الفهرس 
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Abstract
Non-alcoholic fatty liver disease (NAFLD) has been defined as the hepatic manifestation of the metabolic syndrome (MetS). It is closely associated with insulin resistance (IR), obesity, type 2 diabetes mellitus (T2DM), hypertension (HTN), hypercholesterolemia, and hypertriglyceridemia. Multiple insults act together on genetically susceptible individuals to cause NAFLD, including IR, dysregulation of adipokines released from adipose tissue (AT), dietary components, physical activity, and gut microbiota. The complex interaction between some or all of these factors leads to the accumulation of lipotoxic lipid products, which activate liver resident macrophages or Kupffer cells (KCs). Macrophages are cellular components of the innate immune system that play an important role in inflammatory processes. Macrophages are differentiated into one of two phenotypes under the impact of the local microenvironment: M1 macrophages (classically activated) and M2 macrophages (alternatively activated). According to the microenvironment stimuli, tissue-resident macrophages may be polarized towards M1 or M2. In the liver, macrophages can be defined as either KCs or monocyte-derived macrophages. KCs exhibit an M2-like phenotype that plays essential roles in tissue homeostasis and regulation of metabolic function. Several surface molecules have been used to identify M1 and M2 macrophage subpopulations. CD163 is an M2 macrophage-specific protein that is upregulated in conditions with inflammatory macrophage activation. A soluble form of CD163 (sCD163) is released from the macrophage surface into the circulation upon their activation during inflammation.