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#Gastroenterology #Hepatology #Multispeciality
Nonalcoholic fatty liver disease (NAFLD) is a major health problem measured to be the utmost common chronic liver disorder in the Western countries. NAFLD is estimated to touch at least 30% of the general population. Cytokines and adipokines plays a key role in inflammatory processes, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. Accruing evidences divulge that NAFLD as well as insulin resistance is muscularly related to inflammation. Current findings accentuates the role of main inflammatory markers in both NAFLD and insulin resistance and their impending role in modulating hepatic fat content in NAFLD and associated hepatic insulin resistance.
NAFLD nearly always results in insulin resistance through the accumulation of toxic lipid intermediates such as DAGs and ceramides, which lead to inhibition of the insulin signaling cascade. This ectopic fat gathering in the liver and the subsequent hepatic insulin resistance result in inflammation, which is secondary to cytokines release. These cytokines may either exacerbate NAFLD and insulin resistance, such as TNFα or IL6 or try to compensate the situation, such as IL10 and adiponectin. Understanding the role of cytokines in the modulation of hepatic fat content might provide new therapeutic targets for conditions associated with hepatic insulin resistance, such as NAFLD, obesity, and type 2 diabetes.
NAFLD is muscularly related with obesity, insulin resistance, hypertension, and dyslipidemia, suggesting that NAFLD might be considered as the liver manifestation of the metabolic syndrome.
Source: Journal of Endocrinology. September 2013.218:3:R25-R36