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Abstract
Many factors may increase the risk of fibrosis development in chronic viral hepatitis infections. As the burden of obesity and metabolic syndrome has been increasing in recent years, there is growing concern regarding the association between metabolic factors and chronic viral hepatitis cases. However data regarding the influence of metabolic syndrome on progression of fibrosis in chronic hepatitis B virus (HBV) infection is limited. Metabolic syndrome is a constellation of problems that includes insulin resistance, obesity, hypertension, and hyperlipidemia. Initially, epidemiologic data demonstrated that HBsAg-positive serostatus was positively correlated with a high risk of metabolic syndrome; later on, HBV was considered as a “metabolovirus” because the gene expression of HBV and key metabolic genes in hepatocytes was found to be similarly regulated. Metabolic syndrome is not only found to accelerate the progression of liver disease in patients with chronic HBV infection but also found to induce cirrhosis or even hepatocellular carcinoma development. This review article it is aimed to highlight the association of metabolic syndrome with chronic HBV infection.
Highlights
Chronic hepatitis B virus (HBV) infection is well-known as a major risk factor for liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC) [1,2,3,4]
Several reports have suggested that HBV adopts a mode of regulation similar to major gluconeogenesis genes in the liver, such as gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6phosphatase (G6Pase), which are co-regulated by PGC-1α, HNF4α and FOXO1 [25,26]
The results indicated that pre-existing metabolic syndrome, as defined by the 2001 US NCEP-ATP III criteria, confered a statistically significant 2.13 and 1.56 fold increased risk for terminal liver diseases as HCC and intrahepatic cholangiocarcinoma (ICC) which was independent of other risk factors [33]
Summary
Chronic hepatitis B virus (HBV) infection is well-known as a major risk factor for liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC) [1,2,3,4]. A study by Su et al reported an association between asymptomatic chronic HBV infection and lower serum levels of total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) [11]. The GA/HbA1c ratio has been reported to be associated with the histological stage of liver fibrosis and portal hypertension in HCV-positive patients and nonalcoholic steatohepatitis. The GA/HbA1c ratio is found to be increased in association with the stage of liver fibrosis in HBV-positive patients. Extreme obesity (body mass index >or=30 kg/m2) was independently associated with a 4-fold risk of HCC and there was more than 100-fold increased risk in HBV or HCV This evidence suggested metabolic profiles and subsequent development of MS might be associated with chronic HBV infection. It seems vital to explore the relationship between chronic HBV and MS to inform better prevention and control strategies
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