Chapter

Adipose Tissue and Adipokines in Health and Disease

Part of the series Nutrition and Health pp 291-305

Adipokines in Non-Alcoholic Fatty Liver Disease

  • Ancha BaranovaAffiliated withCenter for Liver Diseases, Inova Fairfax HospitalCenter for the Study of Genomics in Liver DiseasesMolecular and Microbiology Department, George Mason UniversityGeorge Mason-Inova Health System’s Translational Research Centers
  • , Zobair M. YounossiAffiliated withCenter for Liver Diseases, Inova Fairfax HospitalGeorge Mason-Inova Health System’s Translational Research Centers

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Abstract

Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of clinicopathological conditions in patients who do not consume excessive amounts of alcohol; these conditions are characterized by hepatic steatosis with or without other pathological changes observed in liver biopsy. The pathogenesis of NAFLD and its progressive form (non-alcoholic steatohepatitis [NASH]) appears to be multifactorial and is the subject of intense investigation. Increasing evidence indicates that the pathogenesis of NAFLD and NASH is hastened by a disturbance in adipokine production. Decreased serum adiponectin and increased tumor necrosis factor-α, which are characteristic of obesity, appear to contribute to the development and progression of NASH. The role of leptin in the pathogenesis of NASH remains controversial and the involvement of serum resistin is primarily documented only in animal models, which may or may not be applicable to the human form of NAFLD. Finally, other adipokines such as vaspin, visfatin, and apelin may play important roles in the pathogenesis of NASH and require further investigation.

Key Words

Non-alcoholic fatty liver disease (NAFLD) non-alcoholic steatohepatitis (NASH) oxidative stress insulin resistance adiponectin leptin resistin TNF-α vaspin visfatin apelin