Aberrant insulin-induced GLUT4 translocation predicts glucose intolerance in the offspring of a diabetic mother

Am J Physiol Endocrinol Metab. 2003 May;284(5):E901-14. doi: 10.1152/ajpendo.00516.2002. Epub 2003 Jan 21.

Abstract

We examined the long-term effect of in utero exposure to streptozotocin-induced maternal diabetes on the progeny that postnatally received either ad libitum access to milk by being fed by control mothers (CM/DP) or were subjected to relative nutrient restriction by being fed by diabetic mothers (DM/DP) compared with the control progeny fed by control mothers (CM/CP). There was increased food intake, glucose intolerance, and obesity in the CM/DP group and diminished food intake, glucose tolerance, and postnatal growth restriction in the DM/DP group, persisting in the adult. These changes were associated with aberrations in hormonal and metabolic profiles and alterations in hypothalamic neuropeptide Y concentrations. By use of subfractionation and Western blot analysis techniques, the CM/DP group demonstrated a higher skeletal muscle sarcolemma-associated (days 1 and 60) and white adipose tissue plasma membrane-associated (day 60) GLUT4 in the basal state with a lack of insulin-induced translocation. The DM/DP group demonstrated a partial amelioration of this change observed in the CM/DP group. We conclude that the offspring of a diabetic mother with ad libitum postnatal nutrition demonstrates increased food intake and resistance to insulin-induced translocation of GLUT4 in skeletal muscle and white adipose tissue. This in turn leads to glucose intolerance and obesity at a later stage (day 180). Postnatal nutrient restriction results in reversal of this adult phenotype, thereby explaining the phenotypic heterogeneity that exists in this population.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Animals, Newborn / physiology
  • Biological Transport
  • Diabetes Mellitus, Experimental
  • Drinking
  • Female
  • Forecasting
  • Glucose Intolerance / etiology*
  • Glucose Transporter Type 4
  • Growth Disorders / etiology
  • Insulin / metabolism*
  • Lactation
  • Monosaccharide Transport Proteins / metabolism*
  • Muscle Proteins*
  • Muscle, Skeletal / metabolism
  • Obesity / etiology
  • Pregnancy
  • Pregnancy in Diabetics / complications*
  • Rats
  • Rats, Sprague-Dawley
  • Sarcolemma / metabolism

Substances

  • Glucose Transporter Type 4
  • Insulin
  • Monosaccharide Transport Proteins
  • Muscle Proteins
  • Slc2a4 protein, rat