Sexually dimorphic metabolic responses to exposure of a high fat diet during pregnancy, lactation and early adulthood in Gipr^-/- mice.

Obesity has a multifactorial origin. It is known that alterations of the intra uterine milieu induce developmental programming effects leading to metabolic diseases in offspring. Obesity is diminished in mice lacking the glucose-dependent insulinotropic polypeptide receptor (Gipr^-/-) when exposed to a high fat diet (HFD). We investigated whether Gipr^-/- mice are still protected from obesity when additionally exposure to a HFD during pregnancy and lactation occurs. Male and female wild type (WT) and Gipr^-/- offspring received either a control/ low fat diet or HFD during pregnancy and lactation and were then either left on this diet or placed on the opposite diet after weaning until 24 weeks of life. Female WT mice showed increased body weight and adiposity when exposed to a HFD during pregnancy and lactation and post-weaning compared to female WT that received the HFD after weaning only. This exacerbated effect of a HFD during pregnancy and lactation was abolished in female Gipr^-/- mice. Male Gipr^-/- mice were protected from obesity to a much lesser extent. Male Gipr^-/- mice exposed to a HFD during pregnancy and lactation and after weaning exhibited significantly increased fed serum glucose compared to Gipr^-/- mice exposed to a HFD after weaning only. In female Gipr^-/- mice no differences in fed blood glucose were observed between these groups. Our data indicate that female Gipr^-/- mice are more protected from obesity. This protection is preserved in female Gipr^-/- mice when additional deleterious effects of a HFD occur during fetal development.

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