Figure 2.

Inter-organ crosstalk in the development of cardiac steatosis and left ventricular (LV) heart failure on the background of insulin resistance. Decreased insulin sensitivity leads to (A) impaired glycogen synthesis in skeletal muscle, promoting hyperglycemia; (B) unrestrained hepatic lipogenesis and gluconeogenesis, promoting hyperglycemia and dyslipidemia; and (C) augmented lipolysis in adipose tissue, promoting dyslipidemia; increased concentrations of insulin, glucose and free fatty acids (FAs) results in increased lipid accumulation in the myocardium and cardiac glucolipotoxicity, which ends up in LV heart failure.