Fetal programming of adipose tissue: effects of intrauterine growth restriction and maternal obesity/high-fat diet

Semin Reprod Med. 2011 May;29(3):237-45. doi: 10.1055/s-0031-1275517. Epub 2011 Jun 27.


A newly recognized primary cause of obesity epidemic is the developmental programming effects of (1) intrauterine growth-restricted (IUGR) newborns exposed in utero to undernutrition, and (2) normal or excessive weight newborns exposed to maternal obesity and high-fat (HF) diets. The mechanisms contributing to offspring obesity have been extensively studied in animal models with adipose tissue identified as one of the principal targets of programming. IUGR and HF offspring exhibit programmed adipocytes, such that an intrinsic enhanced lipogenesis and adipocyte proliferation contribute to the development of obesity. This is attributed to early induction of adipogenic transcription factor peroxisome proliferator-activated receptor (PPAR)γ, whose activity is enhanced under limited or excess nutrient availability. Nonetheless, this occurs via different mechanisms involving PPARγ coregulators: In IUGR, it is upregulation of coactivators, whereas in HF newborns, it is downregulation of corepressors. Thus preventive therapeutic interventions will require target-specific modalities that depend on the primary etiology.

Publication types

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

MeSH terms

  • Adipogenesis
  • Adipose Tissue / embryology*
  • Adipose Tissue / metabolism
  • Adult
  • Animals
  • Dietary Fats / adverse effects*
  • Disease Susceptibility
  • Female
  • Fetal Development*
  • Fetal Growth Retardation / physiopathology*
  • Humans
  • Male
  • Maternal Nutritional Physiological Phenomena
  • Obesity / etiology
  • Obesity / physiopathology*
  • PPAR gamma / metabolism
  • Pregnancy
  • Pregnancy Complications / physiopathology*
  • Prenatal Exposure Delayed Effects*


  • Dietary Fats
  • PPAR gamma