Benfotiamine increases glucose oxidation and downregulates NADPH oxidase 4 expression in cultured human myotubes exposed to both normal and high glucose concentrations

Fraser, David A.; Hessvik, Nina Pettersen; Nikolić, Nataša; Aas, Vigdis; Hanssen, K. F.; Bøhn, Siv Kjølsrud; Thoresen, G. Hege; Rustan, Arild C.

doi:10.1007/s12263-011-0252-8

Cited by 17 publications

(16 citation statements)

References 34 publications

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“…We are unclear how precisely this occurs, but previous research work suggests that this may constitute an energy‐conserving mechanism (by promoting glucose oxidation) (Fraser et al . ) and/or a direct effect of BFT on neurohormonal modulation (Katare et al . ).…”

Section: Discussionmentioning

confidence: 99%

Detrimental effects of acute hyperglycaemia on the rat heart

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Detrimental effects of acute hyperglycaemia on the rat heart

et al. 2013

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“…Several studies have shown that cisplatin treatment decreases GSH levels . BFT increases the thiamine level that activates transketolase and downregulates NADPH oxidase; consequently, NADPH production is increased . This replenishes the cellular GSH; therefore, BFT protects the kidneys from the damaging effect of cisplatin .…”

Section: Discussionmentioning

confidence: 99%

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

Harisa

2013

J Biochem & Molecular Tox

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The objective of the present study was to assess superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), paraoxonase (PON1), glutathione reductase (GR), and catalase (CAT) activities ratio and their relationship with DNA oxidative damage in rats treated with cisplatin (3 mg/kg bwt/day) in the presence and absence of benfotiamine (100 mg/kg/day) for 25 days. Cisplatin-induced renal damage was evidenced by renal dysfunction and elevated oxidative stress markers. SOD activity and levels of nitric oxide, protein carbonyl, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine were significantly increased by cisplatin treatment. Moreover, the ratios of GPx/GR, SOD/GPx, SOD/CAT, and SOD/PON1 were significantly increased compared to control. In contrast, glutathione levels were significantly decreased by cisplatin treatment. Simultaneous treatment of rats with cisplatin and benfotiamine ameliorate these variables to values near to those of control rats. This study suggests that benfotiamine can prevent cisplatin-induced nephrotoxicity by inhibiting formation reactive species of oxygen and nitrogen.

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“…Benfotiamine but not thiamine increased glucose oxidation while lipid oxidation and metabolism was influenced by neither of the two. Benfotiamine also down-regulated NADPH oxidase 4 expression [36] .…”

Section: Thiamine Mishandling In Diabetesmentioning

confidence: 94%

Evidence for altered thiamine metabolism in diabetes: Is there a potential to oppose gluco- and lipotoxicity by rational supplementation?

Pácal¹

2014

WJD

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Growing prevalence of diabetes (type 2 as well as type 1) and its related morbidity due to vascular complications creates a large burden on medical care worldwide. Understanding the molecular pathogenesis of chronic micro-, macro-and avascular complications mediated by hyperglycemia is of crucial importance since novel therapeutic targets can be identified and tested. Thiamine (vitamin B1) is an essential cofactor of several enzymes involved in carbohydrate metabolism and published data suggest that thiamine metabolism in diabetes is deficient. This review aims to point out the physiological role of thiamine in metabolism of glucose and amino acids, to present overview of thiamine metabolism and to describe the consequences of thiamine deficiency (either clinically manifest or latent). Furthermore, we want to explain why thiamine demands are increased in diabetes and to summarise data indicating thiamine mishandling in diabetics (by review of the studies mapping the prevalence and the degree of thiamine deficiency in diabetics). Finally, we would like to summarise the evidence for the beneficial effect of thiamine supplementation in progression of hyperglycemia-related pathology and, therefore, to justify its importance in determining the harmful impact of hyperglycemia in diabetes. Based on the data presented it could be concluded that although experimental studies mostly resulted in beneficial effects, clinical studies of appropriate size and duration focusing on the effect of thiamine supplementation/therapy on hard endpoints are missing at present. Moreover, it is not currently clear which mechanisms contribute to the deficient action of thiamine in diabetes most. Experimental studies on the molecular mechanisms of thiamine deficiency in diabetes are critically needed before clear answer to diabetes community could be given. Key words: Diabetes; Thiamine; Vitamin B1; Transketolase; Benfotiamine; Hyperglycemia; Nephropathy; Metabolic syndrome; Cardiovascular disease; Chronic kidney disease Core tip: Published data suggest deficient action of thiamine in diabetes, however, it is not currently clear by which mechanisms. Plasma levels might be decreased in diabetics (although renal function has a prevailing effect), nevertheless, intracellular concentration of thiamine diphosphate is the crucial parameter and there is not a direct relationship with the plasma thiamine since the rate of transmembrane transport (via thiamine transporters) and intracellular activation by thiamine pyrophosphokinase might affected by hyperglycemia at first place. Experimental studies on the molecular mechanisms of thiamine deficiency in diabetes are critically needed before clear answer to diabetes community could be given.

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Benfotiamine increases glucose oxidation and downregulates NADPH oxidase 4 expression in cultured human myotubes exposed to both normal and high glucose concentrations

Cited by 17 publications

References 34 publications

Detrimental effects of acute hyperglycaemia on the rat heart

Detrimental effects of acute hyperglycaemia on the rat heart

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

Evidence for altered thiamine metabolism in diabetes: Is there a potential to oppose gluco- and lipotoxicity by rational supplementation?

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