ライフサイエンスコーパス: VLDL

1 VLDL cholesterol explained 50% and IDL + LDL cholesterol

2 VLDL cholesterol explained one-half of the myocardial in

3 VLDL cholesterol, triglycerides, and 2-hour OGTT were hi

4 VLDL may contribute to the pathophysiology of atrial fib

5 VLDL-TG levels of polyunsaturated fatty acids (PUFA), in

6 VLDL-TG secretion rates (SRs) were not statistically dif

7 VLDLs (15 microg/g) and equivalent volumes of saline (CT

8 VLDLs were separated from normal (Normal-VLDL) and MetS

9 were obtained for 13 subclasses, including 5 VLDLs (particle size 64-31.3 nm), 4 LDLs (particle size

10 articles (-39.6%; 95% CI, -49.4% to -24.6%), VLDL particles (-19.6%; 95% CI, -40.6% to 10.3%), and VL

11 these sources to liver-triglyceride accrual, VLDL-triglyceride synthesis, and hypertriglyceridemia.

12 iglyceride (TG) secretion, nor did it affect VLDL-TG concentrations.

13 Short-term hypogonadism did not affect VLDL triglyceride (TG) secretion, nor did it affect VLDL

14 ared with 2.74 +/- 0.55 vol %; P < 0.05) and VLDL-triglyceride (0.55 +/- 0.06 compared with 1.40 +/-

15 icles (-19.6%; 95% CI, -40.6% to 10.3%), and VLDL triglycerides (-15.2%; 95% CI, -35.9% to 11.3%) and

16 MCT has a neutral effect on TRL apo B-48 and VLDL apo B-100 kinetics and on the intestinal expression

17 asma lipoprotein profile or TRL apo B-48 and VLDL apo B-100 kinetics.

18 The in vivo kinetics of TRL apo B-48 and VLDL apo B-100 were assessed by using a primed-constant

19 oth the chylomicron (r = -0.46 to -0.52) and VLDL (r = -0.49 to -0.68) fractions were inversely corre

20 f hepatocytes increases both VTV budding and VLDL secretion.

21 ced postprandial chylomicron cholesterol and VLDL apolipoprotein B-48.

22 GPx) and blood lipids (total cholesterol and VLDL) and the interaction with yacon flour, and phytate,

23 eted particles derived from chylomicrons and VLDL that are relatively enriched in cholesteryl esters

24 ionship between plasma FFA concentration and VLDL-TG SRs.

25 tissue insulin sensitivity deteriorated, and VLDL apoB100 concentrations and secretion rates increase

26 ing the fructose conversion into glucose and VLDL-triglyceride and fructose carbon storage into hepat

27 to unravel the collaboration between HCV and VLDL secretion, we studied HCV particles budding from th

28 KO mice also exhibited higher plasma LDL and VLDL cholesterol content, increased circulating apolipop

29 onfinement chamber, individual HDL, LDL, and VLDL particles labeled with three distinct fluorophores

30 ent of all major lipoproteins, HDL, LDL, and VLDL.

31 emoval, via mitochondrial beta-oxidation and VLDL (very low density lipoprotein) secretion, causes ex

32 osis and normalized fatty acid oxidation and VLDL-TG secretion.

33 ed in lipogenesis, fatty acid oxidation, and VLDL secretion was unaltered.

34 on dramatically decreased plasma VLDL TG and VLDL cholesterol concentrations but only moderately incr

35 resulting in smaller increases of HDL-TG and VLDL subparticles.

36 iet but also reduced plasma triglyceride and VLDL concentrations without significantly increasing LDL

37 nificant decrease in plasma triglyceride and VLDL within 5h.

38 hepsin B resulted in decreased OA uptake and VLDL secretion.

39 containing lipoproteins (such as remnant and VLDLs).

40 for the blockade of HCV cell attachment, as VLDL-depleted mouse serum lost HCV-inhibitory activity.

41 ocardial infarction entered by importance as VLDL cholesterol, systolic blood pressure, smoking, and

42 secretion of triglycerides (TG) packaged as VLDLs.

