title: Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats.
abstract: In rats with streptozotocin (STZ) induced diabetes the effect of (watersoluble) thiamine nitrate and of (lipidsoluble) benfotiamine on peripheral nerve function (motor nerve conduction velocity) as well as on the formation of advanced glycation end-products in peripheral nerve tissue was studied. In one group of animals drug administration was started immediately after diabetes induction (prevention study) and in another group two months after diabetes induction (treatment study). Motor nerve conduction velocity (NCV) dropped by 10.5% in diabetic animals, carboxymethyl-lysine (CML) rose to a 3.5fold concentration, deoxyglucosone (3DG)-type AGE formation was increased 5.1fold compared with controls. After three months preventive administration of both vitamin B(1) preparations NCV had increased substantially compared with results in diabetic controls. It was nearly normal after six months with benfotiamine, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfotiamine application but not with thiamine. Furthermore, benfotiamine induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products (CML). Treatment with thiamine did not significantly affect AGE or cmL levels. Unlike treatment with water-soluble thiamine nitrate timely administration of liposoluble prodrug benfotiamine was effective in the prevention of functional damage and of AGE and cmL formation in nerves of diabetic rats.
authors.affiliation: Center of Internal Medicine, Department of Endocrinology and Metabolism, University of Giessen, Rodthohl 6, D-35385 Giessen, Germany. Hilmar.Stracke@innere.med.uni-giessen.de
authors.forename: H
authors.initials: H
authors.lastname: Stracke
authors.forename: H P
authors.initials: HP
authors.lastname: Hammes
authors.forename: D
authors.initials: D
authors.lastname: Werkmann
authors.forename: K
authors.initials: K
authors.lastname: Mavrakis
authors.forename: I
authors.initials: I
authors.lastname: Bitsch
authors.forename: M
authors.initials: M
authors.lastname: Netzel
authors.forename: J
authors.initials: J
authors.lastname: Geyer
authors.forename: W
authors.initials: W
authors.lastname: Köpcke
authors.forename: C
authors.initials: C
authors.lastname: Sauerland
authors.forename: R G
authors.initials: RG
authors.lastname: Bretzel
authors.forename: K F
authors.initials: KF
authors.lastname: Federlin
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006031:Glycosylation / Q000187:drug effects*; D008239:Lysine / Q000031:analogs & derivatives* / Q000378:metabolism; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D010084:Oxidation-Reduction; D010525:Peripheral Nerves / Q000187:drug effects* / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D013831:Thiamine / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D017127:Glycation End Products, Advanced; C048496:N(6)-carboxymethyllysine; D008239:Lysine; D013831:Thiamine; C013835:benphothiamine