, an effect that was entirel

12 Atherogenic very low density lipoprotein and intermediate density li

13 tion and considerably decreases synthesis of very low density lipoprotein and its secretion in both l

14 of a subset of apolipoproteins implicated in very low density lipoprotein and triglyceride metabolism

15 a massive uptake of yolk precursors such as very low density lipoprotein and vitellogenin.

16 nmol/L versus TT, 57.0+/-4.5 nmol/L; P=0.03) very low-density lipoprotein and chylomicron particle nu

17 ations, the variant was also associated with very low-density lipoprotein and high-density lipoprotei

18 ein B (apoB), the major protein component of very low-density lipoprotein and low-density lipoprotein

19 concentration of proatherogenic lipoproteins very low-density lipoprotein and low-density lipoprotein

20 Very low-density lipoprotein and triglyceride concentrat

21 ng aetiology via extensive associations with very-low-density lipoprotein and triglyceride metabolism

22 ipoproteins, including low-density (LDL) and very-low-density lipoproteins and chylomicrons.

23 6449) has been associated with triglyceride, very low-density lipoprotein, and high-density lipoprote

24 Serum triglyceride, very-low-density lipoprotein, and apolipoprotein B level

25 triglyceride secretion, lower lipidation of very-low-density lipoproteins, and increased lipid dropl

26 Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density

27 ptotic activity of HDL is inhibited by APOE4 very-low-density lipoprotein (APOE4-VLDL) in endothelial

28 This tempers triglyceride availabiity for very low density lipoprotein assembly and allows homeost

29 protein B-100 (apoB-100), and beta-migrating very low-density lipoprotein (beta-VLDL) particles, whic

30 sulfate and 2-O-sulfate groups did not block very low density lipoprotein binding and uptake in isola

31 1-tg mice had increased secretion of hepatic very low density lipoprotein but maintained plasma trigl

32 sma from apoA-I(-/-) mice or purified low or very low density lipoproteins but readily opacified HDL.

33 plasmic reticulum export of chylomicrons and very low-density lipoproteins, but not collagen XII.

34 terols isolated from liver, bile, and plasma very low density lipoprotein by a variant of ISA designe

35 arily because of its role in the assembly of very low density lipoproteins by the liver and chylomicr

36 the secretion of cholesteryl ester-enriched very low density lipoproteins by the liver.

37 ty lipoprotein, low-density lipoprotein, and very-low-density lipoprotein, can be easily separated an

38 D-PDMP affected very-low-density lipoprotein catabolism by increasing th

39 C), low density lipoprotein cholesterol, and very low density lipoprotein cholesterol (VLDL-C) assess

40 After 7 days, triglyceride (TG) levels and very low density lipoprotein cholesterol (VLDLc) levels

41 measurements revealed a 3.6-fold decrease of very low density lipoprotein cholesterol in serum and a

42 d fasting levels of plasma triglycerides and very low density lipoprotein cholesterol, and increased

43 rcumference, triglycerides, body mass index, very low density lipoprotein cholesterol, lipoprotein A,

44 actor of 5 for the ratio of triglycerides to very low-density lipoprotein cholesterol (TG:VLDL-C); ho

45 l fibres reviewed reduced total cholesterol, very low-density lipoprotein cholesterol (VLDL-C) and LD

46 HDL-C), triglycerides, and directly measured very low-density lipoprotein cholesterol (VLDL-C), as we

47 patient-specific ratios of triglycerides to very low-density lipoprotein cholesterol.

48 acylglycerols, apolipoproteins A-I and B, or very low-density lipoprotein cholesterol.

