Metabolic characterization of adipocytes in response to serum of rodents subjected to dietary restriction

Abstract

The prevalence of obesity has been growing worldwide alongside the morbidities associated with the disease. Current anti-obesity therapies appear to be poorly efficient, especially on the long-term, and are associated with significant side effects. There are two ways to lose weight: by decreasing the energy intake or increasing energy expenditure. One way to increase energy expenditure in mammals is the stimulation of brown/beige adipocytes and the increase in their function. This phenomenon correlates especially with high levels of UCP1 expression and activity. Some conditions capable of regulating UCP1 expression and function have already been described. Among them, there is chronic cold exposure, exercise, an enriched social environment, and cancer cachexia. These conditions act through cell autonomous mechanisms, such as by regulating transcription factors in preadipocytes or adipocytes, and cell non-autonomous mechanisms, such as by signaling through hormones and other circulating molecules. The study and understanding of the circulating molecules that act in adipose tissue to increase its brown/beige characteristics is essential for the development of more efficient and secure pharmacological strategies that could help to combat the global scenario of obesity. It was noticed, in preliminary results obtained by our group, that serum of mice subjected to dietary restriction is capable of modulating the expression of Ucp1 in vitro in mouse adipocytes derived from brown adipose tissue. The characterization of this phenomenon is the overarching aim of this project and serves as an initial and fundamental step to the future identification of the molecule(s) responsible for this function. This/these molecule(s) may bring insights into the development of new drugs to combat obesity.