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Glucose Intolerance and Resistin Expression in Rat Offspring Exposed to Ethanol in Utero: Modulation by Postnatal High-Fat Diet

Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3A1R9

Address all correspondence and requests for reprints to: B. L. G. Nyomba, M.D., Ph.D., Health Sciences Centre, University of Manitoba, 820 Sherbrook Street Room GG449, Winnipeg, Manitoba, Canada R3A1R9. E-mail: bnyomba{at}cc.umanitoba.ca.

High-fat diet and intrauterine growth retardation may predispose to obesity, insulin resistance, and type 2 diabetes. Because prenatal ethanol (ETOH) exposure causes intrauterine growth retardation, we investigated its interactions with postnatal high-fat diet on glucose tolerance and adipocyte-derived hormones in the rat offspring.

High-fat-fed offspring had increased adiposity, serum leptin, and muscle uncoupling protein-3, but decreased adiponectin mRNA, compared with corresponding chow-fed groups. ETOH-exposed offspring had normal adiponectin, but increased resistin mRNA and protein, compared with controls, regardless of postnatal diet. Skeletal muscle glucose transporter-4 content was decreased after both ETOH exposure and high-fat feeding. Glycemic and insulin responses to an ip glucose challenge were equally increased in non-ETOH-exposed high-fat-fed offspring and in ETOH-exposed chow-fed offspring, with additive effects of ETOH and high-fat diet. Pancreatic insulin content was elevated only in non-ETOH-exposed high-fat-fed offspring.

The data suggest that high-fat diet worsens glucose intolerance in offspring of rats exposed to ETOH. Prenatal ETOH exposure and postnatal high-fat diet might cause insulin resistance through separate mechanisms, involving resistin and adiponectin, respectively.

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