Dapagliflozin: A sodium glucose cotransporter 2 inhibitor in development for type 2 diabetes

被引:18
作者
Tahrani A.A. [1 ,2 ]
Barnett A.H. [1 ,2 ]
机构
[1] Heart of England NHS Foundation Trust, Birmingham Heartlands Hospital, Birmingham B9 5SS, Bordesley Green East
[2] University of Birmingham, Birmingham
关键词
dapagliflozin; diabetes; inhibitor; SGLT2;
D O I
10.1007/s13300-010-0007-3
中图分类号
学科分类号
摘要
Type 2 diabetes mellitus (T2DM) is a growing worldwide epidemic. Patients face lifelong therapy to control hyperglycemia and prevent the associated complications. There are many medications, with varying mechanisms, available for the treatment of T2DM, but almost all target the declining insulin sensitivity and secretion that are associated with disease progression. Medications with such insulin-dependent mechanisms of action often lose efficacy over time, and there is increasing interest in the development of new antidiabetes medications that are not dependent upon insulin. One such approach is through the inhibition of renal glucose reuptake. Dapagliflozin, the first of a class of selective sodium glucose cotransporter 2 inhibitors, reduces renal glucose reabsorption and is currently under development for the treatment of T2DM. Here, we review the literature relating to the preclinical and clinical development of dapagliflozin. © 2010 Springer Healthcare.
引用
收藏
页码:45 / 56
页数:11
相关论文
共 51 条
  • [1] International Diabetes Federation, IDF Diabetes Atlas
  • [2] World Health Organization, Global Strategy on Diet, Physical Activity and Health
  • [3] Weyer C., Tataranni P.A., Bogardus C., Pratley R.E., Insulin resistance and insulin secretory dysfunction are independent predictors of worsening of glucose tolerance during each stage of type 2 diabetes development, Diabetes Care, 24, pp. 89-94, (2001)
  • [4] Defronzo R.A., Pathogenesis of type 2 diabetes mellitus, Med Clin North Am, 88, pp. 787-835, (2004)
  • [5] Tabak A.G., Jokela M., Akbaraly T.N., Brunner E.J., Kivimaki M., Witte D.R., Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study, Lancet, 373, pp. 2215-2221, (2009)
  • [6] Bonner-Weir S., Islet growth and development in the adult, J Mol Endocrinol, 24, pp. 297-302, (2000)
  • [7] Goldstein B.J., Insulin resistance as the core defect in type 2 diabetes mellitus, Am J Cardiol, 90, (2002)
  • [8] Jiang G., Zhang B.B., Glucagon and regulation of glucose metabolism, Am J Physiol Endocrinol Metab, 284, (2003)
  • [9] Nichols G.A., Arondekar B., Herman W.H., Complications of dysglycemia and medical costs associated with nondiabetic hyperglycemia, Am J Manag Care, 14, pp. 791-798, (2008)
  • [10] Fowler M.J., Microvascular and macrovascular complications of diabetes, Clin Diabetes, 26, pp. 77-82, (2008)