ライフサイエンスコーパス: VLDL

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

2 VLDL may contribute to the pathophysiology of atrial fib

3 VLDL receptor deletion significantly impairs the express

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

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

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

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

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

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

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

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

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

13 on in hepatocyte microsomal lumina, and also VLDL secretion into the plasma.

14 takes, large VLDLs (P = 0.042 and 0.018) and VLDL size (P = 0.011 and 0.025) remained negatively asso

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

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

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

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

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

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

21 f hepatocytes increases both VTV budding and VLDL secretion.

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

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

24 ration, VLDL-triglyceride concentration, and VLDL-[(13)C]palmitate production were measured after ora

25 ealth and Human Services on IHTG content and VLDL kinetics in obese persons with NAFLD.

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

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

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

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

30 y and very low-density lipoproteins (LDL and VLDL).

31 um triglyceride, total cholesterol, LDL, and VLDL concentrations significantly decreased by 51.7%, 17

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

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

34 of host lipid metabolism, LD morphology, and VLDL transport appear to negatively influence HCV prolif

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

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

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

38 e (16:0) to linoleate (18:2n-6) in serum and VLDL triglycerides was used as an index of DNL.

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

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

41 amatic improvement in serum triglyceride and VLDL concentrations, a significant increase in serum ome

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

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

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

45 secretion of triglycerides (TG) packaged as VLDLs.

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

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

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

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

50 Both VLDL particle size and plasma cholesterol levels were si

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

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

53 +/- 0.43 vol%; P < 0.05) but did not change VLDL-triglyceride concentrations or VLDL-[(13)C]palmitat

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

55 rahepatocellular lipid (IHCL) concentration, VLDL-triglyceride concentration, and VLDL-[(13)C]palmita

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

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

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

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

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

61 the major function of liver PLTP is to drive VLDL production and makes a small contribution to plasma

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

63 HFr also enhanced VLDL-[(13)C]palmitate production.

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

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

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

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

68 hepatic production of triglyceride-enriched VLDL.

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

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

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

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

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

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

78 re used to evaluate IHTG content and hepatic VLDL-TG and apolipoprotein B-100 (apoB-100) secretion ra

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

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

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

82 sampling, respectively, the rate of hepatic VLDL-TG secretion was measured following tyloxapol (an i

83 in signaling independently regulates hepatic VLDL secretion.

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

85 PY) release during fasting regulates hepatic VLDL-TG secretion.

86 Exercise training did not change the hepatic VLDL-TG secretion rate (17.7 +/- 3.9 mumol/min before an

87 8.4 +/- 3.6%; n = 13) exhibited a 45% higher VLDL-triacylglycerol 16:1n-7 molar percentage (P < 0.01)

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

89 ation of ectodomains in the plasma, impaired VLDL catabolism, and hypertriglyceridemia.

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

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

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

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

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

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

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

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

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

99 to repression of hepatic Sort1 and increased VLDL secretion via Atf3.

100 had larger hepatic fat stores and increased VLDL secretion.

101 etes is typically characterized by increased VLDL secretion but normal LDL cholesterol levels, possib

102 Despite this, diabetes increased VLDL triglycerides and LDL cholesterol in E4LDLR(-/-) mi

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

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

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

106 oventricular administration of NPY increases VLDL-TG secretion by the liver without affecting lipolys

107 iver PLTP expression significantly increases VLDL lipidation in hepatocyte microsomal lumina, and als

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

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

110 rsion into glucose or its incorporation into VLDL triglycerides.

