Abstract
Several metabolic adaptations emerge during pregnancy and continue through lactation, including increases in food intake and body weight, as well as insulin and leptin resistance. These maternal adaptations are thought to play a role in offspring viability and success. Using a model of attenuated maternal metabolic adaptations induced by ablation of the Socs3 gene in leptin receptor expressing cells (SOCS3 KO mice), our study aimed to investigate whether maternal metabolic changes are required for normal offspring development, and if their absence causes metabolic imbalances in adulthood. The litters were subjected to a cross‐fostering experimental design to distinguish the prenatal and postnatal effects caused by maternal metabolic adaptations. Males either born or raised by SOCS3 KO mice showed reduced body weight until 8 weeks of life. Both adult males and females born or raised by SOCS3 KO mice also had lower body adiposity. Despite that, no significant changes in energy expenditure, glucose tolerance or insulin resistance were observed. However, males either born or raised by SOCS3 KO mice showed reduced brain mass in adulthood. Furthermore, animals born from SOCS3 KO mice also had lower proopiomelanocortin fiber density in the paraventricular nucleus of the hypothalamus. In conclusion, these findings indicate that the commonly observed metabolic changes in pregnancy and lactation are necessary for normal offspring growth and brain development.
Highlights
Pregnancy and lactation are exceptional moments, in which females need to attend their own energetic demands and provide energy to their offspring (Ladyman et al 2010; Woodside et al 2012)
Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society
We studied mice deficient of suppressor of cytokine signaling-3 (SOCS3) in LepRexpressing cells since these females have a diminished development of maternal metabolic changes (Zampieri et al 2015, 2016)
Summary
Pregnancy and lactation are exceptional moments, in which females need to attend their own energetic demands and provide energy to their offspring (Ladyman et al 2010; Woodside et al 2012). Some authors suggest that leptin resistance can emerge from defects in the transduction of leptin receptor (LepR) signaling pathways (Balland and Cowley 2015). Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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