Maternal hypothyroxinemia alters the immune function of the adipose tissue in the adult the progeny

Abstract

Abstract Obesity and thyroid hormone deficiency are global problems. Chile has 31,2% of obesity. Obesity is characterized by adipose tissue, that’s able to influence the immune system. Gestational environment can increase the offspring susceptibility to have obesity. It’s been suggested that maternal hypothyroxinemia (HTX) could be a factor for obesity development in the offspring imprinting the adipose tissue contributing to the altered immune response seen in HTX progeny. The aim of this work is to evaluate the effect of HTX in adipose tissue in the progeny and its influence on the adipocyte immune function. For this purpose, weight and body fat content of the offspring gestated or not under HTX using In vivo MRI was asess. Area and number of adipocytes from offspring conditions was evaluated using a deep convolutional neural network approach. Cell infiltration was also analyzed. Expression of cytokines as PPARs and leptin were evaluated. Adipose tissue infiltrating cells were analyzed by FACS. In vitro, the differentiation capacity of control and HTX pre-adipocytes using Oil red staining and quantification and measure adipokine an cytokine production by these cells was evaluated. We show that the HTX offspring present an increased body fat content. Image analysis showed an increase in the number and area of the HTX adipocytes. An increased capacity of HTX pre-adipocytes to differentiate to adipocytes was seen. Alteration in the expression of cytokines, PPARs and leptin and an increase in cell infiltration with more predominant activated CD4+ T cells and monocytes was observed. This work proves that maternal HTX induces alterations of the adipose tissue of the progeny that could contribute to the susceptibility of the HTX to autoimmune diseases.