Adipose tissue comprises of large volumes of biologically functioning fat globule, which employs substantial systemic effect. Adipocytes and adipokines play an active role in autocrine, paracrine, or endocrine metabolic functions. Recent studies demonstrated that the hormonal role of adipocyte and adipose tissue dysfunction contributes to the pathogenesis of alcoholic liver disease (ALD) by the activation of CYP2E1. The gut microbiome and adipose tissue response play a pivotal role in the pathogenesis of ALD. Enteric dysbiosis increases plasma levels of metabolites that activate Kupffer cells. Recent literature suggested that chronic alcohol consumption is also correlated with oxidative stress in adipose tissue, inflammation, and adipocyte cell death, decrease in adiponectin, increase level of leptin and resistin, adipose tissue mass, and insulin resistance that acts on the muscle and liver. Dysbiosis combined with non-nutritional diet has an effect on the luminal metabolism causing immunological changes in the gut that might also contribute to pathogenesis of nonalcoholic fatty liver disease (NAFLD). Understanding the interaction between the altered gut microbiota, diet, environmental factors, and their effects on the gut-liver axis can provide an insight toward the pathogenesis of liver-associated disease.
Part of the book: Adipose Tissue