43 rough the delipidation of larger atherogenic VLDL and large LDL and from direct de novo production by

44 pression, several mouse models of attenuated VLDL particle assembly were subjected to acute hepatoste

45 ucose (gluconeogenesis from fructose), blood VLDL-(13)C palmitate (a marker of hepatic de novo lipoge

46 , Lcad, Ehhadh, Hsd10 and Acaa2, and blunted VLDL export with decreased expression of Mttp and its pr

47 Both VLDL particle size and plasma cholesterol levels were si

48 due to an increased production rate of both VLDL and CM TAG.

49 n (VLDL)-lipoproteins, VLDL-cholesterol (C), VLDL-triglycerides, VLDL-diameter, branched/aromatic ami

50 l, very low-density lipoprotein cholesterol (VLDL-C) and LDL-C.

51 PRAP1 is detectable in chylomicron/VLDL-rich plasma fractions, suggesting that MTTP recogni

52 pectrum of physiological FFA concentrations, VLDL-TG SRs did not vary based on different acute substr

53 r fatty acid ss-oxidation, and 40% decreased VLDL-triglyceride export.

54 rge and extra-large HDL levels and decreased VLDL and amino acid levels were associated with increase

55 ligonucleotides (ASOs) for 6 weeks decreased VLDL secretion and plasma cholesterol without causing st

56 quently, hepatic vigilin knockdown decreases VLDL/low-density lipoprotein (LDL) levels and formation

57 odified the plasma lipid profile, decreasing VLDL levels due to decreased triglyceride biosynthesis.

58 ciated polypeptide 1 (LAP1) caused defective VLDL secretion and steatosis, including intranuclear lip

59 rs required only for cell-free spread (i.e., VLDL pathway components) do not.

60 nockout male mice had significantly elevated VLDL-triglyceride (TG) and strikingly impaired lipid cle

61 torage of "old fat." Interestingly, enhanced VLDL-TG secretion in shSCR-treated L-G6pc(-/-) mice asso

62 c lipogenesis, whereas DHA not only enhances VLDL lipolysis, resulting in greater conversion to LDL,

63 TG-lowering effect of metformin by enhancing VLDL-TG uptake, intracellular TG lipolysis, and subseque

64 ly and secretion of larger, more TG-enriched VLDL particles.

65 ession, and secretion of larger, TG-enriched VLDL, despite a lower rate of TG secretion and a similar

66 dings suggest that reduced ability to export VLDLs is deleterious for the liver.

67 roteins (VLDLs) (P = 0.004), reduced fasting VLDL particle size (P = 0.04), and a reduced postprandia

68 The aim was to determine whether fed VLDL and chylomicron (CM) triacylglycerol (TAG) producti

69 cholesterol, 1.19 (95% CI: 1.14 to 1.25) for VLDL triglycerides, 5.38 (95% CI: 3.73 to 7.75) for IDL

70 confidence interval [CI]: 1.81 to 2.36) for VLDL cholesterol, 1.19 (95% CI: 1.14 to 1.25) for VLDL t

71 TM6SF2, critical for VLDL formation, was identified as a ChREBP target in mou

72 2 is required to mobilize neutral lipids for VLDL assembly but is not required for secretion of apoB-

73 rotein B100 (apoB100), which is required for VLDL formation.

74 fferent sources of fatty acids (FA) used for VLDL-triglyceride synthesis include dietary FA that clea

75 ons contain apoB48, while those derived from VLDL contain apoB100.

76 particles (RLPs), derived by lipolysis from VLDL and chylomicrons, contribute to this residual risk.

77 ructose conversion into blood (13)C glucose, VLDL-(13)C palmitate, and postprandial plasma lactate co

78 positively with afamin, complement factor H, VLDL-associated apolipoproteins, and lipid subspecies co

79 Strikingly, metformin did not affect hepatic VLDL-TG production, VLDL particle composition, and hepat

80 the hypothesis that miR-33 controls hepatic VLDL-TAG secretion.

81 pe-localized torsinA-LAP1 complex in hepatic VLDL secretion and suggest that the torsinA pathway part

82 as an important permissive factor in hepatic VLDL secretion that protects against hepatic steatosis.

