Nonalcoholic fatty liver disease (NAFLD) is expected to touch around 30% of the general population. It is a major health problem measured to be the greatest common chronic liver disorder in the Western countries. Cytokines and adipokines plays an important role in inflammatory processes, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. Accumulating evidences disclose that NAFLD as well as insulin resistance is powerfully related to inflammation. Recent outcomes emphasises the role of main inflammatory markers in both NAFLD and insulin resistance and their imminent role in modulating hepatic fat content in NAFLD and related hepatic insulin resistance.

NAFLD closely always results in insulin resistance through the build-up 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 powerfully related with obesity, insulin resistance, hypertension, and dyslipidemia, suggesting that NAFLD might be considered as the liver appearance of the metabolic syndrome.

Source: Journal of Endocrinology. September 2013.218:3:R25-R36