The exact underlying mechanisms which result in the altered wall thickness and reduced diastolic function, across species, remain undetermined; mitochondrial dysfunction, increased production of reactive oxygen species, insulin resistance, leptin-resistance and intracytoplasmic lipid accumulation in cardiomyocytes all likely play a role in the cardiac changes seen with obesity [3, 32]. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.