The role of adipose tissue as endocrine organ in the metabolic programming of fetuses derived from obese mothers

Abstract

We aim to present the endocrine and paracrine role of the cytokines secreted by hypertrophied maternal fat cells on fetal and later on neonatal metabolic profile. The study used an animal model in order to analyze the influence of maternal adipokines secretion of fetal metabolism. We selected 50 female Wistar rats weighing between 200-250 g (normal weight 100-150g) to whom we induced obesity by high-fat, high-calorie food intake (80% of diet saturated fatty acids) and tracked the correlation of maternal adipokines secretion with placental and fetal lipid peroxidation level. The low adiponectin and increased leptin values as adipokines secreted by adipocytes of obese mothers were correlated with the level of placental and fetal tissue lipid peroxidation (from the liver, pancreas, brain), measured by elevated malonyldialdehyde and total thiols and the decreased levels of glutathione. It has been known for decades that fat tissue is not inert, but a true endocrine organ, which responds by secreting adipokines to different energy and hormonal stimuli. Endocrine secretion of adipokines from the adipocytes of obese mothers is positively correlated with placental and fetal lipid peroxidation levels. Fetal metabolic programming as an inducible phenomenon is explained partly by the influence of excess secretion of maternal adipokines.