49 2 to 63.1%), LDL cholesterol (1.3 to 32.9%), very-low-density lipoprotein cholesterol (27.9 to 60.0%)

50 at individual CpGs as a function of fasting very-low-density lipoprotein cholesterol and triglycerid

51 , hypoxia increased hepatic SCD-1 and plasma very-low-density lipoprotein cholesterol levels and indu

52 lic blood pressure, triglyceride levels, and very-low-density lipoprotein cholesterol levels, lesser

53 mean concentrations of triglycerides (TGs), very-low-density lipoprotein cholesterol, and glucose we

54 triacylglycerols, apolipoprotein A-I and B, very-low-density lipoprotein cholesterol, and lipoprotei

55 first and rate-limiting step in chylomicron/very low density lipoprotein clearance at the luminal su

56 of macrophage LRP decreased uptake of (125)I-very-low-density lipoprotein compared with wild-type cel

57 ssociation results for medium and very large very low-density lipoprotein composition are unlikely to

58 B level, concentration and particle size of very-low-density lipoproteins, concentration of low-dens

59 significantly change serum triglycerides or very-low-density lipoprotein concentrations.

60 lipoproteins, low-density lipoproteins, and very low-density lipoproteins contained elevated apoA-I

61 studies with [(3)H]cholesteryl ether-labeled very-low-density lipoproteins demonstrated that the HL/E

62 nonexchangeable protein in chylomicrons and very low-density lipoprotein-derived lipoprotein particl

63 ents or prepared in vitro by the exchange of very low-density lipoprotein for LDL cholesteryl esters

64 lipoprotein substrate triglyceride content (very low density lipoprotein >> LDL > high density lipop

65 enesis of both apoB48 and apoB100-containing very low density lipoprotein in addition to a phospholip

66 poB-48-carrying remnants of chylomicrons and very low density lipoproteins in the plasma.

67 olesterol into apoB-containing lipoproteins (very low density lipoprotein, intermediate density lipop

68 y lipoprotein levels and increased uptake of very low-density lipoprotein into Cxcr7-expressing white

69 (HDL) to the proatherogenic low-density and very low-density lipoproteins (LDL and VLDL).

70 uction in fasting plasma triacylglycerol and very low-density lipoprotein level coupled with slight i

71 ecombinant Angptl4 causes increase of plasma very low density lipoprotein levels by inhibition of lip

72 Treatment with CCX771 reduced circulating very low-density lipoprotein levels but not low-density

73 0% less body weight gain and lower serum and very low-density lipoprotein levels of triglycerides but

74 er high-density lipoprotein lipids and lower very-low-density lipoprotein lipids, glucose levels, bra

75 poprotein, intermediate-density lipoprotein, very-low-density lipoprotein, lipoprotein (a), or chylom

76 They exist in three major classes: very-low-density lipoprotein, low-density lipoprotein, a

77 nist also produced a significant increase in very low density lipoprotein/low density lipoprotein cho

78 rosclerosis, considering they also had lower very low-density lipoprotein/low-density lipoprotein cho

79 No changes in plasma levels of very low-density lipoprotein/low-density lipoprotein, hi

80 plasma total, high-density lipoprotein, and very-low-density lipoprotein/low-density lipoprotein cho

81 n, 95% confidence interval 3.48-6.78), other very-low-density lipoprotein measures, and branched-chai

82 ether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lip

83 ngivalis levels was directly correlated with very low-density lipoprotein (P = 0.03) and triglyceride

84 protein subclasses were shifted toward lower very-low-density lipoprotein (P<0.001) and higher large

85 0.70, 95% CI 0.65-0.76, p = 2x10(-)(1)(8)), very-low-density lipoprotein particle size (HR 0.69, 95%

86 rly in therapy, whereas TG concentration and very-low-density lipoprotein particle size decreased con

87 reassembly of triacylglycerols that lipidate very low density lipoprotein particles as part of a hepa

88 at the assembled virions piggy-back onto the very low density lipoprotein particles for secretion.

