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 JDM  Vol.4 No.1 , February 2014
Effects of long-term monotherapy with glimepiride vs glibenclamide on glycemic control and macrovascular events in Japanese Type 2 diabetic patients
Abstract: We investigated whether long-term glimepiride (GP) monotherapy improves insulin resistance and exerts a beneficial effect on beta cell function, as compared with glibenclamide (GC). One hundred Japanese Type 2 diabetic patients were randomly assigned to the GP (n = 50) or the GC (n = 50) group. During a 5-year monitoring period, patients received the indicated SU monotherapy, while changes in SU doses were allowed as needed to maintain HbA1C below 7.0%. The GC group, in parallel with fasting insulin, showed a rapid homeostatic model assessment (HOMA)-R increase and maintained a high HOMA-R level. In contrast, HOMA-R in the GP group decreased continuously, from 2.9 at baseline to 1.8 at study completion. In the GC group, HOMA-b was markedly increased in the first 6 months, then gradually decreased through 18 months. While the HOMA-β elevation in the GP group was more moderate than that in the GC group, HOMA-β levels were maintained with a slight decrease. The cumulative macrovascular disease outcome was 1 for the GP and 7 for the GC group, showing a significant difference. These results suggest that glimepiride monotherapy markedly improved HOMA-R with moderate insulin stimulation, which may account for the difference in macrovascular disease development as compared with the group receiving glibenclamide.
Cite this paper: Onuma, H. , Inukai, K. , Watanabe, M. , Sumitani, Y. , Hosaka, T. and Ishida, H. (2014) Effects of long-term monotherapy with glimepiride vs glibenclamide on glycemic control and macrovascular events in Japanese Type 2 diabetic patients. Journal of Diabetes Mellitus, 4, 33-37. doi: 10.4236/jdm.2014.41006.
References

[1]   Rosak, C. (2002) The pathophysiologic basis of efficacy and clinical experience with the new oral antidiabetic agents. Journal of Diabetes and its Complications, 16, 123-132. http://dx.doi.org/10. 1016/S1056-8727(01)00207-0

[2]   Rosenstock, J., Schneider, J., Samols, E. and Mushmore, D.B. (1996) Glimepiride, a new once-daily sulfonylurea. Diabetes Care, 19, 1194-1199. http://dx.doi.org/10.2337/diacare.19.11.1194

[3]   Rosskamp, R., Wernicke-Panten, K. and Draeger, E. (1996) Clinical profile of the novel sulfonylurea glimepiride. Diabetes Research and Clinical Practice, 31, S33-S42. http://dx.doi.org/10.1016/0168-8227(96)01228-4

[4]   Inukai, K., Watanabe, M., Nakashima, Y., Sawa, T., Takata, N., Tanaka, M., Kashiwabara, H., Yokota, K., Suzuki, M., Kurihara, S., Awata, T. and Katayama, S. (2005) Efficacy of glimepiride in Japanese Type 2 diabetic subjects. Diabetes Research and Clinical Practice, 68, 250-257. http://dx.doi.org/10. 1016/j.diabres.2004.10.002

[5]   Haupt, A., Kausch, C., Dahl, D., Bachmann, O., Stumvoll, M., Haring, H.U. and Matthaei, S. (2002) Effect of glimepiride on insulin-stimulated glycogen synthesis in cultured human skeletal muscle cells; a comparison to glibenclamide. Diabetes Care, 25, 2129-2132. http://dx.doi.org/10.1016/j.diabres. 2004.10.002

[6]   Muller, G. and Wied, S. (1993) The sulfonylurea drug, glimepiride, stimulates glucose transport, glucose transporter translocation and dephosphorylation in insulin-resistant rat adipocytes in vitro. Diabetes, 42, 1852-1867. http://dx.doi.org/10.2337/diab.42.12.1852

