Abstract
Thiamine (vitamin B1) is an essential cofactor in most organisms and is required at several stages of anabolic and catabolic intermediary metabolism, such as intracellular glucose metabolism, and is also a modulator of neuronal and neuro-muscular transmission. Lack of thiamine or defects in its intracellular transport can cause a number of severe disorders. Thiamine acts as a coenzyme for transketolase (TK) and for the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism. In particular, TK is able to shift excess fructose-6-phosphate and glycerhaldeyde-3-phosphate from glycolysis into the pentose-phosphate shunt, thus eliminating these potentially damaging metabolites from the cytosol. Diabetes might be considered a thiamine-deficient state, if not in absolute terms at least relative to the increased requirements deriving from accelerated and amplified glucose metabolism in non-insulin dependent tissues that, like the vessel wall, are prone to complications. A thiamine/TK activity deficiency has been described in diabetic patients, the correction of which by thiamine and/or its lipophilic derivative, benfotiamine, has been demonstrated in vitro to counteract the damaging effects of hyperglycaemia on vascular cells. Little is known, however, on the positive effects of thiamine/benfotiamine administration in diabetic patients, apart from the possible amelioration of neuropathic symptoms. Clinical trials on diabetic patients would be necessary to test this vitamin as a potential and inexpensive approach to the prevention and/or treatment of diabetic vascular complications.
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Jansen B, Donath W (1926) Geneeskundig Tijdschrift voor Nederlandsch-Indie 66:1–2 (Reprinted as (1982) The isolation of the anti beri beri vitamin. Nutr Rev 40:53–55)
Frank RAW, Leeper FJ, Luisi BF (2007) Structure, mechanism and catalytic duality of thiamine-dependent enzymes. Cell Mol Life Sci 64:892–905
Bender DA (1999) Optimum nutrition: thiamin, biotin and pantothenate. Proc Nutr Soc 58:427–433
Stryer L (1988) Biochemistry. Freeman WH and Company, New York
Harper C (1979) Wernicke’s encephalopathy, a more common disease than realised (a neuropathological study of 51 cases). J Neurol Neurosurg Psychol 42:226–231
Neufeld EJ, Fleming JC, Tartaglini E, Steinkamp MP (2001) Thiamine-responsive megaloblastic anemia syndrome: a disorder of high-affinity thiamine transport. Blood Cells Mol Dis 27:135–138
Thomson AD (2000) Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke–Korsakoff syndrome. Alcohol Alcohol Suppl 35:2–7
Abbas ZG, Swai AB (1997) Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J 74:803–808
Wu S, Ren J (2006) Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett 394:158–162
Hoyumpa AM Jr, Strickland R, Sheehan JJ, Yarborough G, Nichols S (1982) Dual system of intestinal thiamine transport in humans. J Lab Clin Med 99:701–708
Rindi G (1984) Thiamine absorption by small intestine. Acta Vitaminol Enzymol 6:47–55
Rindi G, Lafarenza U (2000) Thiamine intestinal transport and related issues: recent aspects. PSEBM 224:246–255
Rindi G, Ferrari G (1997) Thiamine transport by human intestine in vitro. Experientia 33:211–213
Lafarenza U, Patrini C, Alvisi C, Faelli A, Licandro A, Rindi G (1997) Thiamine uptake in human intestinal biopsy specimen, including observations from a patient with acute thiamine deficiency. Am J Clin Nutr 66:320–326
Patrini C, Lafarenza U, Gastaldi G, Verri A, Ferrari G, Rindi G (1996) Effects of insulin on thiamine intestinal transport in rat everted jejunal sacs. J Physiol (Lond) 493:100S–101S
Lafarenza U, Gastaldi G, Verri A, Rindi G (1995) Effects of thyroid hormone and insulin on thiamine intestinal transport in vitro. Ital J Gastroenterol 27:129
Fujimara M, Sasakawa S, Itokawa Y, Ikeda K (1964) Affinity of thiamine propyl disulfide-S35 to organs. J Vitaminol (Kyoto) 10:79–87
Fujimara M (1976) Allithiamine and its properties. J Nutr Sci Vitaminol (Tokyo) 22(Suppl):57–62