89 DL particles (0.77, 0.60-0.99, P=0.045), and very-low-density lipoprotein particles (0.78, 0.61-0.99,

90 mall LDL (0.78, 0.61-1.00, P=0.05) and small very-low-density lipoprotein particles (0.78, 0.62-0.99,

91 Hepatic very-low-density lipoprotein particles (VLDL) containing

92 s, LDL particles, and select subfractions of very-low-density lipoprotein particles and LDL particles

93 zed with increasing levels of triglycerides, very-low-density lipoprotein particles, LDL-P, sdLDL-C,

94 ze and concentrations of LDLNMR and VLDLNMR (very-low-density lipoprotein) particles were negatively

95 s C virus (HCV) particles assemble along the very low density lipoprotein pathway and are released fr

96 e appearance in nonesterified fatty acid and very-low-density lipoprotein pools was negatively associ

97 Procollagens, pre-chylomicrons, and pre-very low-density lipoproteins (pre-VLDLs) are too big to

98 ing, quantitative polymerase chain reaction, very-low-density lipoprotein production, adenovirus over

99 antly reduced triglyceride storage and VLDL (very low density lipoprotein) production.

100 Activation of very low density lipoprotein receptor (VLDLR) and apolip

101 Reelin signals via the lipoprotein receptors very low density lipoprotein receptor (VLDLR) and apolip

102 to apolipoprotein E receptor 2 (ApoER2) and very low density lipoprotein receptor (VLDLR) and is int

103 We discovered that miR-200c targets the very low density lipoprotein receptor (Vldlr) and its li

104 For instance, the very low density lipoprotein receptor (VLDLR) and the ap

105 ApoE Receptor 2 (ApoER2) and the very low density lipoprotein receptor (VLDLR) are type I

106 The very low density lipoprotein receptor (VLDLR) is a membe

107 Previously, we have shown that very low density lipoprotein receptor (VLDLR) is virtual

108 induced choroidal neovascularization and the very low density lipoprotein receptor (Vldlr)-knockout m

109 scular entothelial growth factor [VEGF], and very low density lipoprotein receptor [VLDLR]) were test

110 Very low density lipoprotein receptor gene knock-out (Vl

111 ails of the lipoprotein receptors ApoER2 and very low density lipoprotein receptor through an amino-t

112 y, including the receptors ApoER2 and VLDLR (very low density lipoprotein receptor) and the adapter p

113 is dependent on apolipoprotein E receptor 2, very low density lipoprotein receptor, and Dab1.

114 ily, the apolipoprotein E receptor 2 and the very low density lipoprotein receptor, and regulates neu

115 r domains of apolipoprotein E receptor 2 and very low density lipoprotein receptor, Dab1 is preferent

116 ells via apolipoprotein E receptor 2 and the very low density lipoprotein receptor, resulting in the

117 (d), approximately 30 nM) but not to soluble very low density lipoprotein receptor.

118 nt in Reelin, Disabled 1 (Dab1), or both the very low-density lipoprotein receptor (VLDLR) and the ap

119 The very low-density lipoprotein receptor (VLDLR) knockout (

120 le pathways including through the receptors, Very low-density lipoprotein receptor (Vldlr), Apolipopr

121 Mice deficient in another Reelin receptor, very low-density lipoprotein receptor (VLDLR), had norma

122 gnaling pathway that requires its receptors, very low-density lipoprotein receptor and apolipoprotein

123 ation and vascular leakage in the eyecups of very low-density lipoprotein receptor knockout mice, a m

124 Very low-density lipoprotein receptor mutant mice (Vldlr

125 uncation disrupts an interaction with VLDLR (very low-density lipoprotein receptor), while the APOER2

126 an interaction with the RELN receptor VLDLR (very low-density lipoprotein receptor); this was confirm

127 l blood vessels invading photoreceptors: the very low-density lipoprotein receptor-deficient (Vldlr(-

128 ng embryonic neurons requires binding to the very-low-density lipoprotein receptor (VLDLR) and the ap

129 revealed a point mutation, c.2239C>T, in the very-low-density lipoprotein receptor (Vldlr) gene.

130 Very-low-density lipoprotein receptor (VLDLR) in knockou

131 Very-low-density lipoprotein receptor (VLDLR) is a multi

132 The very-low-density lipoprotein receptor (VLDLR) negatively

133 Very-low-density lipoprotein receptor (Vldlr), which is

134 retinopathy and another angiogenic model of very-low-density lipoprotein receptor (Vldlr)-deficient

135 by binding to the two lipoprotein receptors, very-low-density lipoprotein receptor and apolipoprotein

136 ER2 (apolipoprotein E receptor 2) and VLDLR (very-low-density lipoprotein receptor).

137 rs, apolipoprotein E receptor 2 (Apoer2) and very-low-density lipoprotein receptor.