[7]   Inukai, K., Watanabe, M., Nakashima, Y., Takata, N., Isoyama, A., Sawa, T., Kurihara, S., Awata, T. and Katayama, S, (2005) Glimepiride Enhances Intrinsic Peroxisome Proliferator Activated Receptor-g Activity in 3T3-L1 Adipocytes. Biochemical and Biophysical Research Communications, 328, 484-490. http://dx.doi.org/10.1016/j.bbrc.2004.12.190

[8]   Fukuen, S., Iwaki, M., Yasui, A., Makishima, M., Matsuda, M. and Shimomura, I. (2005) Sulphonylurea agents exhibit peroxisome proliferator-activated receptor gamma agonistic activity. The Journal of Biological Chemistry, 280, 23653-23659. http://dx.doi.org/10.1074/jbc.M412113200

[9]   Marco, S., Podvinec, M., Roth, A., Hug, H., Kersten, S., Albrecht, H., Schwede, T., Meyer, U.A. and Rücker, C. (2007) Sulphonylureas and glinide exhibit peroxisome prolierator-activated receptor g activity: A combined virtual screening and biological assay approach. Molecular Pharmacology, 71, 398-406.

[10]   Müller, G., Hartz, D., Pünter, J., Okonomopulos, R. and Kramer, W. (1994) Differential interaction of glimepiride and glibenclamide with the beta-cell sulfonylurea receptor I Binding characteristics. Biochimica et Biophysica Acta, 1192, 267-277. http://dx.doi.org/10.1016/0005-2736(94)90177-5

[11]   Rendell, M. (2004) The role of sulfonylurea in the management of Type 2 diabetes mellitus. Drugs, 64, 1339-1358. http://dx.doi.org/10.2165/00003495-200464120-00006

[12]   Feinb?ck, C., Luger, A., Klinger, A., Egger, T., Bielesz, G.K., Winkler, F., Siebenhofer, A., Grossch?dl, F., Frank, E. and Irsigler, K. (2003) Prospective multicentre trial comparing the efficacy of and compliance with, glimepiride or acarbose treatment in patients with Type 2 diabetes not controlled with diet alone. Diabetes, nutrition & metabolism, 16, 214-221.

[13]   Korytkowski, M., Thomas, A., Reid, L., Tedesco, M.B., Gooding, W.E. and Gerich, L. (2002) Glimepiride improves both first and second phases of insulin secretion in Type 2 diabetes. Diabetes Care, 25, 1607-1611. http://dx.doi.org/10.2337/diacare.25.9.1607

[14]   Muller, G.., Satoy, Y. and Geisen, K. (1995) Extrapancreatic effects of sulfonylurea-A comparison between glimepiride and conventional sulfonylurea. Diabetes Research and Clinical Practice, 28, S115-S137. http://dx.doi.org/10.1016/0168-8227(95)01089-V

[15]   UK Prospective Diabetes Study Group (1995) Overview of 6 year’s therapy of Type 2 diabetes: A progressive disease. Diabetes, 44, 1249-1258. http://dx.doi.org/10.2337/diab.44.11.1249

[16]   Holman, R.R., Paul, S.K., Bethel, M.A., Matthews, D.R. and Neil, H.A. (2008) 10-year follow-up of intensive glucose control in Type 2 diabetes. The New England Journal of Medicine, 359, 1577-1589. http://dx.doi.org/10.1056/NEJMoa0806470

[17]   Miyauchi, H., Minamino, T., Tateno, K., Kunieda, T., Toko, H. and Komuro, I. (2004) Akt negatively regulates the in vitro lifespan of human endothelial cells via a p53/ p21-dependent pathway. The EMBO Journal, 23, 212-220. http://dx.doi.org/10.1056/NEJMoa0806470

[18]   Sato, T., Nishida, H., Miyazaki, M. and Nakaya, H. (2006) Effects of sulfonylureas on mitochondrial ATP-sensitive K+ channels in cardiac myocytes: Implications for sulfonylurea controversy. Diabetes/Metabolism Research and Reviews, 22, 341-347. http://dx.doi.org/10.1002/dmrr.621

 
 
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