| ObjectiveMetabolic syndrome (MS) is a series of clinical diseases, including abdominal obesity, hyperglycemia, dyslipidemia and hypertension, which seriously affect the healthy of human. Diabetes is the most popular metabolic disease induced by the inheritance and environment. Insulin resistance is considered as an importance reason duing to diabetes. Adipose tissues become an important hinge connecting obesity, insulin resistance and diabetes. Inflammatory reactions sufficiently confirm multiple factors act the development of diseases above. Chemerin, a novel adipokine, secreted from adipocytes and interacted with its receptor CMKLR1 through autocrine secretory pathway. Ownan et al isolated and identified the G-protein-coupled receptor from cDNA library of human B lymphocytes. CMKLR1 highly expressed on immature dendritic cells, macrophages and adipocytes. Chemerin affected adipocyte differentiation, lipidolysis, glucose transportation and phosphorylation of IRS-1.It also affected inflammatory cells, adipose tissue and lipid metabolism through paracrine secretory pathway. In addition, the expression of Chemerin gene is association with PPAR-γ.the intervention of rosiglitazone could active PPAR-y to improve the metabolism of glycolipid, affect Chemerin and improve the sensitivity of insulin as well as treat IR. The study assessed the expression level of Chemerin and CMKLR1 mRNA in adipose tissue in spontaneous type 2 diabetic OLETF rats in order to provide a new way for interpretation and treatment of diseases.ContentMake typical model of spontaneous type 2 diabetes.10 male LETO rats (as control) and 30 male OLETF rats aged 4 weeks were selected. Subsequently,20 OLETF rats proved with diabetes through the diagnostic criteria in animals after 30 weeks were classified into rosiglitazone group and diabetes group. OGTT were performed every 4 weeks from 30 to 42 weeks. Detect insulin release test and hyperinsulinemic euglycemic clamp test and serum lipids at 42nd. Tissues were excised and snap froze in liquid nitrogen. The mRNA level of Chemerin and CMKLR1 in adipose tissue among LETO rats and OLETF rats were assessed by real-time PCR. Parts of fresh subcutaneous and visceral adipose tissue (0.5cm×0.5cm×0.5cm) from rats were for HE dyeing, then observation by light microscope. The mean maximum diameter of adipocytes were calculated every unit of vision through using Image-Pro plus Vol 6.0.Methods1,Experimental methods included:(1) Breed model of laboratory animals. (2) Insulin levels were measured by ELISA; TC and TG were measured by enzymic method, FFA by diacetone method. (3) Extraction of total RNA, Gene sequencing, Real-time PCR and Immunohistochemisty.2,Statistic methods:All analysis were performed with SPSS 16.0 software package. Pairing T-test was used to compare means of two groups. Group comparisons were performed with one way analysis of variance. Comparison of any two groups among the groups was performed with Student-Newman-Keuls.Results1,The typical model of obesity, hyperglycosemia, hyperlipemia, hyperinsulinism and type 2 diabetes was bred successfully.2,The expression of Chemerin and CMKLR1 mRNA of subcutaneous and visceral adipose tissue in diabetes group and rosiglitazone group were more than those in LETO group (P<0.01), and the expression of Chemerin in rosiglitazone group was less than that in diabetes group(P<0.01). The expression of Chemerin and CMKLR1 mRNA of visceral were more than those in subcutaneous adipose tissue (P<0.01,P<0.05).3,The average maximum diameter of subcutaneous and visceral adipocytes in diabetes group were increased compared with those in LETO group (P<0.01). However, the average maximum diameter of visceral adipocytes in rosiglitazone group was reduced compared to diabetes group (P<0.01).ConclusionsChemerin and its receptor CMKLR1 are increased in adipose tissue of OLETF rats,and can be down-regulated by rosiglitazone. |
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