138 e gene expression for lipoprotein lipase and very-low-density lipoprotein receptor.

139 eceptors for Reelin, including integrins and very-low-density lipoprotein receptor/apolipoprotein E2

140 the brain involves the binding of Reelin to very-low-density lipoprotein receptors (VLDLR) and apoli

141 Reelin that is not mediated by Disabled1 or very-low-density lipoprotein receptors and apolipoprotei

142 ticles such as very low density lipoprotein, very low density lipoprotein remnants, and intermediate-

143 lls to acetylated low-density lipoprotein or very low density lipoprotein resulted in a time- and con

144 and increased secretion of triglyceride-rich very low density lipoprotein resulting in hypertriglycer

145 els were associated with both a reduction in very low density lipoprotein secretion and an increase i

146 ombined effect of inhibition of lipogenesis, very low density lipoprotein secretion and export of tri

147 Despite increased very low density lipoprotein secretion, apoB/BATless mic

148 cal increase in both hepatic lipogenesis and very low density lipoprotein secretion.

149 nhibiting hepatic triglyceride synthesis and very low density lipoprotein secretion.

150 miR-34a inhibits very low-density lipoprotein secretion and promotes live

151 Blocking hepatic very low-density lipoprotein secretion through genetic o

152 genes involved in fatty acid beta-oxidation, very low-density lipoprotein secretion, and transcriptio

153 Choline metabolism is important for very low-density lipoprotein secretion, making this nutr

154 cal mechanisms and consequences of defective very low-density lipoprotein secretion.

155 and inadequate increases in IHTG export via very low-density lipoprotein secretion.

156 Very-low-density lipoprotein secretion, which is absent

157 atic free fatty acid oxidation, or decreased very-low-density lipoprotein secretion.

158 , via mitochondrial beta-oxidation and VLDL (very low density lipoprotein) secretion, causes excessiv

159 ewly formed lipid droplets, and yolk-derived very low density lipoprotein, shown to be efficiently en

160 protein distribution preference of apoE4 for very low density lipoprotein-sized particles.

161 sity lipoprotein cholesterol subclasses, and very-low-density lipoprotein subclasses did not improve

162 events was also observed for several LDL and very-low-density lipoprotein subfractions but not for io

163 CVD/all-cause death, as were several LDL and very-low-density lipoprotein subfractions, albeit with a

164 nover, which drives hepatic triglyceride and very low-density lipoprotein synthesis.

165 Mttp produced a dramatic reduction in plasma very low density lipoprotein-TG and virtually eliminated

166 the increase in LPL activity, the uptake of very low density lipoprotein-TG is markedly reduced in a

167 RPs bound human apolipoprotein-enriched beta very low density lipoprotein, the canonical ligand for t

168 er of surface components of chylomicrons and very low density lipoprotein to high density lipoprotein

169 ally derived chylomicrons and injected human very low density lipoproteins to the same extent as obse

170 Uptake of DiI-labeled very low-density lipoprotein to adipose tissue was deter

171 lycerol content, plasma triacylglycerol, and very low density lipoprotein triacylglycerol secretion.

172 mol/min for LowLF; P = .41) or production of very-low-density lipoprotein triacylglycerol from FFAs (

173 -IV, C-II, and C-III and increases serum and very low density lipoprotein triglyceride levels.

174 ect has been shown to be caused by decreased very low-density lipoprotein triglyceride secretion rate

175 incorporation into palmitate of circulating very low-density lipoprotein triglyceride.

176 , where rs964184 was associated with various very low density lipoprotein, triglyceride, and high-den

177 ants caused only a small increase in hepatic very low density lipoprotein-triglyceride secretion.