83 Consistent with a role for Them2 in hepatic VLDL secretion, THEM2 levels were increased in livers of

84 ngs suggest that syndecan-1 mediates hepatic VLDL turnover in humans as well as in mice and that shed

85 ed hepatic steatosis and the rate of hepatic VLDL secretion, upregulated hepatic LDLR expression, and

86 in signaling independently regulates hepatic VLDL secretion.

87 he hypothesis that glycine regulates hepatic VLDL-TG secretion by potentiating NMDA receptor-mediated

88 genesis but also strongly suppressed hepatic VLDL lipidation, hence promoting the storage of "old fat

89 erol level, high LDL cholesterol level, high VLDL cholesterol level, high triglyceride level, high to

90 8.4 +/- 3.6%; n = 13) exhibited a 45% higher VLDL-triacylglycerol 16:1n-7 molar percentage (P < 0.01)

91 Both purified mouse and human VLDL could efficiently inhibit HCV infection.

92 DNL, only the abundances of 14:0 and 18:0 in VLDL-TG could discriminate between subjects having high

93 abundances (mol%) of 14:0, 16:0, and 18:0 in VLDL-TG were weakly (r <= 0.35) associated with DNL, whe

94 18:2n-6) nor the SCD index (16:1n-7/16:0) in VLDL-TG was associated with isotopically assessed DNL (r

95 e diet, the low amount of dietary 16:1n-7 in VLDL-triacylglycerols corresponded to a stronger signal

96 cerides in LDL subclasses and cholesterol in VLDL and LDL subclasses.

97 The decrease in VLDL secretion could be attributed to CB1R blockade, whi

98 e contributing mechanism for the decrease in VLDL secretion is enhanced degradation of apolipoprotein

99 n the KO animals due to a 3-fold decrease in VLDL-TG secretion rate without any associated reduction

100 evels, an effect mostly due to a decrease in VLDL-TG, whereas HDL was slightly increased.

101 proteins and has significant implications in VLDL secretion by hepatocytes.

102 ough downstream factors those participate in VLDL assembly/secretion.

103 Highly significant reduction in VLDL cholesterol levels and systolic BP was observed amo

104 epatocytes caused even greater reductions in VLDL secretion and profound steatosis.

105 st models were obtained for triglycerides in VLDL (0.82 < Q(2) <0.92) and HDL (0.69 < Q(2) <0.79) sub

106 Whereas feeding increased VLDL-TG uptake into WAT eightfold in wild-type mice, no

107 e rescue with high physiological T increased VLDL-TG secretion during both basal and clamp conditions

108 ic fatty acid oxidation leading to increased VLDL synthesis, decreased glucose tolerance, and promoti

109 cholesterol concentrations due to increased VLDL/LDL fractions.

110 ely 7% of circulating FFA was converted into VLDL-TG.

111 terations in triglyceride incorporation into VLDL or abnormal lipoprotein remodeling in the plasma.

112 riglyceride synthesis for incorporation into VLDL particles.

113 rsion into glucose or its incorporation into VLDL triglycerides.

114 physiological role of SVIP in intracellular VLDL trafficking and secretion.

115 learance of glycerol tri[(3)H]oleate-labeled VLDL-like emulsion particles into brown adipose tissue (

116 th hepatic fat accumulation along with large VLDL and triglyceride levels.

117 er the curve in plasma (P = 0.041) and large VLDLs (P = 0.004).

118 size (-1.5%; 95% CI, -3.7% to 0.5%), larger VLDL size (2.8%; 95% CI, -5.8% to 12.7%), and lower LPIR

119 The experiments showed that very LDL (VLDL) receptor (VLDLR) interacts with high affinity with

120 significantly higher serum HDL and lower LDL+VLDL levels in comparison to F1 mice from dams on the co

121 een plasma lipoprotein particles HDL and LDL/VLDL, resulting in equilibration between these lipoprote

122 m levels of lipid metabolites (including LDL/VLDL lipoproteins), creatinine and decreased levels of a

123 tivation of Bmal1 led to elevated plasma LDL/VLDL cholesterol levels as a consequence of the disrupti

124 glycerides and very-low-density lipoprotein (VLDL) and its subclasses, which decreased in metabolic g

125 tes in hepatic very low-density lipoprotein (VLDL) assembly and in adipose tissue basal lipolysis.

