It is clear from this derivation that to efficiently harness the energy-converting potential of BAT for the prevention and treatment of obesity and diabetes requires not only knowledge of the substrates and metabolic pathways involved, of the control of these pathways by neurotransmitters and hormones and of the control of gene expression in BAT, but also an appreciation and understanding of the inherently inactive nature of UCP1, the physiological and molecular brakes of UCP1 activation and the exquisite sensitivity of UCP1 activity to temperature-dependent regulation. This evidence concerns the gene UCP1 and obesity due to melanocortin 4 receptor deficiency.