Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats

Am J Physiol Endocrinol Metab. 2007 Nov;293(5):E1451-8. doi: 10.1152/ajpendo.00356.2007. Epub 2007 Sep 25.

Abstract

Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTH-secreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an approximately 70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenocorticotropic Hormone / blood
  • Animals
  • Animals, Newborn
  • Cholesterol / blood
  • Corticosterone / blood
  • Corticosterone / urine
  • Fasting / blood
  • Female
  • Glucose / metabolism
  • Hypothalamo-Hypophyseal System / metabolism*
  • Insulin / blood
  • Insulin Resistance / physiology*
  • Insulin-Like Growth Factor Binding Protein 1 / genetics
  • Insulin-Like Growth Factor Binding Protein 1 / metabolism
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Liver / enzymology
  • Liver / metabolism*
  • Phosphoenolpyruvate Carboxykinase (ATP) / genetics
  • Phosphoenolpyruvate Carboxykinase (ATP) / metabolism
  • Pituitary-Adrenal System / metabolism*
  • Pregnancy
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Glucocorticoid / genetics
  • Receptors, Glucocorticoid / metabolism
  • Restraint, Physical / physiology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Triglycerides / blood

Substances

  • Insulin
  • Insulin-Like Growth Factor Binding Protein 1
  • Receptors, Glucocorticoid
  • Triglycerides
  • Insulin-Like Growth Factor I
  • Adrenocorticotropic Hormone
  • Cholesterol
  • Phosphoenolpyruvate Carboxykinase (ATP)
  • Glucose
  • Corticosterone