126 ol level, high very low-density lipoprotein (VLDL) cholesterol level, high triglyceride level, low hi

127 ein (HDL), and very-low-density lipoprotein (VLDL) cholesterol levels.

128 er remnant and very-low-density lipoprotein (VLDL) cholesterol, but there were no associations on cho

129 tein (LDL) and very-low-density lipoprotein (VLDL) discriminated dengue virus (DENV)-infected subject

130 Nascent very low density lipoprotein (VLDL) exits the endoplasmic reticulum (ER) in a speciali

131 e secretion of very-low-density lipoprotein (VLDL) for its egress.

132 and decreased very low-density lipoprotein (VLDL) fractions.

133 ete lipid-poor very low-density lipoprotein (VLDL) lacking arachidonoyl PLs.

134 ze and reduced very low-density lipoprotein (VLDL) levels, as compared with littermate controls.

135 rge and medium very-low-density lipoprotein (VLDL) particle concentrations and increased LDL peak par

136 ort of nascent very low density lipoprotein (VLDL) particles from the endoplasmic reticulum (ER) to t

137 ficking of pre-very low-density lipoprotein (VLDL) particles.

138 ponents of the very-low-density lipoprotein (VLDL) pathway for assembly/release.

139 contrast, the very low density lipoprotein (VLDL) pathway, which is required for the secretion of ce

140 ssociated with very-low-density lipoprotein (VLDL) play a major role in maintaining overall lipid hom

141 and decreased very-low-density lipoprotein (VLDL) secretion by 50%.

142 gilin controls very-low-density lipoprotein (VLDL) secretion through the modulation of apolipoprotein

143 ide synthesis, very low-density lipoprotein (VLDL) secretion, and fatty acid beta-oxidation.

144 sis, increased very low-density lipoprotein (VLDL) secretion, and improved glucose tolerance and insu

145 lating hepatic very low-density lipoprotein (VLDL) secretion, and subsequently circulating low-densit

146 Genes for very-low-density lipoprotein (VLDL) synthesis (microsomal triglyceride transfer protei

147 d increases in very-low-density lipoprotein (VLDL) triglycerides by decreasing the fructose conversio

148 nce and plasma very low density lipoprotein (VLDL) triglycerides concentrations.

149 ased levels of very low density lipoprotein (VLDL) triglycerides, suggesting alterations in triglycer

150 d secretion as very low-density lipoprotein (VLDL) triglycerides.

151 ted that serum very-low-density lipoprotein (VLDL) was responsible for the blockade of HCV cell attac

152 ased levels of very low-density lipoprotein (VLDL), amino acids, and citrate.

153 ations of LDL, very low-density lipoprotein (VLDL), and high-density lipoprotein (HDL) particles.

154 100-containing very-low-density lipoprotein (VLDL), as well as on the expression of key intestinal ge

155 [chylomicron, very-low-density lipoprotein (VLDL), LDL, high-density lipoprotein].

156 ein (LDL), and very-low density lipoprotein (VLDL), play a critical role in heart disease.

157 affinities for very low density lipoprotein (VLDL), the main carrier of lipophilic drugs.

158 nthesis, e.g., very low-density lipoprotein (VLDL), the precursor of circulating LDL-C.

159 ma kinetics of very-low-density lipoprotein (VLDL)-apolipoprotein B-100 (apoB), intermediate-density

160 icated these 3 very-low-density lipoprotein (VLDL)-associated apolipoproteins in de novo lipogenesis,

161 ll spread, but very-low-density lipoprotein (VLDL)-containing mouse serum did not affect HCV cell-to-

162 ociations with very-low-density lipoprotein (VLDL)-lipoproteins, VLDL-cholesterol (C), VLDL-triglycer

163 e analysis and very low density lipoprotein (VLDL)-TG secretion assays revealed that hepatic ChREBP k

164 Very-low-density lipoprotein (VLDL)-triacylglycerols and plasma free FA [nonesterified

165 t from that of very-low-density lipoprotein (VLDL).

