Abstract

Body weight and adipose mass are thought to be tightly regulated by homeostatic mechanisms, in which leptin, an adipocyte secreted hormone, circulates in concentrations proportional to body fat content and thereby regulates body weight through hypothalamic pathways in a bi-directional manner. However, obesity has become global epidemic over the past several decades, despite of high circulating leptin levels among the obese population. This phenomenon was considered as a result of “leptin resistance” in the central nervous system. Intriguingly, recent evidences show that leptin is still functional under the obese condition, therefore the development of obesity is not due to “leptin resistance”. To date, whether body weight is homeostatically regulated is still controversial. Recently, we found that Rcan2 regulated food intake via a leptin-independent pathway, and could promote a rapid weight gain in mice when fed with a high-fat diet, which provides a novel insight into the mechanisms of obesity epidemic.

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