Such time-dependent progressive increase in mitochondrial dysfunction and collapse of oxidative phosphorylation (OXPHOS) stimulates a shift in metabolism from using mitochondrially produced ATP to dependence on glycolysis as a consequence of the accumulation of hypoxia-inducible factor 1 alpha (HIF-1α) and decreased activity of respiratory complexes I, III and IV [47], which stimulates the Warburg effect involved in the metabolic syndrome, obesity, type 2 diabetes, the onset of cancer and other degenerative diseases [47,48,49,50,51]. This evidence concerns the gene HIF1A and obesity due to melanocortin 4 receptor deficiency.