Elena Makarova
Institute of Cytology and Genetics, Russia
Title: Leptin administration in midpregnancy reduces foetal and early postnatal growth rate and abolishes obesity-associated hyperglycemia in mouse offspring
Biography
Biography: Elena Makarova
Abstract
Maternal obesity increases the risk of obesity in offspring. Leptin is increased in obese animals, and elevation of maternal leptin may affect the metabolic phenotype of the offspring. We explore the effects of leptin elevation during midpregnancy on the offspring metabolic phenotypes, foetal growth, and placental gene expression. C57BL mice received a single injection of leptin or saline on pregnancy day 12. Body weight (BW) was measured weekly in offspring, which consumed standard show or palatable food, and the mRNA expression of glucose and amino acid transporters, insulin-like growth factor 2 and its receptor was measured 3 h, and the placental and foetal weights were measured 24 h after the injection. The offspring born to leptin-treated mothers exhibited growth retardation before and catch-up growth after weaning, and mature male offspring had an increased BW on a standard diet. Prenatal exposure to leptin did not influence the obesity development but prevented the development of obesity-associated hyperglycemia. The leptin injection decreased the foetal weight by 5% and the placental mRNA level of amino acid transporter SNAT2. The results suggest that elevation of maternal leptin in midpregnancy has positive effect on glucose metabolism in mature offspring and this effect is associated with leptin influence on fetal growth and amino acid transporter expression in placentas. (Supported by the RFBR, Grant 17-04-01357).