In addition, expression of MFN2 improved HFD-induced insulin resistance and glucose homeostasis in liver. These findings are consistent with our results that HFDinduced mice showed a molecular shift from fusion towards more fission. Therefore, we next need to carefully examine the changes of mitochondrial dynamics during the development of insulin resistance, so that we could find better ways for when and how to intervene and treat FTY720 obesity and diabetes through targeting mitochondrial dynamics. Retinol binding protein 4 was characterized in 1968 for its transporting role of retinol from storage sites in the liver to extrahepatic tissues. During the beginning of this century, RBP4 was discovered to be an adipokine in that it is produced by adipocytes, induces gluconeogenesis by stimulating phosphoenolpyruvate carboxykinase in the liver and impairs peripheral and hepatic insulin sensitivity. Several RBP4 gene variants are associated with adiposity, the predisposition to visceral accumulation of adipose tissue, insulin secretion or/and insulin resistance and type 2 diabetes. Visceral obesity and liver fat content is associated with high circulating RBP4 concentrations, which relate to metabolic risk factors. A recent cellular study showed that RBP4 consistently stimulates the expression of inflammatory molecules in human retinal capillary and umbilical vein endothelial cells. High RBP4 concentrations are associated with increased atherosclerosis and incident coronary event rates. Several adipokines other than RBP4 and including adiponectin, leptin and resistin can participate importantly in the pathophysiology of rheumatoid arthritis, a prototypic inflammatory disease. In this regard, RBP4 concentrations are also associated with those of inflammatory markers, and successful lifestyle intervention in obese subjects results in reduced RBP4 concentrations that are closely related not only to decreased insulin resistance, triacylglycerol levels and blood pressure but also reduced systemic inflammation. A recent investigation revealed that treatment with tumor necrosis factor-a blockade reduces RBP4 concentrations in ankylosing spondylitis, another inflammatory disorder. Patients with RA sustain a markedly enhanced risk of cardiovascular disease that is effectuated by adverse conventional cardiovascular risk factors, high-grade inflammation and genetic determinants. Nevertheless, atherogenesis in RA remains inadequately elucidated and current recommendations on CVD risk stratification reportedly have important limitations. It is in this context that the need for identifying novel biomarkers of enhanced cardiovascular risk in RA has been raised. The presence of rheumatic disease can impact on the production as well as the relationships of adipokines with cardiometabolic risk and atherogenesis. Lupus alters the effects of leptin on lipid metabolism and atherogenesis. Whereas adiponectin is well recognized for its protective effects against cardiovascular risk in the population at large, adiponectin concentrations associate independently.