178 were used to assess insulin sensitivity and very-low-density lipoprotein-triglyceride (VLDL-TG) secr

179 rate decreased by 27% +/- 7% (P < .01); and very-low-density lipoprotein-triglyceride secretion rate

180 emic free fatty acids (FFA) into circulating very low-density lipoprotein triglycerides (VLDL-TGs) un

181 Rs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postpr

182 sociations were observed for extremely large very-low-density lipoprotein triglycerides (odds ratio [

183 ajor role in promoting uptake of circulating very low density lipoprotein-triglycerides (VLDL-TGs) in

184 pact of anti-miR-33 therapy on the levels of very low-density lipoprotein-triglycerides (VLDL-TAG).

185 ) dictates the formation of chylomicrons and very low-density lipoproteins, two major lipoprotein pre

186 (a), and triglyceride-rich particles such as very low density lipoprotein, very low density lipoprote

187 l four backgrounds, the vitamin E content of very low density lipoprotein (VLDL) and/or LDL was signi

188 Abnormalities in very low density lipoprotein (VLDL) assembly and secreti

189 ridemia was due largely to overproduction of very low density lipoprotein (VLDL) by the liver, a norm

190 Nascent very low density lipoprotein (VLDL) exits the endoplasmi

191 uptake of low density lipoprotein (LDL) and very low density lipoprotein (VLDL) particles by a singl

192 The transport of nascent very low density lipoprotein (VLDL) particles from the e

193 posed that clearance of cholesterol-enriched very low density lipoprotein (VLDL) particles occurs thr

194 In contrast, the very low density lipoprotein (VLDL) pathway, which is re

195 Although very low density lipoprotein (VLDL) receptor (VLDLr) kno

196 Two apolipoprotein E (apoE) receptors, the very low density lipoprotein (VLDL) receptor and apoE re

197 This antitumor mechanism may involve the very low density lipoprotein (VLDL) receptor because the

198 incubations of apoA-I(-)(/)(-) apoE(-)(/)(-) very low density lipoprotein (VLDL) resulted in a 3-fold

199 intrahepatic triglyceride (IHTG) content and very low density lipoprotein (VLDL) triglyceride (TG) se

200 correlated to insulin resistance and plasma very low density lipoprotein (VLDL) triglycerides concen

201 sma apolipoprotein B yet increased levels of very low density lipoprotein (VLDL) triglycerides, sugge

202 erum triglycerides primarily associated with very low density lipoprotein (VLDL) with no difference i

203 (LDL) density lipoprotein as lipid donor to very low density lipoprotein (VLDL), and the preference

204 cells do not express MTP and cannot secrete very low density lipoprotein (VLDL), yet they do not acc

205 ted apoE in accounting for the difference in very low density lipoprotein (VLDL)-induced adipocyte tr

206 oth human high density lipoprotein (HDL) and very low density lipoprotein (VLDL).

207 toma cells can mediate binding and uptake of very low density lipoprotein (VLDL).

208 ed for the hepatic assembly and secretion of very low density lipoprotein (VLDL).

209 h a Golgi-dependent mechanism while bound to very low density lipoprotein (vLDL).

210 secretion of the metabolic precursor of LDL, very low density lipoprotein (VLDL).

211 rations of low density lipoprotein (LDL) and very low density lipoprotein (VLDL).

212 In contrast, serum levels of very low density lipoprotein (VLDL)/low density lipoprot

213 n the hepatic secretion of apoB-100-carrying very low density lipoproteins (VLDL) and a decrease in t

214 core lipid in the assembly and secretion of very low density lipoproteins (VLDL) has been of interes

215 HDL) particles to form triglyceride-enriched very low density lipoproteins (VLDL) has not been identi

216 The major protein component in secreted very low density lipoproteins (VLDL) is apoB, and it is

217 accelerated hepatic fatty acid oxidation and very low density lipoproteins (VLDL) secretion.

218 transient depression of hepatic secretion of very low density lipoproteins (VLDL).

219 riglyceride into plasma through secretion of very low density lipoproteins (VLDL).

220 c reticulum (ER) and is further lipidated to very low density lipoproteins (VLDL).

221 iating FFA uptake or triglyceride release as very low density lipoproteins (VLDL).

