Although the underlying pathophysiologic mechanisms of the association between MetS and HF remain to be fully elucidated, metabolic stress caused by elevated glucose and free fatty acids, including dysregulated insulin signaling, impaired mitochondrial respiration, and reactive oxygen species formation, is thought to decrease adenosine triphosphate (ATP) production, resulting in impaired contraction, myocellular hypertrophy, and fibrosis of the heart, subsequently leading to HF [12]. This evidence concerns the gene INS and hydrops fetalis.