Glyoxalase-1 overexpression partially prevents diabetes-induced impaired arteriogenesis in a rat hindlimb ligation model

Olaf Brouwers, Liang Yu, Petra Niessen, Jos Slenter, Karolien Jaspers, Allard Wagenaar, Mark Post, Toshio Miyata, Walter Backes, Coen Stehouwer, Maya Huijberts, Casper Schalkwijk*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

7 Citations (Web of Science)


We hypothesize that diabetes-induced impaired collateral formation after a hindlimb ligation in rats is in part caused by intracellular glycation and that overexpression of glyoxalase-I (GLO-I), i.e. the major detoxifying enzyme for advanced-glycation-endproduct (AGE) precursors, can prevent this. Wild-type and GLO-I transgenic rats with or without diabetes (induced by 55 mg/kg streptozotocin) were subjected to ligation of the right femoral artery. Laser Doppler perfusion imaging showed a significantly decreased blood perfusion recovery after 6 days in the diabetic animals compared with control animals, without any effect of Glo1 overexpression. In vivo time-of-flight magnetic resonance angiography at 7-Tesla showed a significant decrease in the number and volume of collaterals in the wild-type diabetic animals compared with the control animals. Glo1 overexpression partially prevented this decrease in the diabetic animals. Diabetes-induced impairment of arteriogenic adaptation can be partially rescued by overexpressing of GLO-I, indicating a role of AGEs in diabetes-induced impaired collateral formation.
Original languageEnglish
Pages (from-to)627-630
JournalGlycoconjugate Journal
Issue number4
Publication statusPublished - Aug 2016


  • Glyoxalase-I
  • Diabetes
  • Arteriogenesis
  • Magnetic resonance angiography
  • Advanced glycation end-products

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