Glucose intolerance and resistin expression in rat offspring exposed to ethanol in utero: modulation by postnatal high-fat diet

Endocrinology. 2003 Feb;144(2):500-8. doi: 10.1210/en.2002-220623.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin
  • Adipose Tissue / anatomy & histology
  • Animals
  • Body Weight
  • Carrier Proteins / genetics
  • Central Nervous System Depressants / pharmacology*
  • Dietary Fats / pharmacology*
  • Eating
  • Ethanol / pharmacology*
  • Fatty Acids, Nonesterified / blood
  • Female
  • Gene Expression / drug effects
  • Glucose Intolerance / etiology
  • Glucose Intolerance / physiopathology*
  • Glucose Transporter Type 4
  • Hormones, Ectopic / genetics*
  • Hyperinsulinism / etiology
  • Hyperinsulinism / physiopathology
  • Insulin / analysis
  • Insulin / blood
  • Intercellular Signaling Peptides and Proteins*
  • Ion Channels
  • Leptin / blood
  • Mitochondrial Proteins
  • Monosaccharide Transport Proteins / genetics
  • Muscle Proteins*
  • Muscle, Skeletal / physiology
  • Nerve Growth Factor
  • Organ Size
  • Pancreas / anatomy & histology
  • Pancreas / chemistry
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Proteins / genetics
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Cell Surface / genetics
  • Receptors, Leptin
  • Resistin
  • Uncoupling Protein 3

Substances

  • Adiponectin
  • Carrier Proteins
  • Central Nervous System Depressants
  • Dietary Fats
  • Fatty Acids, Nonesterified
  • Glucose Transporter Type 4
  • Hormones, Ectopic
  • Insulin
  • Intercellular Signaling Peptides and Proteins
  • Ion Channels
  • Leptin
  • Mitochondrial Proteins
  • Monosaccharide Transport Proteins
  • Muscle Proteins
  • Proteins
  • Receptors, Cell Surface
  • Receptors, Leptin
  • Resistin
  • Retn protein, rat
  • Retnla protein, rat
  • Slc2a4 protein, rat
  • Ucp3 protein, rat
  • Uncoupling Protein 3
  • Ethanol
  • Nerve Growth Factor