Accumulation of fructosyl-lysine and advanced glycation end products in the kidney, retina and peripheral nerve of streptozotocin-induced diabetic rats. (1st December 2003)

• Record Type: Journal Article
• Authors: Karachalias, N.; Babaei-Jadidi, R.; Ahmed, N.; Thornalley, P.J.
• Is Part Of: Biochemical Society transactions. Volume 31:Number 6(2003)
• Page Start: 1423
• Page End: 1425
• Publication Date: 2003-12-01
• Subjects: advanced glycation end product (AGE) -- diabetes -- fructosyl-lysine -- nephropathy -- neuropathy -- retinopathy; Biochemistry -- Congresses; 572
• DOI: 10.1042/bst0311423
• Languages: English
• ISSNs: 0300-5127

Abstract

Abstract : The accumulation of AGEs (advanced glycation end products) in diabetes mellitus has been implicated in the biochemical dysfunction associated with the chronic development of microvascular complications of diabetes – nephropathy, retinopathy and peripheral neuropathy. We investigated the concentrations of fructosyl-lysine and AGE residues in protein extracts of renal glomeruli, retina, peripheral nerve and plasma protein of streptozotocin-induced diabetic rats and normal healthy controls. Glycation adducts were determined by LC with tandem MS detection. In diabetic rats, the fructosyl-lysine concentration was increased markedly in glomeruli, retina, sciatic nerve and plasma protein. The concentrations of N ∊ -carboxymethyl-lysine and N ∊ -carboxyethyl-lysine were increased in glomeruli, sciatic nerve and plasma protein, and N ∊ -carboxymethyl-lysine also in the retina. Hydroimidazolone AGEs derived from glyoxal, methylglyoxal and 3-deoxylglucosone were major AGEs quantitatively. They were increased in the retina, nerve, glomeruli and plasma protein. AGE accumulation in renal glomeruli, retina, peripheral nerve and plasma proteins is consistent with a role for AGEs in the development of nephropathy, retinopathy and peripheral neuropathy in diabetes. High-dose therapy with thiamine and Benfotiamine suppressed the accumulation of AGEs, and is a novel approach to preventing the development of diabetic complications.