Corticotropin Releasing Hormone and Body Weight Regulation: The Behavioral Approach

In 1996, Cabanac and Richard revived Hervey's then 25-year old hypothesis explaining the stability of body weight through regulation of blood corticosteroid concentrations. They suggested that glucocorticoids are the regulated variable, the concentration of which ensures body weight stability, and they proposed a descriptive model of this regulation. Because steroids are soluble in lipids, it follows that their concentration in the body depends in part on the volume of lipids stored. Low fat stores increase the glucocorticoid concentration in the blood and, conversely, high fat stores lower the glucocorticoid concentration. Hypothalamic corticotropin-releasing hormone (CRH) and body weight could thus be the final step in the sequence initiated by glucocorticoid regulation. Alternatively, glucocorticoids stimulate leptin production by the adipocytes. The rise in leptin secretion increases hypothalamic CRH production, which lowers the set-point for body weight. In both cases, it may be hypothesized that hypothalamic CRH concentration defines the set-point for body weight regulation. Since 1996, Richard has studied the histological aspects of the hypothesis. In this article we present the results of our behavioral experiments to test the hypothesis. The results of all the experiments support this hypothesis.