*Corresponding author:Xiang-Rong Cheng, School of Food Science and Technology, National Engineering Research Center for Functional Food, Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu Province, Jiangnan University, Wuxi, Jiangsu 214122, PR China
Received: February 20, 2020; Published: March 03, 2020
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Nonalcoholic fatty liver disease (NAFLD) is described as exposition of multiplex liver metabolic disturbance interconnected with obesity. NAFLD is depicted by steatosis, excessive accumulation of fats in liver, due to triglycerides export and oxidation of fatty acid from plasma and de novo synthesis. Hepatic steatosis can therefore be explained as biochemical outcome of inconsistency between interfused mechanisms of lipid biotransformation. This condition is allied to a range of various modifications in lipoproteins, fatty acids, and glucose metabolisms in organism. So, above metabolic disfunctions are suspected to be the origin of possibility for adverse cardiometabolic risk agents related to NAFLD, like dyslipidemia, Type 2 diabetes mellitus (T2DM), and insulin resistance. Reactive oxygen species (ROS) generation participates as known inducer of inflammation and oxidative stress, that exacerbate this disease. These disorders are hallmarks that worsen NAFLD complications, so far participate in developing advanced stages of NAFLD and incline the body to CVD and T2D. The reciprocal risks exist among these diseases. Given the sharp growing prevalence and persistence of NAFLD, and its complexity that provoke additional metabolic syndrome, this review discusses various mechanisms of developing NAFLD, interaction with other associated hallmarks, aiming to clarify beneficial mechanisms for improvement.
Keywords: Nonalcoholic fatty liver disease; oxidative stress; Type 2 diabetes; noncoding RNAs; cardiovascular disease
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