Genetic Obesity in Pregnant Ay Mice Does Not Affect Susceptibility to Obesity and Food Choice in Offspring

Int J Mol Sci. 2023 Mar 15;24(6):5610. doi: 10.3390/ijms24065610.

Abstract

Maternal diet and obesity (MO) may influence taste preferences and increase the susceptibility to obesity in offspring, but the impact of MO per se to these influences is poorly understood. We evaluated the influence of MO on food choice and susceptibility to obesity in offspring when mothers consumed a standard diet (SD). Mice with the Lethal yellow mutation (Ay/a) develop obesity consuming an SD. Metabolic parameters were assessed in pregnant and lactating Ay/a (obesity) and a/a (control) mothers. Metabolic response to the consumption of a sweet-fat diet (SFD: SD, lard, and sweet biscuits) and the choice of components of this diet were evaluated in their male and female offspring. Compared to control mothers, pregnant obese mothers had higher levels of insulin, leptin, and FGF21. MO increased food intake and liver expression of lipogenesis genes in male offspring consuming the SD. SFD consumption caused obesity development and insulin resistance, increased liver expression of glycolytic and lipogenesis genes, and affected hypothalamic expression of anorexigenic and orexigenic genes. In offspring of both sexes, MO had no effect on food choice and metabolic response to SFD intake. Therefore, when obese mothers consume a balanced diet, MO does not affect food choice and development of diet-induced obesity in offspring.

Keywords: Ay/a mice; developmental programming; food choice; maternal obesity; sweet and fatty diet.

MeSH terms

  • Animals
  • Diet
  • Diet, High-Fat / adverse effects
  • Female
  • Food Preferences
  • Humans
  • Lactation*
  • Leptin / metabolism
  • Liver / metabolism
  • Male
  • Mice
  • Obesity / genetics
  • Obesity / metabolism
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / genetics
  • Prenatal Exposure Delayed Effects* / metabolism

Substances

  • Leptin