Perets O. The effect of social-emotional stress of mothers during pregnancy on the morphofunctional state of adipose tissue in female offspring (experimental research).

Object of study - structural and functional state of adipose tissue in the offspring of female rats obtained from females stressed at different stages of pregnancy. The goal of the work - to establish the presence of a causal relationship between the socio-emotional stress of female rats at different stages of pregnancy and the formation of a pathological morphofunctional state of visceral adipose tissue in female offspring, to prove the possibility of influencing the type and severity of obesity in such descendants of environmental factors. Research methods: physiological, preparative, histological, enzyme-linked immunosorbent assay, statistical. It was found that antenatal stress leads to the birth of offspring with reduced body weight and low leptin level, and the period of early postnatal life is characterized by rapid weight gain and hyperleptinemia. Social-emotional stress during pregnancy has a significant effect on changes in body weight in offspring under the influence of external additional stress factors such as two-day food deprivation and three-day hypokinesia. The growth rate of visceral fat and the nature of the histostructure of adipose tissue in intact offspring, which underwent food deprivation and hypokinesia stress, indicates the development of a hypertrophic type of obesity in these animals. The results obtained give grounds to conclude that the severity of obesity and the type of reaction of mesenteric adipose tissue to repeated stresses in adulthood are associated with the conditions of development of an individual in the embryonic period: in the offspring of intact mothers, postnatal stresses induce the formation of a hypertrophic type of obesity; in the offspring of mothers stressed in the first trimester of pregnancy, such stresses are the cause of the hypertrophic-hyperplastic type of obesity; in the offspring of mothers stressed at the end of pregnancy and exposed to stress in adulthood, hypertrophic-hyperplastic obesity and is accompanied by inflammation of adipose tissue. It was found that adipose tissue is a stress-sensitive formation. At the same time, the type of obesity and the cellular composition of adipose tissue depend both on the period of stress during antenatal development and on the influence of stress in adulthood. The severity of obesity and the type of reaction of mesenteric adipose tissue to repeated stresses in adulthood are associated with the conditions for the development of an individual in the embryonic period. This leads to the formation of low levels of leptin at birth. The offspring of mothers stressed in the first trimester of pregnancy are characterized by a low level of leptin at birth and a significant increase in postnatal life, and a hypertrophic type of obesity develops. In descendants of gestational stressed mothers, the presence of leptinoresistance was found, which has been manifested in absence of anorexogenic effects in hyperleptinemia. When loaded with exogenous leptin, the absence of a regulatory effect of leptin on the feeding behavior of offspring from stressed females was established, which indicates the formation of leptin resistance of central genesis in them. Excessive ingestion of fructose into the body of descendants of gestational stressed mothers is shown to deepen gestationally conditioned leptin resistance that exchange and promotes development of obesity in such descendants in peripuberth age. Studies with fructose and exogenous leptin loading in stressed offspring have shown a tendency to gain excess weight and an insensitivity to leptin at a young age. Excessive fructose intake into the body of the offspring of mothers stressed during pregnancy enhances the signs of leptin resistance: a significant increase in body weight due to the accumulation of visceral adipose tissue and in the activation of nutrient consumption against the background of an increase in the level of leptin in blood plasma. Fructose-induced leptin resistance caused the negative effect of fructose on the structural and functional processes in the liver and pancreas. The results obtained substantiate the need to develop measures to limit the use of fructose in food for children and adolescents, especially among those who belong to risk groups, namely, those born with low birth weight and low leptin levels.