Overproduction of insulin in the chromium-deficient rat

The hypothesis that the insulin secretory hyperresponsiveness observed in r ats with diet-induced insulin resistance may be a basic characteristic of d ietary 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 on ly, 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 c ontrols. 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 hyperli pidemia relative to the chow-fed control rats. There were significant effec ts 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 clearanc e during a 40-minute intravenous glucose tolerance test (IVGTT), The rates of glucose clearance (K-G) in -Cr and +Cr rats were similar (4.2 +/- 1.0 an d 4.3 +/- 0.8 %/min, respectively) and were comparable to the K-G in chow-f ed rats (4.6 +/- 0.8). In contrast, insulin secretory responses in -Cr rats were exaggerated (area, 14,083 +/- 3,399 mu U/mL . min), being twofold gre ater (P < .05) relative to the +Cr group (6,183 +/- 864), The insulin secre tory response area in chow-fed rats (7,081 +/- 408 mu U/mL . min) was simil ar to the value in the +Cr group. These observations provide support for th e hypothesis that Cr deficiency can lead to elevated insulin secretory resp onses to glucose. opyright (C) 1999 by W.B. Saunders Company.