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Amylopectin Starch Promotes the Development of Insulin Resistance in Rats¹

Human Nutrition Unit and Department of Biochemistry, University of Sydney, Sydney, New South Wales, 2006, Australia

Starches that are high in amylopectin are digested and absorbed more quickly than starches with a high amylose content and produce larger postprandial glucose and insulin responses. The aim of this study was to test the hypothesis that feeding rats a diet containing quickly digested starch could promote insulin resistance. Sprague-Dawley rats were fed either a high amylopectin or high amylose diet (two 10-g meals per day), and insulin sensitivity was assessed after 9 wk by intravenous glucose tolerance test (IVGTT). In the rats fed the high amylopectin diet, glucose tolerance was significantly lower (P < 0.05) and the insulin response to IVGTT was twice as high as in rats fed the high amylose diet (P < 0.05). A second study using Wistar rats investigated the time course of these changes. Differences in the insulin response to the IVGTT were not evident at 4 wk but began to emerge at 8 wk, and by 12 wk the insulin response was 100% greater in rats fed the high amylopectin diet (P < 0.05) than in those fed the high amylose diet. In addition, basal plasma insulin concentration was higher in rats fed the high amylopectin diet (P < 0.05). There were no differences, however, in glucose tolerance at any time point. The results suggest that quickly digested starch promotes the development of insulin resistance in rats. The relatively slow time course resembles the normal development of insulin resistance in humans.

KEY WORDS: • amylose • starch • rats • glycemic index • insulin resistance

¹ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

² The first author conducted this work as partial fulfillment for the degree of Bsc (Hons).

³ To whom correspondence should be addressed.

Manuscript received 25 July 1994. Revision accepted 4 January 1995.

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