Circulating Very-Low-Density Lipoprotein Characteristics Resulting from Fatty Liver in an Insulin Resistance Rat Model

2010 ◽  
Vol 56 (3) ◽  
pp. 198-206 ◽  
Author(s):  
V. Zago ◽  
D. Lucero ◽  
E.V. Macri ◽  
L. Cacciagiú ◽  
C.A. Gamba ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Liver ◽  
Rat Model ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Very low-density lipoprotein receptor increases in a liver-specific manner due to protein deficiency but does not affect fatty liver in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yui Oshio ◽  
Yuta Hattori ◽  
Hatsuho Kamata ◽  
Yori Ozaki-Masuzawa ◽  
Arisa Seki ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Protein Restriction ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Protein Levels ◽  
Specific Manner ◽  
Density Lipoprotein Receptor

AbstractVery low-density lipoprotein receptor (VLDLR) is a member of the LDL receptor family that is involved in the uptake of VLDL into cells. Increased hepatic VLDLR under endoplasmic reticulum (ER) stress has been shown to cause fatty liver. In this study, the effect of dietary protein restriction on hepatic VLDLR and the role of VLDLR in fatty liver were investigated using Vldlr knockout (KO) mice. Growing wild-type (WT) and KO mice were fed a control diet containing 20% ​​protein or a low protein diet containing 3% protein for 11 days. In WT mice, the amount of hepatic Vldlr mRNA and VLDLR protein increased by approximately 8- and 7-fold, respectively, due to protein restriction. Vldlr mRNA and protein levels increased in both type 1 and type 2 VLDLR. However, neither Vldlr mRNA nor protein levels were significantly increased in heart, muscle, and adipose tissue, demonstrating that VLDLR increase due to protein restriction occurred in a liver-specific manner. Increased liver triglyceride levels during protein restriction occurred in KO mice to the same extent as in WT mice, indicating that increased VLDLR during protein restriction was not the main cause of fatty liver, which was different from the case of ER stress.

scholarly journals Mechanisms of Hepatic Very Low Density Lipoprotein Overproduction in Insulin Resistance

2000 ◽  
Vol 275 (12) ◽  
pp. 8416-8425 ◽  
Author(s):  
Changiz Taghibiglou ◽  
André Carpentier ◽  
Stephen C. Van Iderstine ◽  
Biao Chen ◽  
Debbie Rudy ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Steatohepatitis and liver fibrosis are predicted by the characteristics of very low density lipoprotein in nonalcoholic fatty liver disease

2016 ◽  
Vol 36 (8) ◽  
pp. 1213-1220 ◽  
Author(s):  
Zhenghui G. Jiang ◽  
Elliot B. Tapper ◽  
Margery A. Connelly ◽  
Carolina F. M. G. Pimentel ◽  
Linda Feldbrügge ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Nonalcoholic Fatty Liver

Mechanisms of Hepatic Very Low-Density Lipoprotein Overproduction in Insulin Resistance

2001 ◽  
Vol 11 (5) ◽  
pp. 170-176 ◽  
Author(s):  
Khosrow Adeli ◽  
Changiz Taghibiglou ◽  
Stephen C Van Iderstine ◽  
Gary F Lewis
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Is There a Relation Between Triglyceride Concentrations in Very Low Density Lipoprotein and the Index of Insulin Resistance in Nondiabetic Subjects?

2014 ◽  
Vol 28 (4) ◽  
pp. 269-274 ◽  
Author(s):  
Yoshifumi Kurosaki ◽  
Tomoaki Tsukushi ◽  
Shinichi Munekata ◽  
Yuhsaku Kanoh ◽  
Tatsumi Moriya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Very Low Density Lipoprotein Metabolism and Plasma Adiponectin as Predictors of High-Density Lipoprotein Apolipoprotein A-I Kinetics in Obese and Nonobese Men

2009 ◽  
Vol 94 (3) ◽  
pp. 989-997 ◽  
Author(s):  
Dick C. Chan ◽  
P. Hugh R. Barrett ◽  
Esther M. M. Ooi ◽  
Juying Ji ◽  
Doris T. Chan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Plasma Adiponectin ◽  
Amyloid A ◽  
Vldl Metabolism

Abstract Context: Hypercatabolism of high-density lipoprotein (HDL) apolipoprotein (apo) A-I results in low plasma apoA-I concentration. The mechanisms regulating apoA-I catabolism may relate to alterations in very low density lipoprotein (VLDL) metabolism and plasma adiponectin and serum amyloid A protein (SAA) concentrations. Objective: We examined the associations between the fractional catabolic rate (FCR) of HDL-apoA-I and VLDL kinetics, plasma adiponectin, and SAA concentrations. Study Design: The kinetics of HDL-apoA-I and VLDL-apoB were measured in 50 obese and 37 nonobese men using stable isotopic techniques. Results: In the obese group, HDL-apoA-I FCR was positively correlated with insulin, homeostasis model of assessment for insulin resistance (HOMA-IR) score, triglycerides, VLDL-apoB, and VLDL-apoB production rate (PR). In the nonobese group, HDL-apoA-I FCR was positively correlated with triglycerides, apoC-III, VLDL-apoB, and VLDL-apoB PR and negatively correlated with plasma adiponectin. Plasma SAA was not associated with HDL-apoA-I FCR in either group. In multiple regression analyses, VLDL-apoB PR and HOMA-IR score, and VLDL-apoB PR and adiponectin were independently predictive of HDL-apoA-I FCR in the obese and nonobese groups, respectively. HDL-apoA-I FCR was positively and strongly associated with HDL-apoA-I PR in both groups. Conclusions: Variation in VLDL-apoB production, and hence plasma triglyceride concentrations, exerts a major effect on the catabolism of HDL-apoA-I. Insulin resistance and adiponectin may also contribute to the variation in HDL-apoA-I catabolism in obese and nonobese subjects, respectively. We also hypothesize that apoA-I PR determines a steady-state, lowered plasma of apoA-I, which may reflect a compensatory response to a primary defect in the catabolism of HDL-apoA-I due to altered VLDL metabolism.

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