Peripheral metabolic tissues such as abdominal fat cells are highly physiologically dysfunctional in liver cirrhosis, a progressive and irreversible disease with hepatic fibrosis and deformation of the liver architecture. Visceral adipose tissue (VAT) communicates with the liver bidirectionally through adipokines and free fatty acids (FFAs), and is implicated in systemic metabolism. Metabolic disturbance in the development of cirrhosis disrupts normal function of adipocytes, which is characterized by insulin resistance, on-going inflammation and perturbation in secretion pattern of various adipokines. Hepatic fat accumulation and fibrogenesis are promoted by elevated levels of circulating FFAs, enhanced lipolysis and an inflamed adipose microenvironment. Two major adipokines, leptin and adiponectin, are dysregulated that also impinge on the activation of hepatic stellate cells and add to the rate of fibrosis progression. Moreover, portal hypertension induced by cirrhosis and nutrient deficiency compound the remodeling of adipose tissue, causing fat wasting and sarcopenia. In order to identify additional metabolic targets for therapy and prevention of advance hepatic disease it is important that the interactions between the alterations induced in cirrhotic livers and the activities of abdominal fat cells be better understood.