The IR induced by chronic sugar intake represents a further key aspect, considering that (i) the consequent stimulation of lipolysis results in an increased release of free fatty acids that inhibit the GH/IGF-1 pathway, with a negative effect on muscle regeneration (48) and (ii) the altered suppression of gluconeogenesis induced by compensatory hyperinsulinemia promotes proteolysis and inhibits protein synthesis, causing a loss of SMM (61, 62). The gene discussed is IGF1; the disease is hyperinsulinism.