222 oprotein (HDL(NMR)), 1.71 (1.38 to 2.12) for very low-density lipoprotein (VLDL(NMR)), and 2.25 (1.80

223 00014; African Americans P = 0.00417), large very low-density lipoprotein (VLDL) (Caucasians P = 0.00

224 the accumulation of free cholesterol in the very low-density lipoprotein (VLDL) and HDL region, and

225 apo) E between lipoprotein particles such as very low-density lipoprotein (VLDL) and high-density lip

226 idemia, the esterification of cholesterol of very low-density lipoprotein (VLDL) and high-density lip

227 usly found that EL is capable of hydrolyzing very low-density lipoprotein (VLDL) and LDL lipids ex vi

228 Very low-density lipoprotein (VLDL) and LDL plasma level

229 ) and the apolipoprotein B (apoB)-containing very low-density lipoprotein (VLDL) and low-density lipo

230 hydrolase (Ces3/TGH) participates in hepatic very low-density lipoprotein (VLDL) assembly and in adip

231 de (TG) levels resulting both from increased very low-density lipoprotein (VLDL) clearance and decrea

232 n decreased cholesterol levels and decreased very low-density lipoprotein (VLDL) fractions.

233 Increased production of very low-density lipoprotein (VLDL) is a critical featur

234 TGs, hepatosteatosis, and secrete lipid-poor very low-density lipoprotein (VLDL) lacking arachidonoyl

235 monstrate that Sort1 alters plasma LDL-C and very low-density lipoprotein (VLDL) particle levels by m

236 ting impaired ER-to-Golgi trafficking of pre-very low-density lipoprotein (VLDL) particles.

237 NDGA inhibited very low-density lipoprotein (VLDL) secretion by affecti

238 ic pathways, such as triglyceride synthesis, very low-density lipoprotein (VLDL) secretion, and fatty

239 attenuation of hepatic steatosis, increased very low-density lipoprotein (VLDL) secretion, and impro

240 erized by a 3-fold higher liver secretion of very low-density lipoprotein (VLDL) that had apoC-III bu

241 mbination of size and concentrations of LDL, very low-density lipoprotein (VLDL), and high-density li

242 lthough triglyceride-rich particles, such as very low-density lipoprotein (VLDL), contribute signific

243 ined the lipidation and secretion of nascent very low-density lipoprotein (VLDL), finding that liver

244 experiments demonstrate that the LDLR has a very low-density lipoprotein (VLDL)-induced, FDNPVY-inde

245 ent reversed tumor necrosis factor alpha and very low-density lipoprotein (VLDL)-stimulated endotheli

246 apoCII levels and increased apoB48 levels in very low-density lipoprotein (VLDL)/intermediate-density

247 DL are further isolated by precipitating the very low-density lipoproteins (VLDL) and low-density lip

248 (CE), and triglyceride (TG) from plasma and very low-density lipoproteins (VLDL) was used to measure

249 Raman signature of single optically trapped very low-density lipoproteins (VLDL), a subclass of TGRL

250 re to triglyceride-rich lipoproteins such as very low-density lipoproteins (VLDL).

251 Excessive secretion of triglyceride-rich very low-density lipoproteins (VLDL-TG) contributes to d

252 in (HDL), low-density lipoprotein (LDL), and very-low density lipoprotein (VLDL), play a critical rol

253 Cardiac utilisation of very-low-density lipoprotein (VLDL) and chylomicrons (CM

254 Very-low-density lipoprotein (VLDL) and chylomicrons (CM

255 fects were mainly on serum triglycerides and very-low-density lipoprotein (VLDL) and its subclasses,

256 NT ASO exhibited a significant impairment in very-low-density lipoprotein (VLDL) binding that was ent

257 protein, high-density lipoprotein (HDL), and very-low-density lipoprotein (VLDL) cholesterol levels.

258 36 had significantly lower plasma TC, LDL-C, very-low-density lipoprotein (VLDL) cholesterol, and MDA

259 in plasma low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) discriminated dengue

260 the notion that HCV coopts the secretion of very-low-density lipoprotein (VLDL) for its egress.

