This is extending previous findings which demonstrated a) increased apoptotic rate of the myocardium only 16 weeks after ACF induction using a 18G needle, and b) mainly in non-cardiomyocytes. However, further studies have to confirm these data. Abnormalities in myocardial catecholamine release and in badrenergic receptor density in patients with congestive heart failure have long been recognized. Adrenergic overactivity is one of the hallmarks of the heart failure syndrome and is associated with a poor prognosis. As early as 1992, Hammond et al. reported blunted heart rate responsiveness to b1- AR stimulation in volume overloaded pigs due to b1-AR PCI-32765 Src-bcr-Abl inhibitor downregulation 5 weeks after fistula induction. In failing human myocardium, b1-ARs are downregulated as studied with quantitative polymerase chain reactions in dilated and ischemic cardiomyopathy. Also, Ihl-Vahl et al. were able to describe a decrease in mRNA-levels of beta 2-adrenergic receptors in the failing human heart. In our results we demonstrate a b1- and b2-adrenoreceptor mRNA downregulation in the LV in rats with heart failure. Almost two decades ago, the b3-adrenorecptor has been identified in myocardial tissue. In healthy myocardial tissue from rodents or humans, the mainly Gi-protein coupled b3- AR is only scarcely expressed. However, according to current knowledge, the b3-AR is upregulated in the failing heart of the ACF group which is consistent with our data from the ACF group. In conclusion, our modified experimental model of heart failure using a 16G needle to induce an infrarenal aortocaval fistula has major advantages to investigate cardiac pathophysiology: congestive heart failure can reproducibly be induced within a relatively short and convenient time period. Combining morphometric, hemodynamic and biochemical parameters, the extent of heart failure can be well characterized. This modified model might facilitate the examination of various questions concerning CHF specifically by precisely timed interventions to determine pathophysiological pathways. Non-alcoholic fatty liver disease is a frequent and growing cause of chronic liver disease, affecting about 20%– 30% of the general population worldwide. Patients with NAFLD, and especially those with non-alcoholic steatohepatitis, are at risk of progression to cirrhosis and its complications, presenting also a high rate of cancer and cardiovascular events compared to subjects without fatty liver. Classical risk factors for liver disease severity and its progression are obesity, insulin resistance and necroinflammation. The above-mentioned conventional risk factors do not entirely explain the occurrence and severity of NAFLD, suggesting that a genetic background might also modulate the spectrum of liver disease and its progression. Accordingly, the severity of disease has been variably associated with different single nucleotide polymorphisms in genes involved in metabolic homeostasis, inflammation, oxidative stress and fibrogenesis. Besides the classical PNPLA3, a recent genome wide study identified other genetic variants.