Diabetes

杂志介绍

Diabetes杂志介绍

《Diabetes》是一本以English为主的未开放获取国际优秀期刊，中文名称糖尿病，本刊主要出版、报道医学-ENDOCRINOLOGY & METABOLISM领域的研究动态以及在该领域取得的各方面的经验和科研成果，介绍该领域有关本专业的最新进展，探讨行业发展的思路和方法，以促进学术信息交流，提高行业发展。该刊已被国际权威数据库SCIE收录，为该领域相关学科的发展起到了良好的推动作用，也得到了本专业人员的广泛认可。该刊最新影响因子为6.2，最新CiteScore 指数为12.5。

本刊近期中国学者发表的论文主要有：

• Genetic Regulation of Pigment Epithelium-Derived Factor (PEDF): An Exome-Chip Association Analysis in Chinese Subjects With Type 2 Diabetes.

  Author: Cheung CYY^1,2, Lee CH¹, Tang CS³, Xu A^1,2,4,5, Au KW¹, Fong CHY¹, Ng KKK¹, Kwok KHM¹, Chow WS¹, Woo YC¹, Yuen MMA¹, Hai J¹, Tan KCB¹, Lam TH⁶, Tse HF^7,8, Sham PC^9,10,11, Lam KSL^7,2,4.

• Targeting the CDA1/CDA1BP1 Axis Retards Renal Fibrosis in Experimental Diabetic Nephropathy.

  Author: Chai Z¹, Wu T², Dai A², Huynh P², Koentgen F³, Krippner G⁴, Ren S^2,5, Cooper ME².

• HSPA12A Is a Novel Player in Nonalcoholic Steatohepatitis via Promoting Nuclear PKM2-Mediated M1 Macrophage Polarization.

  Author: Kong Q¹, Li N¹, Cheng H¹, Zhang X², Cao X¹, Qi T¹, Dai L¹, Zhang Z³, Chen X¹, Li C⁴, Li Y⁵, Xue B⁶, Fang L⁷, Liu L⁸, Ding Z⁹.

• Endoplasmic Reticulum-Associated Degradation (ERAD) Has a Critical Role in Supporting Glucose-Stimulated Insulin Secretion in Pancreatic β-Cells.

  Author: Hu Y¹, Gao Y¹, Zhang M¹, Deng KY², Singh R³, Tian Q¹, Gong Y¹, Pan Z¹, Liu Q¹, Boisclair YR³, Long Q⁴.

英文介绍

Diabetes杂志英文介绍

Diabetes publishes original research about the physiology and pathophysiology of diabetes mellitus. Submitted manuscripts can report any aspect of laboratory, animal, or human research. Emphasis is on investigative reports focusing on areas such as the pathogenesis of diabetes and its complications, normal and pathologic pancreatic islet function and intermediary metabolism, pharmacological mechanisms of drug and hormone action, and biochemical and molecular aspects of normal and abnormal biological processes. Studies in the areas of diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus are not published.