Baker H, Frank O (1976) Absorption, utilization and clinical effectiveness of allithiamines compared to water-soluble thiamines. J Nutr Sci Vitaminol (Tokyo) 22(Suppl):63–68
Greb A, Bitsch R (1998) Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther 36:216–221
Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH (1997) Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. Eur J Pharmacol 52:319–320
Loew D (1996) Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther 34:47–50
Brownlee M (1994) Glycation and diabetic complications. Diabetes 43:836–841
Schenk G, Duggleby RG, Nixon PF (1998) Properties and functions of the thiamine diphosphate dependent enzyme transketolase. Int J Biochem Cell Biol 30:1297–1318
Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ (2003) Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes 52:2110–2120
Thornalley PJ, Jahan I, Ng R (2001) Suppression of the accumulation of triosephosphates and increased formation of methylglyoxal in human red blood cells during hyperglycaemia by thiamine in vitro. J Biochem 129:543–549
Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M (2003) Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med 9:294–299
Nixon PF, Price J, Norman-Hick M, Williams GM, Kerr RA (1990) The relationship between erythrocyte transketolase activity and the “TPP effect” in Wernicke’s encephalopathy and other thiamine deficiency states. Clin Chim Acta 192:89–98
Horwitt MK, Kreisler O (1949) The determination of early thiamine deficient states by estimation of blood lactate and pyruvate after glucose administration and exercise. J Nutr 37:411–427
Butterworth RF, Kril JJ, Harper CG (1993) Thiamine-dependent enzyme changes in the brains of alcoholics: relationship to the Wernicke–Korsakoff syndrome. Alcohol Clin Exp Res 17:1084–1088
DCCT: The Diabetes Control and Complications Trial Research Group (1993) The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 329:977–986
UK Prospective Diabetes Study Group (1998) Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 352:837–853
Kaiser N, Sasson S, Feener EP, Boukobza-Vardi N, Higashi S, Moller DE, Davidheiser S, Przybylski RJ, King GL (1993) Differential regulation of glucose transport and transporters by glucose in vascular endothelial and smooth muscle cells. Diabetes 42:80–89
Heilig CW, Concepcion LA, Riser BL, Freytag SO, Zhu M, Cortes P (1995) Overexpression of glucose transporters in rat mesangial cells cultured in a normal glucose milieu mimics the diabetic phenotype. J Clin Invest 96:1802–1814
Giardino I, Edelstein D, Brownlee M (1996) Bcl-2 expression or antioxidants prevent hyperglycemia-induced formation of intracellular advanced glycation end products in bovine endothelial cells. J Clin Invest 97:1422–1428
Nishikawa T, Edelstein D, Brownlee M (2000) The missing link: a single unifying mechanism for diabetic complications. Kidney Int 58:S26–S30
Brignardello E, Beltramo E, Molinatti PA, Aragno M, Gatto V, Tamagno E, Danni O, Porta M, Boccuzzi G (1998) Dehydroepiandrosterone protects bovine retinal capillary pericytes against glucose toxicity. J Endocrinol 158:21–26
Podestà F, Romeo G, Liu WH, Krajewski S, Reed JC, Gerhardinger C, Lorenzi M (2000) Bax is increased in the retina of diabetic subjects and is associated with pericyte apoptosis in vivo and in vitro. Am J Pathol 156:1025–1032
Beltramo E, Berrone E, Buttiglieri S, Porta M (2004) Thiamine and benfotiamine prevent increased apoptosis in endothelial cells and pericytes cultured in high glucose. Diabetes Metab Res Rev 20:330–336
Fiordaliso F, Leri A, Cesselli D, Limana F, Safai B, Nadal-Ginard B, Anversa P, Kaistura J (2001) Hyperglycemia activates p53 and p53-regulated denes leading to myocyte cell death. Diabetes 50:2363–2375
Kang BP, Frencher S, Reddy V, Kessler A, Malhotra A, Meggs LG (2003) High glucose promotes mesangial cell apoptosis by oxidant-dependent mechanism. Am J Physiol Renal Physiol 284:F455–F466
Vincent AM, McLean LL, Backus C, Feldman EL (2005) Short-term hyperglycemia produces oxidative damage and apoptosis in neurons. FASEB J 19:638–640
