Abstract
Shimomura et al. reply — Human lipodystrophy (also called lipoatrophic diabetes) is genetically heterogeneous, with the severity of insulin resistance and diabetes mellitus varying widely depending on the degree of reduction in adipose tissue mass and the age of the patient1,2. It is therefore not surprising that two mouse models of lipodystrophy (created by using two different transgenes, A-ZIP/F-1 and aP2-SREBP-1c ) vary in their disease severity and in their sensitivity to leptin. The aP2-SREBP-1c animals respond to leptin with a decrease in their insulin and blood sugar levels3, whereas the A-ZIP/F-1 animals of Gavrilova et al. apparently manifest leptin resistance. The differences between these two models should not preclude a clinical trial of leptin in leptin-deficient patients with lipodystrophy, with continuation of therapy in those who are leptin-sensitive.
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