Although the mechanism by which HFD increased Npy1r mRNA expression only in the CA1 and CA3 of Npy1rrfb conditional knockout mice is unknown, it could reflect a compensatory response to a metabolic challenge that might be at least in part responsible for their higher predisposition to develop diet-induced obesity and glucose intolerance. The gene discussed is NPY1R; the disease is obesity due to melanocortin 4 receptor deficiency.