Khera T, Martin J, Riley S, Steadman R, Phillips AO (2006) Glucose enhances mesangial cell apoptosis. Lab Invest 86:566–577
Sustzak K, Raff AC, Schiffer M, Böttinger EP (2006) Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes 55:225–231
Romeo G, Liu WH, Asnaghi V, Kern TS, Lorenzi M (2002) Activation of nuclear factor-kappa B induced by diabetes and high glucose regulates a pro-apoptotic program in retinal pericytes. Diabetes 51:2604–2611
Li W, Liu X, Yanoff M, Cohen S, Ye X (1996) Cultured retinal capillary pericytes die by apoptosis after an abrupt fluctuation from high to low glucose levels: a comparative study with retinal capillary endothelial cells. Diabetologia 39:537–547
Li W, Liu X, He Z, Yanoff M, Jian B, Ye X (1998) Expression of apoptosis regulatory genes by retinal pericytes after rapid glucose reduction. IOVS 39:1535–1543
Ihnat MA, Thorpe JE, Kamat CD, Szabó C, Green DE, Warnke LA, Lacza Z, Cselenyák A, Ross K, Shakir S, Piconi L, Kaltreider RC, Ceriello A (2007) Reactive oxygen species mediate a cellular “memory” of high glucose stress signalling. Diabetologia 50:1523–1531
Cagliero E, Maiello M, Boeri D, Roy S, Lorenzi M (1988) Increased expression of basement membrane components in human endothelial cells cultured in high glucose. J Clin Invest 82:735–738
Roy S, Sala R, Cagliero E, Lorenzi M (1990) Overexpression of fibronectin induced by diabetes or high glucose: phenomenon with a memory. Proc Natl Acad Sci USA 87:404–408
Risso A, Mercuri F, Quagliaro L, Damante G, Ceriello A (2001) Intermittent high glucose enhances apoptosis in human umbilical vein endothelial cells in culture. Am J Physiol Endocrinol Metab 281:E924–E930
Quagliaro L, Piconi L, Assaloni R, Martinelli L, Motz E, Ceriello A (2003) Intermittent high glucose enhances apoptosis relate to oxidative stress in human umbilical vein endothelial cells. Diabetes 52:2795–2804
Piconi L, Quagliaro L, Assaloni R, Da Ros R, Maier A, Zuodar G, Ceriello A (2006) Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction. Diab Met Res Rev 22:198–203
Kowluru RA, Abbas SN, Odenbach S (2004) Reversal of hyperglycemia and diabetic nephropathy: effect of reinstitution of good metabolic control on oxidative stress in the kidney of diabetic rats. J Diabet Complications 18:282–288
Bonora E, Muggeo M (2001) Postprandial blood glucose as a risk factor for cardiovascular disease in type II diabetes: the epidemiological evidence. Diabetologia 44:2107–2114
Shichiri M, Kishikawa H, Ohkubo Y, Wake N (2000) Long-term results of the Kumamoto study on optimal diabetes control in type 2 diabetic patients. Diabetes Care 23(suppl.2):B21–B29
Van Ballegooie E, Hooymans JM, Timmerman Z, Reitsma WD, Sluiter WJ, Schweitzer NM, Doorenbos H (1984) Rapid deterioration of diabetic retinopathy during treatment with continuous subcutaneous insulin infusion. Diabetes Care 7:236–242
Dandona P, Bolger JP, Boag F, Fonesca V, Abrams JD (1985) Rapid development and progression of proliferative retinopathy after strict diabetic control. BMJ 290:885–896
Dahl-Jorgensen K, Brinchmann-Hansen O, Hanssen KF, Sandvik L, Aagenages O (1985) Rapid tightening of blood glucose levels leads to transient deterioration of retinopathy in insulin dependent diabetes mellitus. BMJ 290:811–815
Engerman RL, Kern TS (1987) Progression of incipient diabetic retinopathy during good glycaemic control. Diabetes 36:808–812
Williamson JR, Chang K, Frangos M, Hasan KS, Ido Y, Kawamura T, Nyengaard JR, Van Den Enden M, Kilo C, Tilton RG (1993) Hyperglycemic pseudoypoxia and diabetic complications. Diabetes 42:801–813
Lee AY, Chung SS (1999) Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J 13:23–30
Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 414:813–820
Engerman RL, Kern TS, Larson ME (1994) Nerve conduction and aldose reductase inhibition during 5 years of diabetes or galactosaemia in dogs. Diabetologia 37:141–144
Baynes JW (1991) Role of oxidative stress in development of complications in diabetes. Diabetes 40:405–412
