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Metabolism. 1999 Aug;48(8):1063-8.

Overproduction of insulin in the chromium-deficient rat.

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  • 1Beltsville Human Nutrition Research Center, US Department of Agriculture, Agricultural Research Service, MD 20705-2350, USA.


The hypothesis that the insulin secretory hyperresponsiveness observed in rats with diet-induced insulin resistance may be a basic characteristic of dietary chromium (Cr) deficiency was evaluated. Two groups of weanling rats were fed ad libitum a purified diet containing 64% sucrose, 20% casein, 5% corn oil, and the recommended levels of vitamins and minerals without added Cr. Cr-deficient (-Cr) rats were provided with distilled drinking water only, while Cr-supplemented (+Cr) rats received water containing 5 ppm Cr as CrCl3. A third group of rats fed a commercial chow diet served as sucrose controls. Effects of Cr deficiency were assessed by comparing fasting levels of glucose, insulin, and plasma lipids in blood samples collected biweekly from the -Cr and +Cr groups over a 3-month period. Both groups of rats fed the low-Cr sucrose diet developed a transient hyperinsulinemia and hyperlipidemia relative to the chow-fed control rats. There were significant effects of Cr supplementation on plasma triglycerides during the initial 2 weeks of dietary adaptation. Effects of the low-Cr diet were evaluated after the 12-week period by comparing the insulin response area and glucose clearance during a 40-minute intravenous glucose tolerance test (IVGTT). The rates of glucose clearance (KG) in -Cr and +Cr rats were similar (4.2 +/- 1.0 and 4.3 +/- 0.8%/min, respectively) and were comparable to the K(G) in chow-fed rats (4.6 +/- 0.8). In contrast, insulin secretory responses in -Cr rats were exaggerated (area, 14,083 +/- 3,399 microU/mL x min), being twofold greater (P < .05) relative to the +Cr group (6,183 +/- 864). The insulin secretory response area in chow-fed rats (7,081 +/- 408 microU/mL x min) was similar to the value in the +Cr group. These observations provide support for the hypothesis that Cr deficiency can lead to elevated insulin secretory responses to glucose.

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