A number of studies have suggested that vitamin B6 maybe effective inprevent-ing the adverse effects of poor glycemic control that lead to the development of the complications of diabetes mellitus (Jain and Lim, 2001). Many of these effects are mediated by nonenzymic glycation of proteins. Target proteins include the following:
1. hemoglobin, forming hemoglobin A1c, which has a reduced capacity to transport oxygen;
2. a-crystallin in the lens of the eye, reducing its transparency and leading to the development of cataracts;
4. apolipoprotein B, resulting in impaired receptor-mediated clearance of low-density lipoproteins by the liver and increased macrophage uptake, and thus a factor in the development of atherosclerosis.
Administration of vitamin B6 to genetically diabetic mice has been reported to reduce the thickening of the glomerular basement membrane (Hayakawa and Shibata, 1991). In men with non-insulin-dependent diabetes, supplements of 150 mg per day led to a significant reduction in glycated hemoglobin and improved oxygen transport capacity, although there was no change in glycemic control (Solomon and Cohen, 1989).
Pyridoxamine is a potent inhibitor of the irreversible rearrangement of the initial product of reversible glycation to the advanced glycation end-product. Such inhibitors of this reaction are collectively known as amadorins, and the name pyridorin has been coined for pyridoxamine used in this way (Khalifah et al., 1999). Pyridoxamine also inhibits protein modification caused by lipid peroxides; in both cases, it seems to act by trapping carbonyl compounds formed as intermediates (Onorato et al., 2000; Voziyan et al., 2002).
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