{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T17:36:01Z","timestamp":1791135361629,"version":"4.1.0"},"reference-count":59,"publisher":"The Endocrine Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,2,1]]},"abstract":"<jats:p>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.<\/jats:p>\n               <jats:p>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.<\/jats:p>\n               <jats:p>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.<\/jats:p>","DOI":"10.1210\/en.2002-220623","type":"journal-article","created":{"date-parts":[[2003,1,21]],"date-time":"2003-01-21T21:24:46Z","timestamp":1043184286000},"page":"500-508","source":"Crossref","is-referenced-by-count":59,"title":["Glucose Intolerance and Resistin Expression in Rat Offspring Exposed to Ethanol in Utero: Modulation by Postnatal High-Fat Diet"],"prefix":"10.1210","volume":"144","author":[{"given":"Li","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3A1R9"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. L. 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