Vitamin diabetic complications

Ceriello, A., Giugliano, D., Quatrarto, A., Donzella, C., Dipalo, G., and Lefebvre, P.J. 1991. Vitamin E Reduction of Protein Glycosylation in Diabetes. New Prospect for Prevention of Diabetic Complications Diabetes Care. 14 68-72. 

Recent studies clarified novel functions of vitamin Bg forms. All forms are strong quenchers of singlet oxygen. Pyridoxamine reduces the incidence of diabetic complications. PLP prevents the progression of diabetic nephropathy. 

Thornalley, P.J., 2005. The potential role of thiamine (vitamin Bi) in diabetic complications. Current Diabetes Reviews. 1 287-298. 

Not surprisingly, the reducing agent ascorbic acid (vitamin C) has certain chemical features common with the reducing sugar glucose. Briefly, observations made on the effect of ascorbic acid supplementation in diabetic individuals, the prooxidant ability of ascorbic acid in vitro, and the ability of ascorbic acid to modify proteins are of interest in the context of the development of diabetic complications. 

It has been proposed that the development of the complications of diabetes mellitus may be linked to oxidative stress and therefore might be attenuated by antioxidants such as vitamin E. Furthermore, it is discussed that glucose-induced vascular dysfunction in diabetes can be reduced by vitamin E treatment due to the inactivation of PKC. Cardiovascular complications are among the leading causes of death in diabetics. In addition, a postulated protective effect of vitamin E (antioxidants) on fasting plasma glucose in type 2 diabetic patients is also mentioned but could not be confirmed in a recently published triple-blind, placebo-controlled clinical trial [3]. To our knowledge, up to now no clinical intervention trials have tested directly whether vitamin E can ameliorate the complication of diabetes. 

Vitamin B6 (pyridoxine) and its derivative pyridoxamine are apparently able to inhibit superoxide production, reduce lipid peroxidation and glycosylation in high glucose-exposed erythrocytes [353], It was suggested that the suppression of oxidative stress in erythrocytes may be a new mechanism by which these natural compounds inhibit the development of complication in diabetes mellitus. 

A number of studies have suggested that vitamin Bg may he effective in preventing 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 hy nonenzymic glycation of proteins. Target proteins include the following ... 

Weller and Fichtenbaum (WIO) followed the urinary excretion of xanthurenic acid in 48 arteriosclerotic patients after an oral dose of 10 g DL-tryptophan. On the basis of urinary xanthurenic acid above the range of normal controls, 29% of these patients showed a deficiency of vitamin Bg. Using the same criterion, pyridoxine deficiency was found in 60% of diabetic patients with arteriosclerotic complications. 

Because of the lipase deficiency, fat-soluble vitamin (A, D, E, and K) deficiencies may occur. Whether lipase activity or bile acids (e.g., in micelle formation) are involved in fat-soluble vitamin absorption with steatorrhea is unclear. Vitamin and zinc deficiencies also may occur as aresult of pancreatic enzyme deficiency. Although pancreatic involvement is predominantly exocrine in nature, insulin deficiency with glucose intolerance also occurs in CF patients, especially as they advance in age. Carbohydrate intolerance is characterized by low insulin concentrations and enhanced peripheral sensitivity to insulin but not by the presence of islet cell or anti-insulin antibodies. Carbohydrate intolerance in CF is not usually associated with the ketosis as commonly occurs in type 1 diabetes. This complication involves an increase in the number of insulin receptors with decreased affinity for insulin. Despite a concomitant increase in tissue affinity for insulin, 8% of CF children over 12 years of age require insulin therapy. 

Jain, S.K., 2007. Vitamin Bg (pyridoxamine) supplementation and complications of diabetes. Metabolism Clinical and Experimental. 56 168-171. 

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