Expansion of BMAds has been reported in response to changes in nutrient availability including starvation (reviewed in Devlin(63)), leptin deficiency,(64) dietary restriction (DR),(65) and HFD feeding(43, 49) in mice, and also in human with anorexia nervosa patients.(66) BMAT expansion, under restricted dietary conditions, was shown to be responsible for elevated circulating adiponectin levels that promote systemic improvements in glucose metabolism(66, 67, 68) and, as such, elevated serum adiponectin levels could contribute to the improved metabolic phenotype of Rptorob−/− mice. Here, ADIPOQ is linked to anorexia nervosa.