Objective To analyze the central effect of Qi-Yin Deficiency Syndrome (QYDS) scoring in clinical trials of diabetes.Methods Dispensation degree analysis and multiple linear regression analysis were adopted to compare the differences of central effects among the Qi-Yin deficiency syndrome scoring,fasting plasma glucose (FPG) level and 2-hour postprandial blood sugar (2 hPG)level before and after treatment in the suited databases from two phase Ⅲclinical trials of type two diabetes performed in 2004～2005.Results The variation coefficients of QYDS scoring treated with drug A and drug B varied from one tenth to half times of those of FPG and 2 hPG levels before and after treatment.And the influence of centers on QYDS is weaker than those on blood sugar levels (FPG &2 hPG) either referring to the numbers of significant centers or referring to the absolute values of standard regression coefficients in multiple linear regression equation.Conclusion There exists a central effect in QYDS scoring before and after treatment,and the central effect of QYDS scoring is weaker than that of blood sugar levels (FPG &2 hPG) in clinical trials of diabetes.

Zinc levels are high in pancreatic β-cells, and zinc is involved in the synthesis, processing and secretion of insulin in these cells. However, precisely how cellular zinc homeostasis is regulated in pancreatic β-cells is poorly understood. By screening the expression of 14 Slc39a metal importer family member genes, we found that the zinc transporter Slc39a5 is significantly down-regulated in pancreatic β-cells in diabetic db/db mice, obese ob/ob mice and high-fat diet-fed mice. Moreover, β-cell-specific Slc39a5 knockout mice have impaired insulin secretion. In addition, Slc39a5-deficient pancreatic islets have reduced glucose tolerance accompanied by reduced expression of Pgc-1α and its downstream target gene Glut2. The down-regulation of Glut2 in Slc39a5-deficient islets was rescued using agonists of Sirt1, Pgc-1α and Ppar-γ. At the mechanistic level, we found that Slc39a5-mediated zinc influx induces Glut2 expression via Sirt1-mediated Pgc-1α activation. These findings suggest that Slc39a5 may serve as a possible therapeutic target for diabetes-related conditions.