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Bolton, W.K., Cattran, D. C., Williams, M.E., Adler, S.G., Appel, G.B., Cartwright, K., Foiles, P.G., Freedman, B.I., Raskin, P., Ratner, R.E., Spinowitz, B.S., Whittier, F.C. and Wuerth, J.P. (2004) Randomized Trial of an Inhibitor of Formation of Advanced Glycation End Products in Diabetic Nephropathy. American Journal of Nephrology, 24, 32-40. http://dx.doi.org/10.1159/000075627

has been cited by the following article:

• TITLE: Effects of AGE Inhibition with Aminoguanidine in a Diabetic db/db Mouse Wound Model

  AUTHORS: Margrete Berdal, Trond Jenssen

  KEYWORDS: Diabetes, Wound, Glycation, Inhibition, Animals

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.4 No.2, May 6, 2014

  ABSTRACT: Advanced glycation end products (AGEs) react non-enzymatically with tissue proteins to form irreversible structures involved in atherosclerosis, nephropathy, retinopathy, neuropathy, and wound healing. Studies on AGE-inhibitors have demonstrated possible prevention of diabetes complications. The present open label study was conducted on aminoguanidine (AGu), an inhibitor of AGE-formation, to examine potential effects on wound healing in diabetes type 2-like db/db mice during 5 - 6 weeks. The animals were divided into 4 groups: AGu from the day of wounding (day 0) topically and/or systemically in drinking water (1 g/L; group 1, n = 13); AGu 1 g/L in drinking water from 7 weeks prior to day 0 (group 2, n = 21); AGu 5 g/L in drinking water from 9 - 11 weeks prior to day 0 (group 3, n = 6); placebo controls (group 4, n = 8). Results: Glycated hemoglobin (A1C) was significantly lower in group 3 compared to the other groups (P P = 0.01; weight-change, P = 0.04, both for linear trend across groups 4, 2, and 3, respectively). Even so, percentage wound closure was not improved in the AGu-treated groups compared to controls (P ≥ 0.8).