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Am J Physiol Endocrinol Metab (January 15, 2002). doi:10.1152/ajpendo.00173.2001
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Articles in PresS, published online ahead of print January 15, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00173.2001
Submitted on April 19, 2001
Accepted on January 9, 2002

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

Simon M Chalkley1*, Manthinda Hettiarachchi1, Donald J Chisholm1, and Edward W Kraegen1

1 Metabolism, Garvan, Darlinghurst, NSW, Australia

* To whom correspondence should be addressed. E-mail: s.chalkley{at}garvan.org.au.

Although lipid excess can impair ß-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 months) high polyunsaturated fat feeding on glucose tolerance in Wistar rats. The high fat fed group was 30% heavier and 60% fatter than chow fed, 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 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 to intravenous glucose was similar in both groups. Following the intravenous glucose bolus, plasma glucose decline was slower in the high fat fed 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 a genetic or congenital susceptibility to ß-cell impairment is required for overt hyperglycemia to develop in the presence of severe insulin resistance.




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