The Relationship Between Expression Of GSK-3β Gene And The Statement Of Type 2 Diabetes Patients

Type 2 diabetes is a disease with multifactorial pathogenesis. This result is leaded by many complex genetic factors and environmental factors together, so there is no clearly articulated about its etiology and pathogenesis nowadays. The insulin cell signal transduction is constantly the focus of the study, and the molecules related with the Insulin signal transduction has also become the research hotspot. Through extensive researches the function of these molecules have gradually been confirmed in the past 20 years. Glycogen synthase kinase-3 is well-known as a rate-limiting enzyme to inhibit glycogen synthesis, and participate in the regulation of a variety of signals, including insulin-secreting cells signal transduction, GSK-3βisoforms chiefly. Hence GSK-3βand Type 2 diabetes the correlation study was payed more and more attention. In recent years, high expression of GSK-3βand decreased insulin sensitivity was related to study the function of GSK-3βactivity at home and abroad. The development of GSK-3βinhibitors have become the hotpot of new drug research. For example, the protein expression of GSK-3βin skeletal muscle and liver significantly increased in type 2 diabetes more than in healthy subjects. And GSK-3 inhibitors have effective therapeutic effect in animal models of type 2 diabetes and Alzheimer's disease. However, the mechanism of GSK-3βis not clear. Based on these data, we have understand that the protein expression of GSK-3βin type 2 diabetes patient may affect its function. As a serine/threonine protein kinase,the gene expression of GSK-3βin patients which is whether or not changed leads to its impact in their original normal signal transduction pathways. while activating each relative pathway. In order to verify whether the GSK-3βactively participates in an important pathogenic factor in T2DM, we select the glycogen synthase kinase-3βas the research object, using SYBR real-time fluorescent PCR technology research in the nucleated cells of type 2 diabetes patients, GSK-3βgene expression to explore in patients with type 2 diabetes pathogenesis of relevance.Object:To evaluate the relative quantitative real-time PCR detection of GSK-3βgene in type 2 diabetes patients and healthy expression of peripheral blood nucleated cells, the amount of GSK-3βin type 2 diabetes patients the clinical significance of gene expression in vivo.Methods:Collected in the morning in type 2 diabetic patients and healthy fasting venous blood, EDTA anticoagulant, then tested fasting plasma glucose, total cholesterol and triglyceride. Designed GSK-3βgene primers and detected 40 cases of diabetic patients and 40 healthy human PBMC gene expression with real-time fluorescence relative quantitative RT-PCR. Apply Delta-Delta Ct method to deal with raw data, compare and analyze the clinical significance of expression in the human body and application value of GSK-3βgene.Result:1. The fasting blood glucose, serum total cholesterol and triglycerides of the type 2 diabetic patients group were higher than the healthy control group (P<0.05), but the age is no difference (P>0.05).2. The type 2 diabetic patient group's GSK-3βin the relative mRNA expression levels is 0.94±0.34, and the healthy group is 0.92±0.19, which compared no significant difference between the two groups (P> 0.05).Conclusion:In peripheral blood monucleated cells of type 2 diabetic patients, GSK-3βgene relative expression has no significant difference compared with the healthy control group. GSK-3βin the pathogenesis of type 2 diabetes does not have a significant impact, while restraining the GSK-3βgene relative expression can block part of the signal transduction and play a role in lowering blood glucose, but GSK-3βcan not be the target gene for the treatment of type 2 diabetes.