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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.

has been cited by the following article:

• TITLE: Effects of long-term monotherapy with glimepiride vs glibenclamide on glycemic control and macrovascular events in Japanese Type 2 diabetic patients

  AUTHORS: Hirohisa Onuma, Kouichi Inukai, Masaki Watanabe, Yoshikazu Sumitani, Toshio Hosaka, Hitoshi Ishida

  KEYWORDS: Glibenclamide; Glimepiride; Macrovascular Events; HOMA-R/β

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.4 No.1, January 20, 2014

  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.