The incidence of obesity has dramatically increased in recent years.Consequently,obesity and associated disorders such as nonalcoholic fatty liver disease constitute a serious problem.Therefore,the contribution of adipose tissue to metabolic homeostasis has become a focus of interest.In this review,we discuss the latest discoveries that support the role of lipids in nonalcoholic fatty liver disease.We describe the common mechanisms(cJun aminoterminal kinases,endoplasmic reticulum stress,unfolded protein response,ceramide,lowgrade chronic inflammation)by which lipids and their derivatives impair insulin responsiveness and contribute to inflammatory liver and promote plaque instability in the arterial wall.Presenting the molecular mechanism of lipid activation of proinflammatory pathways,we attempt to find a link between nonalcoholic fatty liver disease,metabolic syndrome and cardiovascular diseases.Describing the common mechanisms by which lipid derivatives,through modulation of macrophage function,promote plaque instability in the arterial wall,impair insulin responsiveness and contribute to inflammatory liver and discussing the molecular mechanism of lipid activation of proinflammatory pathways,the key roles played by the proliferatoractivated receptor and liver X receptorα,nuclear receptorslipid sensors that link lipid metabolism and inflammation,should be emphasized.Further studies are warranted of antiinflammatory drugs such as aspirin,antiinterleukin6 receptors,immunemodulators(calcineurin inhibitors),substances enhancing the expression of heat shock proteins(which protect cells from endoplasmic reticulum stressinduced apoptosis),and anticJun aminoterminal kinases in welldesigned trials to try to minimize the high impact of these illnesses,and the different expressions of the diseases,on the whole population. The incidence of obesity has increased increased in recent years. Conclusion, obesity and associated disorders such as nonalcoholic fatty liver disease constitute a serious problem. Beforefore, the contribution of adipose tissue to metabolic homeostasis has become a focus of interest. This review, we discuss the latest discoveries that support the role of lipids in nonalcoholic fatty liver disease. We describe the common mechanisms (cJun aminoterminal kinases, endoplasmic reticulum stress, unfolded protein response, ceramide, lowgrade chronic inflammation) by which lipids and their derivatives impair insulin responsiveness and contribute to inflammatory liver and promote plaque instability in the arterial wall. Presentation of the molecular mechanism of lipid activation of proinflammatory pathways, we attempt to find link between nonalcoholic fatty liver disease, metabolic syndrome and cardiovascular diseases. Describing the common mechanisms by which lipid derivatives , through modulation of macroph age function, promote plaque instability in the arterial wall, insulin-responsive responsiveness and contribute to inflammatory liver and discussing the molecular mechanism of lipid activation of proinflammatory pathways, the key roles played by the proliferatoractivated receptor and liver X receptor alpha, nuclear receptors lipids that that lipid metabolism and inflammation, should be emphasized. Future studies are warranted of antiinflammatory drugs such as aspirin, antiinterleukin 6 receptors, immune modulators (calcineurin inhibitors), substances enhancing the expression of heat shock proteins (which protect cells from endoplasmic reticulum stress induced apoptosis), and anticJun aminoterminal kinases in welldesigned trials to try to minimize the high impact of these illnesses, and the different expressions of the diseases, on the whole population.