Ingestion of Carbohydrate-Rich Supplements during Gestation Programs Insulin and Leptin Resistance but not Body Weight Gain in Adult Rat Offspring

Abstract

Prenatal nutritional conditions can predispose to development of obesity and metabolic syndrome in adulthood. Gestation with its important modifications in hormonal status is a period of changes in normal feeding habits with pulses of consumption or avoidance of certain categories of food. We tried to mimic in an animal model some changes in food consumption patterns observed in pregnant women. For this purpose, Long–Evans female rats were fed during the dark period, their usual pre-gestational food quantity, and were allowed to complete their daily intake with either a restricted control (Cr), high-fat (HF), or high-carbohydrate (HC) diet available ad libitum during the light period. Dams fed a control diet ad libitum (Ca) served as controls. Body weight and composition, food intake, and metabolic hormones (insulin, leptin) were recorded in male offspring until 20 weeks after birth. Cr and HC females ate less than Ca females (−16%; p < 0.001) and their offspring presented a weight deficit from birth until 6 (HC group) and 10 (Cr group) weeks of age (p < 0.05 or less). Plasma leptin corresponded to low body weight in Cr offspring, but was increased in HC offspring that in addition, had increased plasma insulin, blood glucose, and subcutaneous adipose tissue mass. HF dams ate more than Ca dams (+13%; p < 0.001), but plasma leptin and insulin were similar in their offspring. Hypothalamic Ob-Rb expression was increased in Cr, HC, and HF offspring (+33–100% vs Ca; p < 0.05 or less). HC supplement ingestion during gestation therefore leads to insulin and leptin resistance in adult offspring independently of lower birth weight. These hormonal changes characterize obesity-prone animals. We therefore suggest that attention should be paid to the carbohydrate snacking and overall carbohydrate content in the diet during the last weeks (or months) preceding delivery to limit development of later metabolic disorders in offspring.

Dietary Glycemic Index during Pregnancy Is Associated with Biomarkers of the Metabolic Syndrome in Offspring at Age 20 Years

“…These results are in full agreement with a recent study reporting that carbohydrate-rich diet supplementation in pregnant rats was associated with increased insulin, leptin and glucose levels among their adult male offspring, while no association was found with the offspring’s body weight [25]. These results in rats together with ours in humans support the idea that GI (and perhaps GL) during pregnancy may exhibit a causal programming effect in the adult offspring.…”

Feed Your Head: Neurodevelopmental Control of Feeding and Metabolism

“…However, in contrast to HPD and HFD, HCD does not increase offspring weight gain (147). Supplementation of maternal diets with 20% fructose have yielded inconsistent metabolic effects in offspring; one study reported elevated blood leptin and glucose in P10 female rat pups, but not in male rat pups, although whether this effect persisted into adulthood was unclear (148).…”

Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring

“…In fact, several studies demonstrate that metabolic events during pre- and postnatal development modulate metabolic disease risks in later life [ 2 ]. Among them, feeding conditions likely constitute one of the most influential parameters on the health of the adult [ 3 ]. Thus, diet manipulation in mothers during critical developmental periods (such as gestation and/or the early postnatal) has been used to identify their contribution to obesity and diabetes development in offspring [ 4 ].…”