ISSN: 2574-7770
Authors: Tangvarasittichai S*
Metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) are associated with artherogenic dyslipidemia and abnormal postprandial lipoprotein metabolism which consists with elevated fasting and postprandial triglyceride-rich lipoproteins (TRLs), small dense low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol as cardiovascular disease risk factors. These abnormal lipids concentrations can result from alterations in the production, conversion, or catabolism of lipoprotein particles. Whereas the liver is the central organ in lipogenesis, gluconeogenesis and cholesterol metabolism and the intestine is also a major role in lipoprotein production. However, many research studies demonstrated a variety of pathological conditions focused on the metabolic functions within the liver. As observed in the world population, increase in the prevalence of MetS and T2DM promotes pathophysiological from atherogenic dyslipidemia and cause non-alcoholic fatty liver disease (NAFLD). Alterations in insulin activity, response and signaling are held accountable for these alterations in lipid storage, transport andï¢-oxidation. This review focuses on dysfunctions and alterations in increased lipoprotein production prolongs dyslipidemia, hepatic lipid uptake, storage and metabolism in the clinical of NAFLD in MetS and T2DM patients, and may directly contribute to cause atherogenesis in these patients.
Keywords: Metabolic Syndrome; Type 2 Diabetes Mellitus; Insulin Resistance; Adipose Tissue; Dyslipidemia;De Novo Lipogenesis; Non-Alcoholic Fatty Liver Disease
