Abstract
Chronic hepatitis C (CHC) is generally a slowly progressive disease, but some factors associated with rapid progression have been identified. Steatosis, independently of its metabolic or viral origin, leads to liver injury and fibrosis. It is suggested that hepatitis C virus may contribute to a wide spectrum of metabolic disturbances-namely, steatosis, insulin resistance, increased prevalence of impaired glucose tolerance, type 2 diabetes mellitus and lipid metabolism abnormalities. Adipokines, which are produced mainly by adipose tissue, may influence the inflammatory response and insulin sensitivity and contribute to the development of metabolic abnormalities in CHC and also regulate fibrogenesis and angiogenesis. Visfatin was described as an adipokine with immunomodulating and proinflammatory properties that promotes B-cell maturation and enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines. Visfatin exerts insulin-mimetic effects, decreases plasma glucose levels and regulates cell energy balance. Chemerin stimulates chemotaxis of dendritic cells, macrophages and natural killer (NK) cells toward the site of inflammation. On the other hand, it inhibits synthesis of proinflammatory mediators and enhances adiponectin production, influences adipocyte differentiation and maturation and regulates glucose uptake in adipocytes. Vaspin expression in human adipose tissue seems to be a compensatory mechanism associated with obesity and insulin resistance. Vaspin suppresses leptin, tumor necrosis factor (TNF)-α and resistin expression. Leptin protects against liver steatosis but accelerates fibrosis progression and exacerbates the inflammatory process. In contrast, adiponectin exerts a hepatoprotective effect. In this report, data indicating a possible role of these adipokines in the pathogenesis of chronic hepatitis are summarized.
Highlights
Regulation of insulin sensitivity by adipokines seems to play a key role in fibrosis progression
Recent studies point to the potential role of novel adipokines in chronic hepatitis pathogenesis
Precise evaluation of the role of adipokines in chronic hepatitis would facilitate management and new therapeutic approaches
Summary
Chronic hepatitis C (CHC) has a number of features that suggest that it should be recognized as a viral disease and as a metabolic liver disease that encompasses insulin resistance (IR), liver steatosis, impaired glucose tolerance or type 2 diabetes mellitus (T2DM) and disturbances in lipid metabolism (Figure 1). Increasing data suggest that IR is closely related to the extent of steatosis and inflammatory activity in the liver [2,3]. Adipokines (adipocytokines)—agents secreted primarily by adipocytes—modulate lipid and glucose metabolism and insulin sensitivity [10]. In addition to their wellestablished role in controlling adipose tissue physiology, adipokines have been shown to be involved in regulation of the inflammatory response, angiogenesis and fibrogenesis [11,12]. A better understanding of the pathogenic role of novel adipokines in the inflammatory process and in mechanisms underlying IR development and fibrosis progression in CHC may have a prophylactic implication in preventing progression of liver fibrosis and improving response to antiviral therapy. Development of hepatocellular carcinoma (HCC) [16,17,18,19,20,21,22]
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