Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner

Int J Obes (Lond). 2017 Sep;41(9):1420-1426. doi: 10.1038/ijo.2017.136. Epub 2017 Jun 7.


Background/objectives: The current world-wide obesity epidemic partially results from a vicious circle whereby maternal obesity during pregnancy predisposes the offspring for accelerated weight gain and development of metabolic syndrome. Here we investigate whether low-grade inflammation, characteristic of the obese state, provides a causal role for this disastrous fetal programming in mice.

Methods: We exposed pregnant and lactating C57BL/6JBom female mice to either high-fat diet (HFD), or continuous infusion of lipopolysaccharide (LPS), a potent trigger of innate immunity, and studied offspring phenotypes.

Results: Both maternal LPS or HFD treatments rendered the offspring hyperphagic and inept of coping with a HFD challenge during adulthood, increasing their adiposity and weight gain. The metabolic effects were more pronounced in female offspring, while exposed male offspring mounted a larger inflammatory response to HFD at adulthood.

Conclusions: This supports our hypothesis and highlights the programming potential of inflammation in obese pregnancies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects*
  • Disease Models, Animal
  • Female
  • Fetal Development / physiology*
  • Genetic Predisposition to Disease
  • Inflammation / metabolism
  • Inflammation / physiopathology*
  • Insulin Resistance / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Obesity / metabolism
  • Obesity / physiopathology*
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • Prenatal Nutritional Physiological Phenomena / physiology
  • Weight Gain / physiology*