166 tein (HDL) and very low density lipoprotein (VLDL).

167 and uptake of very low density lipoprotein (VLDL).

168 evels, and low very-low-density lipoprotein (VLDL)/high high-density lipoprotein (HDL) profile.

169 he LDL signal, very-low-density-lipoprotein (VLDL) yields 1-3%, and human serum albumin (HSA) yields

170 ipitating the very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) with phosphotun

171 Very-low-density lipoproteins (VLDL) is a hallmark of metabolic syndrome (MetS) and eac

172 om plasma and very low-density lipoproteins (VLDL) was used to measure FA and cholesterol synthesis u

173 de release as very low density lipoproteins (VLDL).

174 secretion of very low density lipoproteins (VLDL).

175 very-low, low and high density lipoproteins (VLDL, LDL and HDL) with less of an increase in HDL.

176 lomicrons and very-low-density lipoproteins (VLDLs) (P = 0.004), reduced fasting VLDL particle size (

177 23) and large very-low-density lipoproteins (VLDLs) (P = 0.016) and postprandial triglyceride total a

178 ins including very low density lipoproteins (VLDLs) and chylomicrons, and regulates their distributio

179 secretion of very-low-density lipoproteins (VLDLs).

180 pectively, in very low-density lipoproteins (VLDLs).

181 vitamin E) to very-low-density lipoproteins (VLDLs).

182 .1 mm Hg) and very-low-density lipoproteins (VLDLs; 5.16 mg/dL) in group E.

183 low-density lipoprotein (VLDL)-lipoproteins, VLDL-cholesterol (C), VLDL-triglycerides, VLDL-diameter,

184 Direct DVC infusion of glycine lowered VLDL-TG secretion, whereas NMDA receptor blocker MK-801

185 The secretion of mature VLDL particles occurs through the Golgi secretory pathwa

186 ion of [1,1,2,3,3-(2)H5]glycerol (to measure VLDL-TG kinetics) and either [1-(14)C]palmitate or [9,10

187 to adipose tissue inflammation and mediates VLDL-induced lipid accumulation and induction of inflamm

188 MetS-VLDL induced downregulation of Cx40 and Cx43 at transcri

189 In conclusion, MetS-VLDL modulates gap junctions and delays both atrial and

190 ted from normal (Normal-VLDL) and MetS (MetS-VLDL) individuals.

191 d conduction on atria and ventricles of MetS-VLDL mice.

192 Electrocardiograms demonstrated that MetS-VLDL induced prolongation of P wave (P = 0.041), PR inte

193 n into the endoplasmic reticulum for nascent VLDL particle assembly activates CREBH processing and en

194 ieved to latch onto or fuse with the nascent VLDL particle in either the ER or the Golgi compartment,

195 that TM6SF2 activity is required for normal VLDL secretion and that impaired TM6SF2 function causall

196 nd QTc interval (both P = 0.003), but Normal-VLDL did not.

197 VLDLs were separated from normal (Normal-VLDL) and MetS (MetS-VLDL) individuals.

198 The strong associations of VLDL-associated apolipoproteins with incident CVD in the

199 The biogenesis of VLDL particles occurs in the endoplasmic reticulum (ER),

200 tly accelerated the fractional catabolism of VLDL-apoB (P<0.001 and P.032, respectively), intermediat

201 Clearance of VLDL and chylomicron remnants was hampered, leading to a

202 and smaller increases of most components of VLDL (very low density lipoprotein) subparticles.

203 and cholesterol and triglyceride content of VLDL, intermediate-density lipoproteins (IDLs), and low-

204 nisms underlying the postprandial control of VLDL-TAG secretion remain unclear.

205 Tm6sf2 level is an important determinant of VLDL metabolism and further implicate TM6SF2 as a causat

206 also imply that reduction or elimination of VLDL production will likely enhance HCV infection in the

207 ly, our findings suggest that elimination of VLDL will lead to the development of more robust mouse m

208 Inhibition of VLDL secretion reduces plasma levels of atherogenic apol

209 of this pathway indicates that inhibition of VLDL secretion remains a viable target for therapies aim

210 es in blood plasma due to a reduced level of VLDL-secreted triglycerides from the liver.

