Transgenic mice overexpressing BNP or PKG increased the mitochondrial muscle content and fat oxidation through upregulation of PGC-1α and PPARδ, preventing obesity and glucose intolerance; moreover, treatment of myotubes with ANP and BNP stimulates mitochondrial biogenesis and mitochondrial respiration [171]. Here, NPPB is linked to obesity due to melanocortin 4 receptor deficiency.