The Implications of Maternal Obesity on Offspring Physiology and Behavior in the Nonhuman Primate

Abstract

Exposure to maternal obesity and high-fat diet (HFD) consumption during perinatal development impacts numerous aspects of offspring physiology and behavior. Epidemiologic studies indicate that maternal obesity is associated with increased risk for metabolic, mental health, and neurodevelopmental disorders. As factors such as a shared environment and genetics could contribute to this association, animal studies are critical. The use of nonhuman primates is particularly important as they have a similar developmental timeline, physiology, and behavior as humans. Evidence from animal models supports the findings from human studies and indicates that maternal obesity induced by HFD consumption impairs the development of many organ systems including the brain, pancreas, liver, and cardiovascular system. These studies suggest that offspring are predisposed to obesity due to hyperphagia, increased preference for fat and sugar, and reductions in energy expenditure. Rodent and nonhuman primate offspring exposed to maternal HFD consumption exhibit increased anxiety, impairments in social behavior, and decreased cognitive performance. These observed behavioral changes are though to be due to alterations in the development of neural circuitry critical in behavioral regulation such as the serotonin, dopamine, and melanocortin systems and increased activity of the hypothalamic–pituitary axis. Mechanisms for these developmental changes include alternations in maternal behavior due to HFD consumption and the increased levels of inflammatory factors, nutrients and hormones that are associated with maternal obesity. Given the high levels of maternal obesity and HFD consumption in developed nations, we postulate that future generations are at increased risk for obesity and metabolic, neurodevelopmental, and mental health disorders.