| PrefaceInsulin resistance is the mechanism that leads to the disorder of human metabolism. Evidences demonstrate that hypertension, atherosclerosis, and cardiac vascular heart is on the pathogenic basis of insulin resistance. Insulin resistance not only causes the metabolic disorder such as sugar metabolic disorder, fat metabolic disorder and so on, but also results in inflammation. Many factors causing inflammation increase in the insulin-resistant state. So many scientists propose hypothesis concerning the relation of insulin and atherosclerosis.Materials and MethodsWe purchase 40 Wistar male rats from experimental animal center of China Medical University. The rats are divided in three groups according to random principle. We feed the rats in Group One on the normal diet,which contains 21% protein, 19% fat and 60% carbohydrate. We feed the rats in Group Two on the more fat diet, which contains 21% protein, 60% fat and 19% carbohydrate. We feed the rats on the more fat and more sugar diet, which contains 21% protein, 60% fat, 19% carbohydrate and 40 grammers extra sugar. We have cultivated three groups of rats for eight weeks in order to build the rat models that are in the insulin resistance state.We examine insulin resistance in the experimental rats by glucose clamp test(GCT). Glucose intaking rate(GIR) gotten in GCT reflects the situation of IR of the experiment.We get the serum samples of these rats afer clamp technique examination. We examine the serum insulin, blood lipid series, and free fat acid by ELISA. Afer killing the rats we get the catorid samples, which are stored under 4% PFA. All samples are preserved in low temperature. Carotid samples are routine paraffin imbeddinged after dehydration, transparent, immerse wax as immunochemistrical samples. The expression of eNOSand ICAM-1 in endothelial cells is examined by immunochemical method. Continuous distribution measurement data is demonstrated with mean±S.D. We proceed ANOVA on them by. Noncontiuous distribution measurement data is demonstrated with mean ranks. We proceed rank sum test on these datum. All statistic analysis are completed by SPSS package.Result1,GIR: the GIR of the rats in Group One is higher than Group Tow and Group Three(P>0.05), and the GIR of the rats in Group Two is higher than Group Three(P>0.05);2,Serum insulin: the insulin level of the rats in Group Two and Group Three is higher than Group One(P>0.05), but there's no difference between Group Two and Group Three(P>0.05);3,Serum free fat acid(FFA): the FFA level of the rats in Group Two and Group Three is higher than Group One(P<0.05), and the FFA of the rats in Group Three is higher than Group Two(P<0.05);4,Immunohistochemistry index: the expression ofeNOS in arterial endothedial cells of Group Two and GroupThree were lower than Group One(P<0.05), but there's no significantly difference here's no difference between Group Two and Group Three(P>0.05); the expression of ICAM-1 in arterial endothedial cells of Group Two and Group Three were higher than Group One(P<0.05), but there's no significantly difference here's no difference between Group Two and Group Three(P>0.05).ConclusionHe people that have high fat diets in the long term have surplus energy metabolism. On the one hand, surplus energy metabolism increases the level of insulin in human body, which makes insulin receptor of aim cell downregulation as to lead to insulin resistance; on the other hand, fat accumulation under lipidolytic hormone increases the level of serum FFA in human body. On the contrary, FFA strengthens the situation of insulin resistance in human body. Insulin resistance decreases the expression of eNOS in arterial endothelial, which promotes arterial inflammation... |
PDF Full Text Request