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1 Division of Endocrinology, Metabolism and Diabetes, University of Colorado Health Sciences Center, Denver, Colorado 80262; 2 Department of Physiology and Biophysics, University of Southern California, Los Angeles, California 90089; and 3 Exercise Science Research Institute, Arizona State University, Tempe, Arizona 85287
Sucrose feeding
reduces the ability of insulin to suppress glucose production and
hepatic gluconeogenesis. The present study examined the effect of a
high-sucrose diet on early insulin-signaling steps in the liver. Rats
were provided a high-starch (STD, control diet) or high-sucrose diet
(HSD) for 3 wk. On the day of study, overnight-fasted rats were
anesthetized and injected with either saline (n = 5/diet group) or insulin (2 mU/kg, n = 5/diet group) via the portal vein. Portal venous blood and liver tissue were harvested 2 min after injections. Portal vein plasma glucose levels were not significantly different among groups, pooled average 147 ± 12 mg/dl. Western blot analysis revealed no significant differences
in the amount of insulin receptor (IR), insulin receptor substrates-1
and -2 (IRS-1, IRS-2), and the p85 subunit of phosphatidylinositol (PI)
3-kinase. In contrast, the amount of the p110
subunit of PI 3-kinase
was increased ~2-fold in HSD vs. STD (P < 0.05).
After saline injection, tyrosine phosphorylation (pY) of IR, IRS-1, and
IRS-2 was not significantly different between groups. However, PI
3-kinase activity associated with phosphorylated proteins was increased
~40% in HSD vs. STD (P < 0.05). After insulin
injection, pY of the IR was not different between groups, whereas pY of
IRS-1 and IRS-2 was reduced (P < 0.05) in HSD vs. STD.
In addition, association of IRS-1 and IRS-2 with p85 was significantly
reduced in HSD vs. STD. These data demonstrate that an HSD impairs
insulin-stimulated early postreceptor signaling (pY of IRS proteins,
IRS interaction with p85). Furthermore, the increased amount of p110
and increased basal PI 3-kinase activity suggest a diet-induced
compensatory response.
phosphatidylinositol 3-kinase; diet; insulin action; insulin receptor substrates; rats
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