Previously, it has been found that mice selectively deficient for LEPR in POMC neurons developed modest obesity that was associated with reduced energy expenditure independent of changes in food intake.38 Therefore, the reduced effect of leptin in the regulation of energy expenditure in the present study could be related to low expression of LEPR or deficiency in leptin down-stream signalling on POMC neurons important for regulation of energy expenditure.38 The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.