Study On Relationship Between Insulin Resistance And Nonalcoholic Fatty Liver And Its Partial Mechanism

Objective Through the analysis of the physical examination data,human bodycomposition, serum index to target population, and normal human liver cells cultured invitro, study the relationship under the state of IR and lipid metabolism and liver injury.The expression of PGC-1α and liver cells compared with different levels of insulinstimulation caused by abnormal liver cells as well as energy metabolism imbalanceexpression of PGC-1α liver mitochondria injury, and relation with liver fataccumulation, help to further clarify the pathogenesis of NAFLD, in order to providedata basis and some experimental evidence.Method This study selects the Affiliated Hospital of An University of medical groups,including history taking, physical examination, biochemical tests, liver ultrasoundexamination. The subjects were divided into NAFLD group and control group, analysisof the general situation of the two groups, compare the biochemical, MS and itscomponents of the prevalence rate, related risk factors of NAFLD group and Correlationsof body fat, blood lipids and IR in NAFLD group. Further by L02cells induced by highconcentration of IR model; Using transmission electron microscopy (TEM) to observethe ultrastructural changes without insulin and insulin induced group of liver cells; Takewithout insulin and insulin induced normal human liver cell line L02group for RT-PCRsemi quantitative method for the determination of PGC-1α mRNA expression level. Result1. NAFLD group than in the control group, SBP, DBP, FBS, TC, TG, HDL-C, LDL-C,ALT, AST, UA, FFA, FINS, BMI, WC, WHR, VFA, HOMA-IR and body fat percentageincreased, with statistical significance (P<0.01).2. The prevalence of NAFLD in group MS and its components (obesity, high serum TG,low HDL-C levels, increased blood pressure, abnormal FBS) were higher prevalencethan those in the control group, with statistical significance (P<0.01).3. The NAFLD groupof FINS and TG, FFA, BMI, WC was positively correlated (P<0.05, P <0.01), FINS and HDL-C was negatively correlated (P <0.01). The NAFLDgroup of HOMA-IR and TG, FFA, BMI, WC, WHR was positively correlated (P<0.05,P<0.01), HOMA-IR and HDL-C was negatively correlated (P<0.01).4. Normal human liver cell line L02cell extract total RNA as a template, nonspecificamplification PGC-1α gene and β-actin gene, purpose strip size of approximately247bpand100bp. Insulin group than in the control group value PGC-1α mRNA increased andinsulin E group difference was statistically significant (P<0.05).5. The electron microscopy display: control group that did not add insulin group,showing that cells of different sizes, rough endoplasmic reticulum was arranged tracklike mitochondrial small crest complete, rare lipid droplets appear. Group ofinsulin-induced increase concentration, visible lipid droplets gradually accumulated toreduce the number of mitochondria, the structure is unclear, the reduction in the numberof cristae.Conclusions1.In the pathogenesis of NAFLD, IR, hyperinsulinemia and hyperlipidemia.2.Successful high insulin concentrations build liver IR model cells. 3. In the pathogenesis of NAFLD, insulin levels may be closely related to PGC-1αexpression.