Our results indicate that visfatin may play a role in the pathogenesis of T2DM.

Objective-Adiponectin, an adipocyte-derived peptide with antiinflammatory and antiatherogenic effects, is known to protect against the initiation and progression of atherosclerosis. In this study, we investigate whether hypoadiponectinemia is present in patients with ischemic cerebrovascular disease (CVD). Methods and Results-In this case-control study, plasma adiponectin concentration was measured by an enzyme-linked immunosorbent assay in type 2 diabetic and nondiabetic subjects with or without ischemic CVD. A total of 534 subjects were studied. The mean plasma level of adiponectin of the 228 patients with ischemic CVD was significantly lower than that of 306 subjects without CVD. When the analysis was stratified according to diabetes status, plasma levels of adiponectin in CVD subjects with or without type 2 diabetes were significantly lower than those of their counterparts. Decreasing concentrations of adiponectin were independently and significantly associated with a higher risk of CVD when concentrations were analyzed by quartile and as a continuous variable. When patients with CVD were subgrouped according to the comorbidity with or without type2 diabetes, the same trend of association between plasma adiponectin and risk of CVD was observed in each group. Conclusion-These data show that there are significantly lower levels of plasma adiponectin in patients with ischemic CVD. Acrp30, an adipose tissue-specific protein that has structural homology to collagen VIII and X and complement factor C1q, circulates at high levels in human plasma. [1][2][3][4] It is one of the adipocyte-expressed proteins that contribute to the homeostatic control of glucose, lipid, energy metabolism, and antiinflammatory activity. 5,6 According to several studies, dysregulation of adiponectin has been implicated in metabolic X syndrome and atherosclerosis disorders, including insulin resistance, obesity, type 2 diabetes, hypertension, and coronary artery disease (CAD). 7-10 Decreased plasma adiponectin levels have been found to be independently associated with the presence of CAD after adjustment for other well-known CAD risk factors in men, with male patients with hypoadiponectinemia (Ͻ4.0 g/mL) having a significant 2-fold increase in CAD prevalence. 9 Adiponectin has a potential inhibitory effect on all molecular mechanisms of atherosclerosis, 11 including the inhibition of monocyte adhesion to endothelial cells, 12 the inhibition of oxidized lowdensity lipoprotein (LDL) uptake of macrophage through scavenger receptors, 13 and inhibition of proliferation of migrated smooth muscle cells by the action of growth factors. 14 Recently, Pischon et al, in a nested case-control study of 19 225 men who had been followed-up for Ͼ6 years, have associated high plasma adiponectin concentrations with lower risk of myocardial infarction in men. 15 Although these findings indicate that adiponectin plays a crucial role in the development of atherosclerosis, to the best of our knowledge, there have been no studies of the association between plasma...

Our results indicate that differential leukocyte counts are associated with MetS and that peripheral leukocytes may play a role in the pathogenesis of macrovascular complications in patients with T2DM.

The ENPP1 K121Q polymorphism is not related to T2DM, features of the metabolic syndrome, or diabetic macrovascular complications in a Chinese population.

Role of tumor necrosis factor-␣, leptin, and white blood cell count in betel nut chewing-related metabolic derangements A reca nut (Areca catechu)/betel quid (BQ) is said to be the fourth most commonly used psychoactive substance in the world and is chewed regularly by at least 10% of the world's population (1). High prevalences of BQ chewing were observed especially in South and Southeast Asia (1). High prevalences of insulin resistance and metabolic syndrome were also observed in this area (2). Specific areca alkaloids act as competitive inhibitors of ␥-aminobutyric acid receptors in the brain, cardiovascular system, and pancreas, which may promote one's appetite or altered insulin secretion (3). Moreover, BQ components have recently been shown to induce keratinocytes to secrete tumor necrosis factor-␣ (TNF-␣) and interleukin-6, as well as induce reactive oxygen species and activate nuclear factor-B expression (4), which may potentially provoke chronic inflammation. Recently, we confirmed that BQ chewing was associated with a higher risk of type 2 diabetes and central obesity in Taiwanese men (5). The detrimental effects of BQ chewing on selected components of the metabolic syndrome, and the induction of inflammatory cytokines and factors, raise the possibility that BQ chewing may increase the risk of metabolic syndrome.In this study, a total of 1,466 aboriginal subjects of Southern Taiwan, 30 -95 years of age, were enrolled. Metabolic syndrome was defined according to the National Cholesterol Education Program Adult Treatment Panel III definition. The age-adjusted prevalence of metabolic syndrome in the aborigines studied was 41.1% in men and 42.4% in women. BQchewing subjects had significantly higher prevalences of central obesity, hypertriglyceridemia, dysglycemia, and metabolic syndrome than those of nonchewers. Peripheral leukocyte count also significantly increased in chewers of both sexes, with plasma TNF-␣ level increased in men and plasma leptin level elevated in women. All were parallel to the number of components of the metabolic syndrome. Multiple logistic regression modeling adjusted for age, educational level, socioeconomic level, exercise, drinking, and smoking status showed that BQ chewing is an independent risk factor for the metabolic syndrome. The adjusted OR (95% CI) for male BQ chewers was 1.92 (1.15-3.27) and that of female chewers was 1.60 (1.03-2.50). The study shows that chronic BQ chewing is an independent contributor of metabolic syndrome. TNF-␣, leptin, and leukocyte count are involved in BQ chewing-related metabolic derangements.