The Critical Role of

The discovery of increased formation of methylglyoxal (MG) by cell metabolism in high glucose concentration in vitro suggested possible relevance to diabetes and di-abetes complications (1,2). MG is the precursor of quantitatively important advanced glycation end prod-ucts (AGEs) of protein and DNA- and MG-derived AGEs increase in experimental and clinical diabetes (3,4). In-creased MG and its metabolism by glyoxalase 1 (Glo1) was linked to clinical microvascular complications (ne-phropathy, retinopathy, and neuropathy) (5). Current clinical treatment decreasing MG and MG-derived AGEs, such as insulin lispro (6,7), has some clinical benefit in diabetic nephropathy (8), although the decrease in MG-derived AGE exposure is minor—;17 % (7). Greater benefits may be achieved with specific and effective anti