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J. Biol. Chem., Vol. 277, Issue 1, 793-803, January 4, 2002
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From the A fructose-fed hamster model of insulin
resistance was previously documented to exhibit marked hepatic very low
density lipoprotein (VLDL) overproduction. Here, we investigated
whether VLDL overproduction was associated with down-regulation of
hepatic insulin signaling and insulin resistance. Hepatocytes isolated
from fructose-fed hamsters exhibited significantly reduced tyrosine
phosphorylation of the insulin receptor and insulin receptor substrates
1 and 2. Phosphatidylinositol 3-kinase activity as well as
insulin-stimulated Akt-Ser473 and
Akt-Thr308 phosphorylation were also significantly reduced
with fructose feeding. Interestingly, the protein mass and activity of
protein-tyrosine phosphatase-1B (PTP-1B) were significantly higher in
fructose-fed hamster hepatocytes. Chronic ex vivo exposure
of control hamster hepatocytes to high insulin also appeared to
attenuate insulin signaling and increase PTP-1B. Elevation in PTP-1B
coincided with marked suppression of ER-60, a cysteine protease
postulated to play a role in intracellular apoB degradation, and an
increase in the synthesis and secretion of apoB. Sodium orthovanadate, a general phosphatase inhibitor, partially restored insulin receptor phosphorylation and significantly reduced apoB secretion. In summary, we hypothesize that fructose feeding induces hepatic insulin resistance at least in part via an increase in expression of PTP-1B. Induction of
hepatic insulin resistance may then contribute to reduced apoB degradation and enhanced VLDL particle assembly and secretion.
Hepatic Very Low Density Lipoprotein-ApoB Overproduction Is
Associated with Attenuated Hepatic Insulin Signaling and Overexpression
of Protein-tyrosine Phosphatase 1B in a Fructose-fed Hamster Model
of Insulin Resistance*
§,,,
Division of Clinical Biochemistry,
Department of Laboratory Medicine and Pathobiology, Hospital for
Sick Children and ¶ Department of Medicine, Division of
Endocrinology and Metabolism, Mount Sinai Hospital and University
Health Network, University of Toronto, Toronto,
Ontario M5G 1X8, Canada
*
This work was supported by Heart and Stroke Foundation of
Ontario Grant T-4809 (to K. A.).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.
To whom correspondence should be addressed. Tel.:
416-813-8682; Fax: 416-813-6257; E-mail: k.adeli@utoronto.ca.
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