Giardino I, Edelstein D, Brownlee M (1994) Nonenzymatic glycosylation in vitro and in bovine endothelial cells alters basic fibroblast growth factor activity. A model for intracellular glycosylation in diabetes. J Clin Invest 94:110–117
Charonis AS, Reger LA, Dege JE, Kouzi-Koliakos K, Furcht LT, Wohlhueter RM, Tsilibary EC (1990) Laminin alterations after in vitro nonenzymatic glycosylation. Diabetes 39:807–814
Beltramo E, Pomero F, Allione A, D’Alù F, Ponte E, Porta M (2002) Pericyte adhesion is impaired on extracellular matrix produced by endothelial cells in high hexose concentrations. Diabetologia 45:416–419
Beltramo E, Buttiglieri S, Pomero F, Allione A, D’Alù F, Ponte E, Porta M (2003) A study of capillary pericyte viability on extracellular matrix produced by endothelial cells in high glucose. Diabetologia 46:409–415
Doi T, Vlassara H, Kirstein M, Yamada Y, Striker GE, Striker LJ (1992) Receptor-specific increase in extracellular matrix production in mouse mesangial cells by advanced glycosylation end products is mediated via platelet-derived growth factor. Proc Natl Acad Sci USA 89:2873–2877
Schmidt AM, Hori O, Chen JX, Li JF, Crandall J, Zhang J, Cao R, Yan SD, Brett J, Stern D (1995) Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes. J Clin Invest 96:1395–1403
Skolnik EY, Yang Z, Makita Z, Radoff S, Kirstein M, Vlassara H (1991) Human and rat mesangial cell receptors for glucose-modified proteins: potential role in kidney tissue remodelling and diabetic nephropathy. J Exp Med 174:931–939
Hammes HP, Martin S, Federlin K, Geisen K, Brownlee M (1991) Aminoguanidine treatment inhibits the development of experimental diabetic retinopathy. Proc Natl Acad Sci USA 88:11555–11558
Koya D, King GL (1998) Protein kinase C activation and the development of diabetic complications. Diabetes 47:859–866
Koya D, Jirousek MR, Lin YW, Ishii H, Kuboki K, King GL (1997) Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. J Clin Invest 100:115–126
Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M (2000) Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature 404:787–790
Ishii H, Jirousek MR, Koya D, Takagi C, Xia P, Clermont A, Bursell SE, Kern TS, Ballas LM, Heath WF, Stramm LE, Feener EP, King GL (1996) Amelioration of vascular dysfunctions in diabetic rats by an oral PKC beta inhibitor. Science 272:728–731
Koya D, Haneda M, Nakagawa H, Isshiki K, Sato H, Maeda S, Sugimoto T, Yasuda H, Kashiwagi A, Ways DK, King GL, Kikkawa R (2000) Amelioration of accelerated diabetic mesangial expansion by treatment with a PKC beta inhibitor in diabetic db/db mice, a rodent model for type 2 diabetes. FASEB J 14:439–447
Schleicher ED, Weigert C (2000) Role of the hexosamine biosyntetic pathway in diabetic nephropaty. Kidney Int 77:S13–S18
Du XL, Edelstein D, Rossetti L, Fantus IG, Goldberg H, Ziyadeh F, Wu J, Brownlee M (2000) Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. Proc Natl Acad Sci USA 97:12222–12226
DeRubertis FR, Craven PA, Melhem MF, Salah EM (2004) Attenuation of renal injury in db/db mice overexpressing superoxide dismutase: evidence for reduced superoxide-nitric oxide interaction. Diabetes 53:762–768
Du X, Matsumura T, Edelstein D, Rossetti L, Zsengellér Z, Szabó C, Brownlee M (2003) Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest 108:341–1057
La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M (1996) Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia 39:1263–1268
Booth AA, Khalifah RG, Hudson BG (1996) Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation end-products: comparison with aminoguanidine. Biochem Biophis Res Commun 220:113–119
Thornalley PJ, Jahan I, Ng R (2001) Suppression of the accumulation of triosephosphates and increased formation of methylglyoxal in human red blood cells during hyperglycaemia by thiamine in vitro. Jpn J Biochem 129:543–549
Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M (2001) Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol 38:135–138
Bakker SJ, Heine RJ, Gans RO (1997) Thiamine may indirectly act as an antioxidant. Diabetologia 40:741–742