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

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

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

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

115 as significantly associated with fewer large VLDLs (P = 0.022 in women, P = 0.064 in men), a smaller

116 nt for carbohydrate and sugar intakes, large VLDLs (P = 0.042 and 0.018) and VLDL size (P = 0.011 and

117 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

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

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

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

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

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

123 .00417), large very low-density lipoprotein (VLDL) (Caucasians P = 0.001; African Americans, P = 0.03

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 impairment in very-low-density lipoprotein (VLDL) binding that was entirely corrected in db/db mice

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

128 sma TC, LDL-C, very-low-density lipoprotein (VLDL) cholesterol, and MDA than had the PC group after 8

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

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

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

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

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

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

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

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

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

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

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

145 G) content and very low density lipoprotein (VLDL) triglyceride (TG) secretion rate.

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

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

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

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

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

151 100-containing very-low-density lipoprotein (VLDL), as well as on the expression of key intestinal ge

152 ion of nascent very low-density lipoprotein (VLDL), finding that liver PLTP expression significantly

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

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

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

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

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

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

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

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

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

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

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

164 that maternal very-low-density-lipoprotein (VLDL) receptor deletion in mice causes the production of

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

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

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

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

169 secretion of very low density lipoproteins (VLDL).

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

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

172 lyceride-rich very low-density lipoproteins (VLDL-TG) contributes to diabetic dyslipidemia.

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

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

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

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

177 .1 mm Hg) and very-low-density lipoproteins (VLDLs; 5.16 mg/dL) in group E.

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

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

180 s the sympathetic nervous system to maintain VLDL-TG secretion at a postprandial level.

181 thetic innervation are necessary to maintain VLDL-TG secretion.

182 AH secretion, but also identify the maternal VLDL receptor as a key genetic program that ensures milk

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

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

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

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

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

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

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

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

191 sults indicate that hepatic LPCAT3 modulates VLDL production by regulating LysoPC levels and MTP expr

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Importantly, the hypersecretion of VLDL-TG from the liver induced by a model of high-fat fe

206 DVC glycine normalized the hypersecretion of VLDL-TG induced by high-fat feeding.

207 Inhibition of VLDL secretion reduces plasma levels of atherogenic apol

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

209 This is not because of inhibition of VLDL-[(13)C]palmitate production.

210 m cell formation induced excessive levels of VLDL remnants.

211 lipoprotein profile with increased levels of VLDL.

212 epatic LDLR protein, and increased levels of VLDL/LDL cholesterol in WT but not Pcsk9-/- mice.

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

214 e level of degradation and the regulation of VLDL production.

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 ese findings not only reveal a novel role of VLDL receptor in suppressing inflammation by maintaining

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

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

220 y of glycine to inhibit hepatic secretion of VLDL-TG in vivo.

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

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

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

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

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

226 acerebroventricular administration of NPY on VLDL-TG secretion.

227 t change VLDL-triglyceride concentrations or VLDL-[(13)C]palmitate production.

228 esicle accumulation after exposure to LDL or VLDL.

229 nd 16.8 +/- 5.4 mumol/min after training) or VLDL-apoB-100 secretion rate (1.5 +/- 0.5 nmol/min befor

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

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

232 '-tetramethylindodicarbocyanine perchlorate)-VLDL binding to cells, and shed syndecan-1 ectodomains b

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

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

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

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

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

238 lpha expression along with elevated LDL plus VLDL export.

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

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

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

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

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

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

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

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

247 y polyunsaturated fatty acid (PUFA), reduces VLDL levels and is used therapeutically for hypertriglyc

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

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

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

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

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

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

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

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

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

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

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

259 0.022 in women, P = 0.064 in men), a smaller VLDL size (P = 0.018 and P = 0.036), more large HDLs (P

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 in profile with decreased cholesterol in the VLDL and the LDL fractions, concomitant with elevated hi

276 ys-regulated molecule, SULF2, normalizes the VLDL-binding capacity of their hepatocytes and abolishes

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

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

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

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

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

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

283 These VLDLs are then circulated throughout the body to maintai

284 lls, and shed syndecan-1 ectodomains bind to VLDL.

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

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

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

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

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

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

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

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

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

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

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

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

297 When VLDL particle assembly and secretion was inhibited by he

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),