261 y reduced triglycerides and large and medium very-low-density lipoprotein (VLDL) particle concentrati

262 patitis C virus (HCV) uses components of the very-low-density lipoprotein (VLDL) pathway for assembly

263 hepatic triglycerides (TAG) associated with very-low-density lipoprotein (VLDL) play a major role in

264 FPIct) has been shown to be a ligand for the very-low-density lipoprotein (VLDL) receptor, we hypothe

265 ght but is associated with increased hepatic very-low-density lipoprotein (VLDL) secretion and elevat

266 glyceride content by threefold and decreased very-low-density lipoprotein (VLDL) secretion by 50%.

267 oaches, we demonstrate that vigilin controls very-low-density lipoprotein (VLDL) secretion through th

268 TG content, we measured hepatic lipogenesis, very-low-density lipoprotein (VLDL) secretion, and lipid

269 Genes for very-low-density lipoprotein (VLDL) synthesis (microsoma

270 rcise prevents fructose-induced increases in very-low-density lipoprotein (VLDL) triglycerides by dec

271 spectrometric analysis suggested that serum very-low-density lipoprotein (VLDL) was responsible for

272 -48-containing TRLs and apo B-100-containing very-low-density lipoprotein (VLDL), as well as on the e

273 inal) in lipoprotein fractions [chylomicron, very-low-density lipoprotein (VLDL), LDL, high-density l

274 While preincubation of HCV-LPs with very-low-density lipoprotein (VLDL), low-density lipopro

275 weeks) for 8 weeks on the plasma kinetics of very-low-density lipoprotein (VLDL)-apolipoprotein B-100

276 ic and proteomic profiles implicated these 3 very-low-density lipoprotein (VLDL)-associated apolipopr

277 a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycer

278 e important for HCV cell-to-cell spread, but very-low-density lipoprotein (VLDL)-containing mouse ser

279 e observed strong positive associations with very-low-density lipoprotein (VLDL)-lipoproteins, VLDL-c

280 Very-low-density lipoprotein (VLDL)-triacylglycerols and

281 uh7 cells via pathways distinct from that of very-low-density lipoprotein (VLDL).

282 TG) and apolipoprotein C-III levels, and low very-low-density lipoprotein (VLDL)/high high-density li

283 Very-low-density lipoproteins (VLDL) are metabolic precu

284 Very-low-density lipoproteins (VLDL) is a hallmark of me

285 in a manner that parallels the formation of very-low-density lipoproteins (VLDL).

286 rocessed human milk and O-glycoproteins from very-low-density-lipoprotein (vLDL) particles.

287 Here we show that maternal very-low-density-lipoprotein (VLDL) receptor deletion in

288 protein (HDL) yields 4-6% of the LDL signal, very-low-density-lipoprotein (VLDL) yields 1-3%, and hum

289 epatitis C virus (HCV) and triglyceride-rich very low-density lipoproteins (VLDLs) both are secreted

290 ip between CD36 expression and serum HDL and very low-density lipoproteins (VLDLs) levels was also ex

291 ccomplished primarily through the actions of very low-density lipoproteins (VLDLs).

292 fasting triacylglycerol in chylomicrons and very-low-density lipoproteins (VLDLs) (P = 0.004), reduc

293 actor ANOVA) in plasma (P = 0.023) and large very-low-density lipoproteins (VLDLs) (P = 0.016) and po

294 at transfers alpha-tocopherol (vitamin E) to very-low-density lipoproteins (VLDLs).

295 ty liver as a result of reduced secretion of very-low-density lipoproteins (VLDLs).

296 was observed in systolic BP (7.1 mm Hg) and very-low-density lipoproteins (VLDLs; 5.16 mg/dL) in gro

297 in B (apoB)-containing lipoproteins (hepatic very-low density lipoproteins), which leads to hyperlipi

298 ich lipoproteins, including chylomicrons and very low density lipoprotein, which is the precursor to

299 cholesterol to triglycerides ratio (1.52) in very low-density lipoproteins with elevated levels of sm

300 by the inability to produce chylomicrons or very low-density lipoproteins, with the absence of apoli