| PrefaceDiabetes mellitus is a chronic metabolic disease that leads to complications including kidney failure, blindness, nerve damadge and cardiovascular disease. Type 2 diabetes mellitus (T2DM) , characterized by insulin secreted deficiency and target - tissue resistance to insulin, is globally epidemic and is strangly associated with obesity, morbidity and mortality of complications are gradually increased, in recent years, there has been a tremendous progress in the pathophysiological mechanisms and pathogenesis of Diabetes mellitus, more and more evidence show that adipocytokines is strangly associated with insulin resistance (IR).Recent study show that adipose tissue not only plays an active role in energy balance but also is the body's largest endocrine organ producing hormones, cytokines and other proteins, like Leptin, Adiponectin, Resistin, Plasminogen - activator inhibitor - 1 ( PAI - 1) , Agouti relattion protein ( AGRP) , Renin angiotensinogen system ( RAS) , Tumor necrosis factor alpha (TNF - α) , Inter-leukin — 6 (IL - 6). These actions are mediated by a number of molecules that are secreted by adipocytes and act in an endocrine, paracrine, or autoctine fashion. Resistin is peptide hormone specifically secreted from adipocytes and was recently postulated to be an important link between obesity and T2DM by Step-pan et al. at animal experiment in 2000. Resistin may affect glucose metabolism, Lipid metabolism in relation to insulin action, and become a novel study topic between obesity and IR. However, the mechamism by which increased ad-iposity causes insulin resistance is unclear. Its putative role as a mediator of insulin resistance is controversial at the present.Soluble intercellular adhesion molecules - 1 ( sICAM - 1) is an inducible intercellular adhesion protein which secreted from leucocytes and vascular endo-thelioid cells, immune globin exceed familial member, which mediates the adhesion between leucocytes and vascular cells. It exerts important roles in maintaining vascular endothelioid cells function and inflammatory response. sICAM -1 low expression levels in the normal condition, is regulated by multiple transcription factors. But, it is expressions increases in a course IL - 1β, TNF - α inflammatory cell, endothelioid cells function abnormal is a component of insulin resistant syndrome, so sICAM - 1 may was correlated with IR. In the present study, Serum resistin, sICAM - 1 different glucose tolerance status with different body mass index, was measured by enzyme - linked immunoassay assay ( ELISA) , and observe the relationship bewteen Serum resistin, sICAM - 1 concentration different glucose tolerance status and insulin resistance, To study mechanism during Resistin, sICAM - 1 is developing T2DM.MethodsFasting serum resistin concentration was measured by enzyme - linked immunosorbent assay (ELISA) in 52 subjects suffering from T2DM, 18 subjects impaired glucose ragulation (IGR) , and 30 subjects non - diabetic control individuals with normal glucose tolerance. All subjects resistin, sICAM - 1 was measured by ELISA, and was subgrouped by impaired glucose regulation, namely DM group 52 individuals, IGR group 18 individuals, NGT group ( normal glucose tolerance) 30 individuals.Total study subjects were respectively subgrouped by ( BMI ≥25kg/m2or BMI < 25 kg/m2) , namely A group ( BMI ≥25) 26 obese subjects with T2DM, B group ( BMI < 25) 26 nonobese subjects with T2DM, C group (BMI ≥25) 14 obese subjects with non - diabete, D group ( BMI < 25 ) 16 nonobese subjects with non - diabete, E group 18 ( BMI≥25) with IGR. HOMA - IR was calculated. Blood pressure, height, other data including body weight, waist circum-ference and hip circumference were measured to calculate BMI, waist - hip ratio (WHR). All characteristics of T2DM were not treated with insulin and thiazo-lidinediones.ResultsIn patients with diabetes and non - diabetic controls, fasting serum insulin concentration (ng/ml) , HOMA - IR were higher in obese subjects than that in those persons with normal weight ( P <0. 01). FINS was not markedly difference in obese DM group and NGT group as well as non - obese DM group and NGT group( P > 0. 05 ). HOMA - IR in DM, IGR was markedly higher than that in NGT( P <0. 01) , HOMA - IR in DM was slightly higher than in IGR ( P > 0. 05 ). In patients with diabetes and non - diabetic controls, fasting serum resistin concentration (ng/ml) were higher in obese subjects than that in those persons with normal weight, but only the diabetes group was significant (P <0.05) , In non - diabetic group resistin was higher in obese subjects than that in those obese diabetes group, normal person resistin was higher than normal weight in diabetic group, but difference was not statistical significance( P >0.05) ; Resistin was higher in IGR than that in those patients with diabetes and non - diabetic controls ( P < 0. 05, P > 0. 05 ). Fasting serum resistin was significantly increased in DM group of Famine.sICAM - 1 in DM, IGR group was significantly higher than that in those NGT( P < 0. 01, P < 0. 05 ) , sICAM - 1 in DM was higher than IGR ( P < 0. 05 ); In patients with diabetes, fasting serum sICAM - 1 concentration ( ng/ml) were higher in obese subjects than that in those persons with normal weight , but not significant ( P <0. 05). Correlate analysis showed that fasting serum resistin concentration was a positive correlated with BMI , HOMA - IR, Fasting insulin (FINS) and Triglyceridemia (TG) (r=0.466, r=0.402, r=0.691, r=0. 320, P <0.01, P <0. 05) , and fasting serum resistin concentration was a negative correlated with HbAlc. No correlation between resistin and fasting plasma glucose ,blood pressure, WHR, age, cholesterol, high density lipoprotein,low density lipoprotein was found. Correlate analysis showed fasting serum sICAM -...
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