Abstract
It has been widely demonstrated that adverse environmental factors in prenatal period cause changes in the normal pattern of fetal growth and development, leading to a susceptible phenotype, in adulthood, to diseases such as hypertension, glucose intolerance, insulin resistance, hyperlipidemia , hyperinsulinemia and obesity. In fact, failure of the maternal-placental supply to meet fetus nutritional demand leads to a series of fetal adaptations, and may induce permanent changes in body structure and metabolism. Probably these adaptations prepare the fetus for adverse extrauterine life and although they are beneficial in short term, they can lead to cardiovascular and metabolic diseases in adult life. In previous studies, our grioup demonstrated that global intrauterine malnutrition caused, in male Wistar rats, hypocellularity in bone marrow and peripheral blood. In addition, reduction in adhesion molecules expression, in extracellular matrix compounds and in inflammatory mediators generation, caused a reduction in the leukocyte migration in these animals. We also observed elevated basal corticosterone levels and failure in increasing leptin levels after inflammatory stimulation. So, permanent changes in homeostatic regulation systems could lead to an increased risk of diseases, especially when the offsprings are on stressed conditions after the birth, due to additional risk factors, such as aging and obesity. There is a strong positive correlation between the amount of adipose tissue and circulating leptin levels, but, during periods of fasting or food restriction, the correlation between leptin and adipose tissue levels is apparently lost. A relationship between HPA axis activity and circulating levels of leptin is observed, demonstrating that the leptin effects on the immune system are due to both direct and indirect effect, modulated by circulating glucocorticoid levels. Increase or decrease in body adiposity occurs due to changes in balance of storage/availability energy as triacylglycerols (lipogenesis and lipolysis). Furthermore, an imbalance in cellular turnover, involving the phenomena of adipogenesis and apoptosis could be correlated with gain or loss of fat mass, whether or not accompanied by insulin resistance and inflammation. Metabolic alterations related to low birth weight are still little explored in the literature. Considering that global nutritional restriction (50%) causes low birth weight and may promote increase of adiposity in adult offspring, we propose to perform the characterization of the inflammatory and metabolic profile of adipose tissue of the mesenteric perivascular region. This study may contribute to a greater understanding of the development of chronic non-communicable diseases (NCD), such as diabetes, and diabetes, in low birth weight individuals. (AU)