211 m cell formation induced excessive levels of VLDL remnants.

212 lipoprotein profile with increased levels of VLDL.

213 t mass was the only independent predictor of VLDL-TG secretion, explaining 33-57% of the variance.

214 These were attributable to reduced rates of VLDL secretion owing to decreased incorporation of plasm

215 Regulation of VLDL-TG secretion is complex in that, despite a broad sp

216 utonomic nervous system in the regulation of VLDL-TG.

217 show that miR-33 limits hepatic secretion of VLDL-TAG by targeting N-ethylmaleimide-sensitive factor

218 factors affecting synthesis and secretion of VLDL-TAG using the growth hormone-deficient Ames dwarf m

219 from each of these sources for synthesis of VLDL-triglyceride.

220 dex, and the pattern in NEFAs echoed that of VLDL-triacylglycerols.

221 eting apoB synthesis, which lies upstream of VLDL secretion, have potential to effectively reduce dys

222 The life cycles of VLDLs and most LDLs occur within plasma.

223 hepatitis, likely from a secretion defect of VLDLs.

224 ASO reduction of ApoC-III had no effect on VLDL secretion, heparin-induced TG reduction, or uptake

225 acerebroventricular administration of NPY on VLDL-TG secretion.

226 s by controlling lipid droplet growth and/or VLDL production.

227 esicle accumulation after exposure to LDL or VLDL.

228 nificant impairment of fatty acid oxidation, VLDL-triglyceride (TG) secretion, and AMPK signaling.

229 in FFA-driven esterification and oxidation, VLDL-TAG secretion is maintained to support peripheral l

230 Plasma VLDL-TG levels were reduced in the KO animals due to a 3

231 Plasma VLDL/IDL/LDL cholesterol levels were significantly decre

232 Tgh expression dramatically decreased plasma VLDL TG and VLDL cholesterol concentrations but only mod

233 mic properties, metformin also lowers plasma VLDL triglyceride (TG).

234 s global hepatic secretion and raises plasma VLDL-TAG.

235 lpha expression along with elevated LDL plus VLDL export.

236 s, in the export of pre-chylomicrons and pre-VLDLs from the ER.

237 , and pre-very low-density lipoproteins (pre-VLDLs) are too big to fit into conventional COPII-coated

238 BMI, systolic and diastolic blood pressure, VLDL cholesterol, and glucose parameters were higher in

239 pies because they might raise proatherogenic VLDL-TAG levels.

240 n did not affect hepatic VLDL-TG production, VLDL particle composition, and hepatic lipid composition

241 oxidation by activating AMPK and to promote VLDL-TG secretion from the liver.

242 increased the levels of the Reelin receptor (VLDL receptor (VLDLR)) in hippocampal neurons by increas

243 d adipocyte hypertrophy and strongly reduced VLDL-induced ER stress and inflammation.

244 ally, we show that silencing of SVIP reduces VLDL secretion, suggesting a physiological role of SVIP

245 ese data indicate that cathepsin B regulates VLDL secretion and free fatty acid uptake via cleavage o

246 CA1-mediated nascent HDL formation regulates VLDL-triglyceride production and contributes to the inve

247 T is not a major determinant of resting VLDL-TG kinetics in men.

248 ccompanied by larger, triglyceride (TG)-rich VLDL, and a higher lipoprotein insulin resistance (LP-IR

249 the liver and larger, more triglyceride-rich VLDL particles.

250 composition, multiorgan insulin sensitivity, VLDL apolipoprotein B100 (apoB100) kinetics, and global

251 mice, which displayed strongly reduced serum VLDL cholesterol levels.

252 lectively, these findings suggest that serum VLDL serves as a major restriction factor of HCV infecti

253 d postprandial concentration of medium-sized VLDL particles (P = 0.02).

