Document Detail


Circulating very-low-density lipoprotein characteristics resulting from fatty liver in an insulin resistance rat model.
MedLine Citation:
PMID:  20203480     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The close association between nonalcoholic fatty liver and insulin resistance is now widely recognized. While the former is characterized by excessive intrahepatic triglyceride accumulation, the latter induces overproduction of very-low-density lipoprotein (VLDL) particles. It has not been well elucidated whether these apparently opposite mechanisms impact on VLDL characteristics or not. The aim of the present study was to evaluate the VLDL secretion and features resulting from insulin resistance and fatty liver in rats fed a sucrose-rich diet (SRD, i.e. addition of sucrose to drinking water during 12 weeks). No differences in calorie intake were observed in comparison to controls. Both groups showed similar weight gains throughout the treatment period. However, SRD rats showed an increased proportion of body fat as assessed by X-ray absorptiometry, increased visceral obesity, liver weight and fat accumulation in the liver (p < 0.04). Histological study revealed moderate micro- and macrovesicular steatosis. Fasting insulin, triglyceride and free fatty acid (FFA) levels increased while VLDLs decreased in SRD rats (p < 0.05). The chemical composition of VLDLs of SRD rats showed a higher percentage of triglycerides, and the VLDL triglyceride/protein ratio, an estimator of lipoprotein size, suggests that VLDL particles of SRD rats are larger than those of controls (p < 0.0005). FFA levels correlated with VLDL triglycerides (r = 0.49, p = 0.03) and liver fat content correlated with plasma triglycerides (r = 0.65), VLDL triglycerides (r = 0.55) and triglyceride/protein ratio (r = 0.52, p < 0.02). The VLDL secretion rate assay showed an increase in SRD rats (p < 0.02), confirming an overproduction despite liver fat accumulation. Our findings are consistent with an insulin resistance development model in which hepatic lipid content would constitute an important determinant of a triglyceride-rich, large-particle VLDL secretion; both features would increase its atherogenic potential.
Authors:
V Zago; D Lucero; E V Macri; L Cacciagiú; C A Gamba; V Miksztowicz; G Berg; R Wikinski; S Friedman; L Schreier
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-04
Journal Detail:
Title:  Annals of nutrition & metabolism     Volume:  56     ISSN:  1421-9697     ISO Abbreviation:  Ann. Nutr. Metab.     Publication Date:  2010  
Date Detail:
Created Date:  2010-04-16     Completed Date:  2010-07-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8105511     Medline TA:  Ann Nutr Metab     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  198-206     Citation Subset:  IM    
Copyright Information:
(c) 2010 S. Karger AG, Basel.
Affiliation:
Laboratory of Lipids and Lipoproteins, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, INFIBIOC, University of Buenos Aires, Buenos Aires, Argentina.
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MeSH Terms
Descriptor/Qualifier:
Absorptiometry, Photon
Adipose Tissue / metabolism
Animals
Blood Glucose / metabolism
Body Weight / physiology
Cholesterol, HDL / blood
Energy Intake
Fatty Acids, Nonesterified / blood
Fatty Liver / blood*
Insulin Resistance / physiology*
Lipid Metabolism
Lipid Peroxidation
Lipoproteins, VLDL / blood*
Liver / metabolism,  pathology
Male
Rats
Rats, Wistar
Thiobarbituric Acid Reactive Substances / metabolism
Triglycerides / blood
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Cholesterol, HDL; 0/Fatty Acids, Nonesterified; 0/Lipoproteins, VLDL; 0/Thiobarbituric Acid Reactive Substances; 0/Triglycerides
Comments/Corrections
Erratum In:
Ann Nutr Metab. 2010;56(4):259

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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