Study On The Relationship Between Plasma Resistin Levels Of Nonalcoholic Fatty Liver Disease And Insulin Resistance

The adipose tissue is the body's largest endocrine organ producing hormones, cytokines and other proteins like leptin, tumor necrosis factor-a (TNF-a), adipokines, and interleukin-6 (IL-6). They regulate the body's energy metabolize through internal secretion and side secretion. They play a pathogenic role in insulin resistance. Resistin was original identified by Steppan et al. in 2001 as an adipocyte secreted factor overexpressed in murine models of obesity and downregulated by thiazolidinediones (TZDs) which are known to increase insulin sensitivity. It belongs to a family of proteins (Resistin-like molecules, RELMs) characterized by a cystein-rich C-terminal domain but a limited homology between the three members. Nonalcoholic fatty liver disease (NAFLD) is a complex metabolic condition in which both lifestyle and genetic factors play a pathogenic role and has been increasingly recognized as a major cause of liver-related morbidity and mortality. Moreover NAFLD has been convincingly associated with the metabolic syndrome and insulin resistance states, such as obesity and diabetes. Insulin resistance, through inhibition of lipid oxidation and increased fatty acid and triglycerides synthesis, is believed to be a key factor in the development of fatty liver. People proposed that resistin is an important link between obesity and diabetes. However, the role of resistin in obesity and insulin resistance has not been confirmed in several recent studies.In the present study, we measured fasting plasma resistin in NAFLD patients and control subjects. Insulin resistance by homeostasis model (HOMA-IR), height, weight, waist circumstance, hip girth, waist to hip ratio (WHR), body mass index (BMI), blood pressure, fasting glucose, total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and fasting insulin were measured as well. We found plasma resistin levels were higher in NAFLD patients as compared to controls. There was no significant correlation between plasma resistin and blood pressure, BMI, %FAT, WHR and a number of biochemical variables (glucose, total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, ALT, AST). Plasma resistin levels were correlation with fasting insulin. Our results suggest that increased resistin in NAFLD patients might be related to insulin resistance. However, no indication of possible relation between resistin and obesity was discovered. In part two study, we found the serum resistin, TNF-a, IL-6 levels were higher in NAFLD model rats as compared to controls. These cytokines play a pathogenic role in NAFLD. Although polyene phosphatidylcholine and berberine treatment obviously decreased serum lipids and fasting glucose of NAFLD model rats induced by high-fat diet, both of them deteriorate hepatocellular steatosis and aggravate hepatocellular inflammation and damage. In conclusion, polyene phasphatidylcholine and berberine may not be used to prevent and treat nonalcoholic fatty liver disease.