The rescue of PGC1α expression by reducing proinflammatory cytokine load could both prevent and ameliorate metabolic remodelling in HF and diabetes: improve mitochondrial function and organisation, reduce insulin resistance by enhancing glucose uptake (GLUT4) and metabolism (PDK4), reducing myocardial steatosis by promoting FFA β-oxidation (due to relationship between myocardial triglyceride accumulation and insulin resistance) [258, 262]. Here, PPARGC1A is linked to hydrops fetalis.