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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #97125

Title: ENHANCED INSULIN SECRETION IN THE CHROMIUM DEFICIENT RAT

Author
item STRIFFLER, JOHN - CITY OF HOPE NATL MED CTR
item Polansky, Marilyn
item Anderson, Richard

Submitted to: Diabetes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/3/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: There are roughly 100 million people in the world with type 2 diabetes and this number is expected to double in the next 10 to 20 years. The causes of this disease are poorly understood. We tested the postulate that diets high in sugar and low in chromium would lead to early signs of diabetes. We have shown previously that people eating diets high in table sugar have increased losses of the essential nutrient, chromium. Rats fed a high sugar diet with required amounts of vitamins and minerals, except chromium, displayed early signs of diabetes including a more that 50% increase in circulating insulin in response to sugar. These results show that high sugar diets low in chromium are associated with signs and symptoms of diabetes. This work demonstrates a link between low chromium and high sugar diets in the causes of diabetes. This work will be of benefit to the medical and scientific communities as well as the millions of people world-wide with diabetes and the even larger numbers of people who may become diabetic. Chromium is only one of the many causes of diabetes and will only be of benefit to those whose diabetes is related to low dietary chromium intake.

Technical Abstract: The hypothesis that insulin secretory hyper-responsiveness observed in rats with diet-induced insulin resistance may be a basic characteristic of deficiency in dietary chromium (Cr) was evaluated. Two groups of weanling rats were fed ad lib a purified diet containing 64% sucrose, 20% casein, 5% corn oil and recommended levels of vitamins and minerals without added Cr. Cr-deficient rats (-Cr) were provided with distilled drinking water only while supplemented rats (+Cr) received water containing 5 ppm Cr as CrCl3. 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 observed during the initial two weeks of dietary adaptation. Effects of the low Cr diet were evaluated after the 12 week period by comparing insulin response areas and glucose clearances during 40-minute intravenous glucose tolerance tests. Rates of glucose clearance (KG) in the -Cr and +Cr rats were similar, KG = 4.2 +/- 1.0 and +Cr, 4.3 +/- 0.8%/min and were comparable to the chow fed rats, KG = 4.6 +/- 0.8. In contrast, insulin secretory responses in the -Cr rats were exaggerated with an area, 14083 +/- 3399 uU/ml x min being two-fold greater (p< 0.05) relative to the +Cr group (6183 +/- 864). Insulin secretory response area in the chow fed rats (7081 +/- 408 uU/ml x min) was similar to the +Cr group. These observations provide support for the hypothesis that Cr deficiency can lead to enhanced insulin secretory responses to glucose.