The timing of "catch-up growth" affects metabolism and appetite regulation in male rats born with intrauterine growth restriction

Am J Physiol Regul Integr Comp Physiol. 2009 Sep;297(3):R813-24. doi: 10.1152/ajpregu.00201.2009. Epub 2009 Jul 15.

Abstract

Epidemiological studies demonstrated a relationship between low birth weight mainly caused by intrauterine growth restriction (IUGR) and adult metabolic disorders. The concept of metabolic programming centers on the idea that nutritional and hormonal status during the key period of development determines the long-term control of energy balance by programming future feeding behavior and energy expenditure. The present study examined the consequence of early or late "catch-up growth" after IUGR on feeding behavior and metabolic cues of male offspring of rat dams exposed to protein restriction during gestation and/or lactation. Our results suggest that early catch-up growth may be favorable for fasting metabolic parameters at weaning, as no differences were observed on plasma leptin, triglyceride, glucose, and insulin levels compared with controls. In contrast, if pups remained malnourished until weaning, low insulin concentration was detected and was accompanied by hyperphagia associated with a large increase in hypothalamic NPY and AgRP mRNA expression. At adult age, on a regular chow diet, only the meal structure was modified by fetal programming. The two IUGR groups demonstrated a reduced meal duration that enhanced the speed of food ingestion and consequently increased the rest period associated to the satiety state without changes in the hypothalamic expression of appetite neuropeptides. Our findings demonstrate that in IUGR, regardless of postnatal growth magnitude, metabolic programming occurred in utero and was responsible for both feeding behavior alteration and postprandial higher insulin level in adults. Additionally, catch-up growth immediately after early malnutrition could be a key point for the programming of postprandial hyperleptinemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Aging / metabolism*
  • Animals
  • Appetite Regulation*
  • Biomarkers / blood
  • Body Weight
  • Circadian Rhythm
  • Diet, Protein-Restricted
  • Disease Models, Animal
  • Eating
  • Energy Metabolism*
  • Fasting / metabolism
  • Feeding Behavior*
  • Female
  • Fetal Growth Retardation / metabolism*
  • Fetal Growth Retardation / physiopathology*
  • Gestational Age
  • Hypothalamus / metabolism
  • Insulin / blood
  • Lactation
  • Male
  • Maternal Nutritional Physiological Phenomena
  • Nerve Tissue Proteins / genetics
  • Postprandial Period
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Satiety Response

Substances

  • Biomarkers
  • Insulin
  • Nerve Tissue Proteins
  • RNA, Messenger