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J. Biol. Chem., Vol. 277, Issue 35, 31646-31655, August 30, 2002
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From the Insulin-resistant states are
characterized by hypertriglyceridemia, predominantly because of
overproduction of hepatic very low density lipoprotein
particles. The additional contribution of intestinal lipoprotein
overproduction to the dyslipidemia of insulin-resistant states has not
been previously appreciated. Here, we have investigated intestinal
lipoprotein production in a fructose-fed hamster model of insulin
resistance previously documented to have whole body and hepatic insulin
resistance, and hepatic very low density lipoprotein overproduction.
Chronic fructose feeding for 3 weeks induced significant oversecretion of apolipoprotein B48 (apoB48)-containing lipoproteins in the fasting
state and during steady state fat feeding, based on (a) in vivo Triton WR1339 studies of apoB48 production as well
as (b) ex vivo pulse-chase labeling of
intestinal enterocytes from fasted and fed hamsters. ApoB48 particle
overproduction was accompanied by increased intracellular apoB48
stability, enhanced lipid synthesis, higher abundance of microsomal
triglyceride transfer protein mass, and a significant shift toward the
secretion of larger chylomicron-like particles. ApoB48 particle
overproduction was not observed with short-term fructose feeding or
in vitro incubation of enterocytes with fructose. Secretion
of intestinal apoB48 and triglyceride was closely linked to intestinal
enterocyte de novo lipogenesis, which was up-regulated in
fructose-fed hamsters. Inhibition of fatty acid synthesis by cerulenin,
a fatty acid synthase inhibitor, resulted in a
dose-dependent decrease in intestinal apoB48 secretion. Overall, these findings further suggest that intestinal overproduction of apoB48 lipoproteins should also be considered as a major contributor to the fasting and postprandial dyslipidemia observed in response to
chronic fructose feeding and development of an insulin-resistant state.
Fasting and Postprandial Overproduction of Intestinally Derived
Lipoproteins in an Animal Model of Insulin Resistance
EVIDENCE THAT CHRONIC FRUCTOSE FEEDING IN THE HAMSTER IS
ACCOMPANIED BY ENHANCED INTESTINAL DE NOVO LIPOGENESIS AND
ApoB48-CONTAINING LIPOPROTEIN OVERPRODUCTION*
,,
,
Department of Laboratory Medicine and
Pathobiology, Hospital for Sick Children and the § Division
of Endocrinology and Metabolism, Department of Medicine, University of
Toronto, Toronto, Ontario M5G 1X8, Canada
*
This work was supported in part by Canadian Institutes of
Health Research Operating Grants MOP53093 (to K. A.) and MOP43839 (to G. F. L.).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.
Recipient of a Research Fellowship from the Heart and Stroke
Scientific Research Corporation of Canada.
**
Canada Research Chair in Diabetes and a Career Investigator of the
Heart and Stroke Foundation of Canada.
To whom correspondence should be addressed: Division of
Clinical Biochemistry, Hospital for Sick Children, 555 University Ave.,
Toronto, Ontario M5G 1X8, Canada. Tel.: 416-813-8682; Fax: 416-813-6257; E-mail: k.adeli@utoronto.ca.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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