Compensatory mechanisms for methylglyoxal detoxification in experimental & clinical diabetes.

ABSTRACT:

Objectives

The deficit of Glyoxalase I (Glo1) and the subsequent increase in methylglyoxal (MG) has been reported to be one the five mechanisms by which hyperglycemia causes diabetic late complications. Aldo-keto reductases (AKR) have been shown to metabolize MG; however, the relative contribution of this superfamily to the detoxification of MG in vivo, particularly within the diabetic state, remains unknown.

Methods

CRISPR/Cas9-mediated genome editing was used to generate a Glo1 knock-out (Glo1^-/-) mouse line. Streptozotocin was then applied to investigate metabolic changes under hyperglycemic conditions.

Results

Glo1^-/- mice were viable and showed no elevated MG or MG-H1 levels under hyperglycemic conditions. It was subsequently found that the

SUBMITTER: Schumacher D 

PROVIDER: S-EPMC6308908 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature