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The Pharmaceutical
Journal Vol 267 No 7159 p151-153 |
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Primary care |
DiabetesRepaglinide not a sulphonylurea derivativeFrom Dr A. J. Bragg, MFPM In your article New diabetes drug targets postprandial glucose (PJ, 5 May), nateglinide is described as an amino acid derivative and repaglinide as a sulphonylurea derivative. Whereas your description of nateglinide is correct, I would like to point out that the description of repaglinide as a sulphonylurea derivative is incorrect. Repaglinide does not contain the sulphonylurea moiety that characterises the sulphonylurea class.1,2 It is important to clarify this for your readers, because there are implications in terms of the pharmacology of the drug. Repaglinide has a unique pharmacology arising from the action of the drug at a site distinct from the common site used by both nateglinide and sulphonylureas.1,3,4 Repaglinide, like nateglinide and sulphonylureas, causes insulin release by closure of ATP-sensitive potassium channels in pancreatic beta cells.1–4 However, repaglinide, in contrast to nateglinide and sulphonylureas, does not cause unwanted direct exocytosis of glucagon and growth hormone.3,5 The pharmacological differences between repaglinide and nateglinide/sulphonylureas will be presented at the forthcoming meeting of the American Diabetes Association in Philadelphia. 1. Landgraf R. Meglitinide analogues in the treatment of type 2 diabetes mellitus. Drugs and Aging 2000;17: 411–25. 2. Lebovitz HE. Insulin secretagogues: old and new. Diabetes Rev 1999;7:139–53. 3. Bokvist K, Hoy M, Buschard K, Holst JJ, Thomsen MK, Gromada J. Selectivity of prandial glucose regulators: nateglinide, but not repa-glinide, accelerated exocytosis in rat pancreatic A-calls. Eur J Pharmacol 1999; 386:105–11. 4. M Massi-Benedetti M, Damsbo P. Pharmacology and clinical expertise with repaglinide. Exp Opin Invest Drugs 2000;9:885–98. 5. Bokvist K, Gromada J, Hoy M, Olsen HI, Lindström P, Hansen BS et al. Diabetologia 2000;43(Suppl 1):A187. A. J. Bragg |
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