Hsu GM, Chow BF (1960) Effect of thiamine deficiency on glutathione contents of erythrocytes and tissues in the rat. Proc Soc Exp Biol Med 104:178–180
Singh R, Barden A, Mori T, Beilin L (2001) Advanced glycation end-products: a review. Diabetologia 44:129–146
Berrone E, Beltramo E, Solimine C, Ape AU, Porta M (2006) Regulation of intracellular glucose and polyol pathway by thiamine and benfotiamine in vascular cells cultured in high glucose. J Biol Chem 281:9307–9313
Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, Jacob T (2001) Thiamine reverses hyperglycemia-induced dysfunctions in cultured endothelial cells. Surgery 130:851–858
Gadau S, Emanueli C, Van Linthout S, Graiani G, Todaro M, Meloni M, Campesi I, Invernici G, Spillmann F, Ward K, Madeddu P (2006) Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis. Diabetologia 49:405–420
Marchetti V, Menghini R, Rizza S, Vivanti A, Feccia T, Lauro D, Fukamizu A, Lauro R, Federici M (2006) Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via Akt/FoxO signaling. Diabetes 55:2231–2237
Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Köpcke W, Sauerland C, Bretzel RG, Federlin KF (2001) Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes 109:330–336
Ceylan-Isik AF, Wu S, Li Q, Li SY, Ren J (2006) High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus. J Appl Physiol 100:150–156
Babaei-Jadidi R, Karachalias N, Kupich C, Ahmed N, Thornalley PJ (2004) High-dose thiamine therapy counters dyslipidaemia in streptozotocin-induced diabetic rats. Diabetologia 47:2235–2246
Hilbig R, Rahmann H (1998) Comparative autoradiographic investigations on the tissue distribution of benfotiamine versus thiamine in mice. Arzneimittelforschung 48:461–468
Yenilmez A, Ozçifçi M, Aydin Y, Turgut M, Uzuner K, Erkul A (2006) Protective effect of high-dose thiamine (B1) on rat detrusor contractility in streptozotocin-induced diabetes mellitus. Acta Diabetol 43:103–108
Frank T, Bitsch R, Maiwald J, Stein G (2000) High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfotiamine. Eur J Clin Pharmacol 56:251–257
Woelk H, Lehrl S, Bitsch R, Kopcke W (1998) Benfotiamine in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAPI Study). Alcohol Alcohol 33:631–638
Stracke H, Lindemann A, Federlin K (1996) A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes 104:311–316
Haupt E, Ledermann H, Kopcke W (2005) Benfotiamine in the treatment of diabetic polyneuropathy—a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther 43:71–77
Saito N, Kimura M, Kuchiba A, Itokawa Y (1987) Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol 33:421–430
Valerio G, Franzese A, Poggi V, Patrini C, Laforenza U, Tenore A (1999) Lipophilic thiamine treatment in long-standing insulin-dependent diabetes mellitus. Acta Diabetol 36:73–76
Jermendy G (2006) Evaluating thiamine deficiency in patients with diabetes. Diab Vasc Dis Res 3:120–121
Thornalley PJ, Babaei-Jadidi R, Al Ali H, Rabbani N, Antonysunil A, Larkin J, Ahmed A, Rayman G, Bodmer CW (2007) High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia 50:2164–2170
Stepuro II, Piletskaya TP, Stepuro VI, Maskevich SA (1997) Thiamine oxidative transformations catalyzed by copper ions and ascorbic acid. Biochemistry 62:1409–1414
Stirban A, Negrean M, Stratmann B, Gawlowski T, Horstmann T, Götting C, Kleesiek K, Mueller-Roesel M, Koschinsky T, Uribarri J, Vlassara H, Tschoepe D (2006) Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care 29:2064–2071
Arora S, Lidor A, Abularrage CJ, Weiswasser JM, Nylen E, Kellicut D, Sidawy AN (2006) Thiamine (vitamin B1) improves endothelium-dependent vasodilatation in the presence of hyperglycemia. Ann Vasc Surg 20:653–658
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Beltramo, E., Berrone, E., Tarallo, S. et al. Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications. Acta Diabetol 45, 131–141 (2008). https://doi.org/10.1007/s00592-008-0042-y
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DOI: https://doi.org/10.1007/s00592-008-0042-y