title: Glucose intolerance and resistin expression in rat offspring exposed to ethanol in utero: modulation by postnatal high-fat diet.
abstract: 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.
authors.affiliation: Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3A1R9.
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.forename: B L G
authors.initials: BL
authors.lastname: Nyomba
mesh_terms: D052242:Adiponectin; D000273:Adipose Tissue / Q000033:anatomy & histology; D000818:Animals; D001835:Body Weight; D002352:Carrier Proteins / Q000235:genetics; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D004041:Dietary Fats / Q000494:pharmacology*; D004435:Eating; D000431:Ethanol / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D018149:Glucose Intolerance / Q000209:etiology / Q000503:physiopathology*; D051275:Glucose Transporter Type 4; D006729:Hormones, Ectopic / Q000235:genetics*; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology; D007328:Insulin / Q000032:analysis / Q000097:blood; D036341:Intercellular Signaling Peptides and Proteins; D007473:Ion Channels; D020738:Leptin / Q000097:blood; D024101:Mitochondrial Proteins; D009004:Monosaccharide Transport Proteins / Q000235:genetics; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000502:physiology; D020932:Nerve Growth Factor; D009929:Organ Size; D010179:Pancreas / Q000033:anatomy & histology / Q000737:chemistry; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011506:Proteins / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000235:genetics; D054411:Receptors, Leptin; D052243:Resistin; D000071247:Uncoupling Protein 3
chemical_list: D052242:Adiponectin; D002352:Carrier Proteins; D002492:Central Nervous System Depressants; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D051275:Glucose Transporter Type 4; D006729:Hormones, Ectopic; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D011506:Proteins; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D052243:Resistin; C499622:Retn protein, rat; C486575:Retnla protein, rat; C495694:Slc2a4 protein, rat; C000604394:Ucp3 protein, rat; D000071247:Uncoupling Protein 3; D000431:Ethanol; D020932:Nerve Growth Factor