Reductions in caloric intake and early postnatal growth prevent glucose intolerance and obesity associated with low birthweight

Diabetologia. 2006 Aug;49(8):1974-84. doi: 10.1007/s00125-006-0311-7. Epub 2006 Jun 8.


Aims/hypothesis: Low birthweight (LBW) and rapid postnatal weight gain, or catch-up growth, are independent risk factors for the development of obesity and diabetes during adult life. Individuals who are both small at birth and have postnatal catch-up growth are at the highest risk. We hypothesised that dietary interventions designed to attenuate catch-up growth in LBW subjects may have long-term beneficial consequences.

Materials and methods: We used our previously described mouse model of LBW-associated diabetes, created by restricting maternal food intake to 50% during the last week of gestation. Control (C) dams and dams that had been subjected to undernutrition (U) were then provided either chow ad libitum after delivery or 50% food restriction on a per-day basis from delivery until weaning. We designated the resulting four groups control-control (CC), undernutrition-control (UC), control-undernutriton (CU) and undernutrition-undernutrition (UU), indicating the prenatal and postnatal experimental conditions, respectively. Carbohydrate metabolism and adiposity were assessed prospectively in offspring until age 6 months.

Results: Males that were small at birth and exhibited early postnatal catch-up growth developed glucose intolerance and obesity by age 6 months. In contrast, LBW mice without catch-up growth (UU) remained smaller than controls (CC), and glucose intolerance and obesity was prevented. Similarly, mice with normal birthweight that had blunted catch-up growth (CU) were leaner and had better tolerance test than CC mice. Catch-up growth during the first week of life correlated better than birthweight with glucose, fat mass and glucose tolerance up to 6 months of age.

Conclusions/interpretation: Prevention of early catch-up growth reversed the development of glucose intolerance and obesity in our mouse model of LBW-associated diabetes.

Publication types

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

MeSH terms

  • Diet, Reducing*
  • Energy Intake*
  • Glucose Intolerance / epidemiology
  • Glucose Intolerance / prevention & control*
  • Growth / physiology*
  • Humans
  • Infant
  • Infant, Low Birth Weight / physiology*
  • Infant, Newborn
  • Insulin / blood
  • Leptin / blood
  • Obesity / epidemiology
  • Obesity / prevention & control*


  • Insulin
  • Leptin