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Am J Physiol Endocrinol Metab 282: E1231-E1238, 2002. First published January 15, 2002; doi:10.1152/ajpendo.00173.2001
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Vol. 282, Issue 6, E1231-E1238, June 2002

Long-term high-fat feeding leads to severe insulin resistance but not diabetes in Wistar rats

Simon M. Chalkley, Manthinda Hettiarachchi, Donald J. Chisholm, and Edward W. Kraegen

Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia 2010

Although lipid excess can impair beta -cell function in vitro, short-term high-fat feeding in normal rats produces insulin resistance but not hyperglycemia. This study examines the effect of long-term (10-mo) high polyunsaturated fat feeding on glucose tolerance in Wistar rats. The high fat-fed compared with the chow-fed group was 30% heavier and 60% fatter, with approximately doubled fasting hyperinsulinemia (P < 0.001) but only marginal fasting hyperglycemia (7.5 ± 0.1 vs. 7.2 ± 0.1 mmol/l, P < 0.01). Insulin sensitivity was ~67% lower in the high-fat group (P < 0.01). The acute insulin response to intravenous arginine was approximately double in the insulin-resistant high-fat group (P < 0.001), but that to intravenous glucose was similar in the two groups. After the intravenous glucose bolus, plasma glucose decline was slower in the high fat-fed group, confirming mild glucose intolerance. Therefore, despite severe insulin resistance, there was only a mildly elevated fasting glucose level and a relative deficiency in glucose-stimulated insulin secretion; this suggests that a genetic or congenital susceptibility to beta -cell impairment is required for overt hyperglycemia to develop in the presence of severe insulin resistance.

insulin secretion; arginine; long-chain acyl-coenzyme A; body composition; glucose tolerance


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