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J. Biol. Chem., Vol. 277, Issue 32, 28795-28802, August 9, 2002
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From the To determine whether reduction of
insulin resistance could ameliorate fructose-induced very low density
lipoprotein (VLDL) oversecretion and to explore the mechanism of this
effect, fructose-fed hamsters received placebo or rosiglitazone for 3 weeks. Rosiglitazone treatment led to normalization of the blunted
insulin-mediated suppression of the glucose production rate and to a
~2-fold increase in whole body insulin-mediated glucose disappearance
rate (p < 0.001). Rosiglitazone ameliorated the
defect in hepatocyte insulin-stimulated tyrosine phosphorylation of the
insulin receptor, IRS-1, and IRS-2 and the reduced protein mass of
IRS-1 and IRS-2 induced by fructose feeding. Protein-tyrosine
phosphatase 1B levels were increased with fructose feeding and were
markedly reduced by rosiglitazone. Rosiglitazone treatment led to a
~50% reduction of VLDL secretion rates (p < 0.05)
in vivo and ex vivo. VLDL clearance assessed directly in vivo was not significantly different in the FR
(fructose-fed + rosiglitazone-treated) versus F
(fructose-fed + placebo-treated) hamsters, although there was a trend
toward a lower clearance with rosiglitazone. Enhanced stability of
nascent apolipoprotein B (apoB) in fructose-fed hepatocytes was
evident, and rosiglitazone treatment resulted in a significant
reduction in apoB stability. The increase in intracellular mass of
microsomal triglyceride transfer protein seen with fructose feeding was
reduced by treatment with rosiglitazone. In conclusion, improvement of
hepatic insulin signaling with rosiglitazone, a peroxisome
proliferator-activated receptor
Ameliorated Hepatic Insulin Resistance Is Associated with
Normalization of Microsomal Triglyceride Transfer Protein Expression
and Reduction in Very Low Density Lipoprotein Assembly and Secretion in
the Fructose-fed Hamster*
§,,,,
,**
Department of Medicine, Division of
Endocrinology and Metabolism, University Health Network, and
¶ Department of Laboratory Medicine and Pathobiology, Hospital for
Sick Children, University of Toronto, Toronto, Ontario M5G 2C4,
Canada, and GlaxoSmithKline, Clinical Development & Medical
Affairs, New Frontiers Science Park (South),
Harlow, Essex CM19 5AW, United Kingdom
agonist, is associated with reduced
hepatic VLDL assembly and secretion due to reduced intracellular apoB stability.
*
These studies were supported in part by operating grants
from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Ontario and GlaxoSmithKline.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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