254 hsa-miR-122-5p levels associated with small VLDL, IDL, and large LDL lipoprotein subclass components

255 In all subjects, VLDL-triacylglycerol 16:1n-7 was significantly (P < 0.01

256 of phospholipid biosynthesis and subsequent VLDL-TAG secretion, leading to increased postprandial TA

257 epatic triglyceride synthesis and subsequent VLDL/LDL secretion by directly and noncompetitively inhi

258 patic insulin signaling is known to suppress VLDL production from the liver, it is unknown whether br

259 result of reduced glycolysis and suppressed VLDL-TG secretion.

260 x 1 (mTORC1) is essential for this sustained VLDL-TAG secretion and lipid homeostasis.

261 lesterol (TG:VLDL-C); however, the actual TG:VLDL-C ratio varies significantly across the range of tr

262 very low-density lipoprotein cholesterol (TG:VLDL-C); however, the actual TG:VLDL-C ratio varies sign

263 -HDL-C values, a 180-cell table of median TG:VLDL-C values was derived and applied in the validation

264 In the derivation data set, the median TG:VLDL-C was 5.2 (IQR, 4.5-6.0).

265 LDL-C using an adjustable factor for the TG:VLDL-C ratio provided more accurate guideline risk class

266 vels explained 65% of the variance in the TG:VLDL-C ratio.

267 We conclude that VLDL assembly and CREBH activation play key roles in the

268 Mechanistic studies demonstrated that VLDL is the major restriction factor that blocks HCV inf

269 The authors tested the hypothesis that VLDL cholesterol and triglycerides each explain part of

270 We hypothesized that VLDL can modulate and reduce atrial gap junctions.

271 These findings suggest that VLDL is beneficial to patients by restricting HCV infect

272 ons were found for lipid compositions in the VLDL, IDL, and LDL lipoprotein subclasses.

273 ted with a ChREBP-dependent induction of the VLDL lipidation proteins microsomal TG transfer protein

274 r B (CIDEB) is an important regulator of the VLDL pathway.

275 ing new insight into the exploitation of the VLDL regulator CIDEB by HCV.

276 rent data provide support for the use of the VLDL-triacylglycerol 16:1n-7 molar percentage as a bioma

277 cell-to-cell spread, while showing that the VLDL pathway, which is required for the secretion of cel

278 ted by a specialized ER-derived vesicle, the VLDL transport vesicle (VTV).

279 ER) in a specialized ER-derived vesicle, the VLDL transport vesicle (VTV).

280 These VLDLs are then circulated throughout the body to maintai

281 roteins ApoA-IV and ApoC-II, contributing to VLDL/HDL distribution and lipolysis.

282 portion of systemic FFA that is converted to VLDL-TG can confound the expected relationship between p

283 portion of systemic FFA that is converted to VLDL-TG.

284 In addition to total VLDL, LDL, and HDL lipoproteins, statistically significa

285 During the SBe+MD treatment, VLDL fractions and serum triglycerides increased.

286 f very low-density lipoprotein triglyceride (VLDL-TG) palmitate.

287 Reduction in triglyceride, VLDL, total WBC, lymphocyte, and neutrophil counts and i

288 very low-density lipoprotein triglycerides (VLDL-TGs) under postabsorptive, postprandial, and walkin

289 very low-density lipoprotein-triglycerides (VLDL-TAG).

290 very low density lipoprotein-triglycerides (VLDL-TGs) into white adipose tissue (WAT) rather than ox

291 s, VLDL-cholesterol (C), VLDL-triglycerides, VLDL-diameter, branched/aromatic amino acids, glycoprote

292 mportant for HCV cell-to-cell spread, unlike VLDL-containing mouse serum, which did not affect HCV ce

293 hat the molecules that changed the most were VLDL, LDL, and amino acids.

294 When VLDL particle assembly and secretion was inhibited by he

295 smoking, and IDL + LDL cholesterol, whereas VLDL triglycerides did not enter the model.

296 evated apoB-containing lipoproteins, whereas VLDL triglycerides did not explain risk.

297 n from apoB-containing lipoproteins, whereas VLDL triglycerides did not explain risk.

298 a 39% increase in [(3)H]TAG associated with VLDL secretion.

299 00 (apoB100) and specifically interacts with VLDL apoB100 and coat complex II proteins.

300 ealed that CideB specifically interacts with VLDL structural protein, apolipoprotein B100 (apoB100),