Sexual dimorphism is frequently reported in murine models of HFD-induced dysmetabolism.57 We have recently shown a permissive role for androgens in glucocorticoid-induced insulin resistance.58 Last, it is possible that altered secretion of adipose-derived signaling molecules (such as leptin) from expanded fat stores could have influenced bone formation in our model.59 The gene discussed is LEP; the disease is Insulin resistance.