Biography
Dr. Elena Makarova (PhD – biology) now is a senior researcher in the Laboratory of Physiological Genetics in the Institute of Cytology and Genetics (Novosibirsk, Russia). Her researches focus on the studies of sex-specific influence of maternal leptin on metabolic characteristics in progeny of rodents. She with her colleagues found maternal leptin retarded obesity development in male progeny and improves glucose metabolism in progeny of both sexes in mice.
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).
Biography
Tatiana Iakovleva graduated Novosibirsk University in 1988. At the University, she studied the properties and function of estradiol secreted by the adrenal gland. She then studied effects of colour mutations (agouti and non agouti) on the function of pituitary-adrenal system in females and males of Arvicola terestris, effects of colour mutation Agouti yellow on the function of pituitary-adrenal system in mice C57Bl, effects of melanocortin system and estradiol on obesity development and insulin sensitivity in females of C57Bl mice.
Abstract
The energy-burning capacity of brown adipose tissue (BAT) makes it an attractive target for use in anti obesity therapies. There are sex differences in the metabolic disorders development: high fat diet induces hyperglycemia development in males, but not in females. Serum FGF21 levels are associated with BAT activity. We investigated the effects of high fat and sugar diet (10 weeks) on blood levels of FGF21, insulin, leptine, glucose, on mRNA levels of genes involved in FGF21 signaling (Fgf21, Klotho beta, Pparg), and on mRNA levels of genes related to BAT activity (Ucp1, Slc2a1, Cpt1, Dio2, Hsl) in females and males of C57Bl mice. We found that diet induced obesity, increased blod levels of FGF21, glucose and leptin in females and males and induced hyperinsulinemia development in males. We found also that diet impaired BAT FGF21 signaling only in males: increased mRNA level of Fgf21 and reduced mRNA levels of Klotho beta and Ppargï€ . Obviously due to impaired FGF21 signaling high blood FGF21 levels and increased BAT Fgf21 expression were associated with decreased expression of Slc2a1 and unaltered expression of Ucp1 genes in BAT of obese males. In females, the diet did not affect FGF21 signaling.