Recent studies have shown that LV hypertrophy and interstitial fibrosis can also be triggered by activation of several insulin-related signaling pathways, altered adipokine levels (including leptin and adiponectin), or the activity of peroxisome proliferator-activated receptors, all indicating that metabolic disorders may play a role in the pathophysiology of LV dysfunction[30]. This evidence concerns the gene LEP and cardiac hypertrophy.