Thiamin status, diuretic medications and the management of congestive heart failure

Brady, J.A; Rock, Cheryl L.; Horneffer, M.D

doi:10.1016/0002-8223(93)91019-m

Cited by 22 publications

(35 citation statements)

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“…The conventional indicator of thiamine sufficiency is the "thiamine effect," the increase of TK activity with a saturating amount of exogenous TPP in ex vivo assay. When this increase is Ն15% of TK activity in the presence of saturating TPP, there is thiamine deficiency (16). In this study, incipient nephropathy developed over a 24-week period in the STZ diabetic rats, as judged by hyperfiltration and microalbuminuria, and both high-dose thiamine and benfotiamine therapy prevented it.…”

mentioning

confidence: 59%

“…Investigating the effect of high-dose thiamine and benfotiamine therapy on STZ diabetic rats to prevent the development of nephropathy, we found that STZ diabetic rats had abnormally low plasma thiamine concentration and glomerular TK activity, although they were not thiamine deficient by the "thiamine effect" criterion (16). Plasma thiamine was decreased in diabetic rats by increased renal clearance.…”

Section: Discussionmentioning

confidence: 98%

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Prevention of Incipient Diabetic Nephropathy by High-Dose Thiamine and Benfotiamine

et al. 2003

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Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycemia is the trigger for biochemical dysfunction leading to the development of diabetic nephropathy-a common complication of diabetes associated with a high risk of cardiovascular disease and mortality. Here we report that stimulation of the reductive pentosephosphate pathway by high-dose therapy with thiamine and the thiamine monophosphate derivative benfotiamine countered the accumulation of triosephosphates in experimental diabetes and inhibited the development of incipient nephropathy. High-dose thiamine and benfotiamine therapy increased transketolase expression in renal glomeruli, increased the conversion of triosephosphates to ribose-5-phosphate, and strongly inhibited the development of microalbuminuria. This was associated with decreased activation of protein kinase C and decreased protein glycation and oxidative stress-three major pathways of biochemical dysfunction in hyperglycemia. Benfotiamine also inhibited diabetes-induced hyperfiltration. This was achieved without change in elevated plasma glucose concentration and glycated hemoglobin in the diabetic state. High-dose thiamine and benfotiamine therapy is a potential novel strategy for the prevention of clinical diabetic nephropathy.

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mentioning

confidence: 59%

Section: Discussionmentioning

confidence: 98%

Prevention of Incipient Diabetic Nephropathy by High-Dose Thiamine and Benfotiamine

et al. 2003

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“…14 Red blood cell transketolase activity is valuable to assess impact on the pentosephosphate pathway and αETKA to explore cause of transketolase activity deficit. 48 Where competitive inhibition of transketolase by OTPP or similar antimetabolite is suspected, care is required to ensure the inhibitor does not dissociate from the holoenzyme before the activity is recorded. Plasma oxythiamine offers an assessment of oxythiamine exposure with analytical standard available commercially.…”

Section: In Clinical Translation Dietary Deficiency Of Thiamine -Leamentioning

confidence: 99%

The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity

Zhang

Masania

Anwar

et al. 2016

Kidney International

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(2016) The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity. Kidney International, 90 (2). pp. 396-403. Permanent WRAP URL:http://wrap.warwick.ac.uk/78200 Copyright and reuse:The Warwick Research Archive Portal (WRAP) makes this work by researchers of the University of Warwick available open access under the following conditions. Copyright © and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable the material made available in WRAP has been checked for eligibility before being made available.Copies of full items can be used for personal research or study, educational, or not-for-profit purposes without prior permission or charge. Provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way. A note on versions:The version presented here may differ from the published version or, version of record, if you wish to cite this item you are advised to consult the publisher's version. Please see the 'permanent WRAP url' above for details on accessing the published version and note that access may require a subscription.For more information, please contact the WRAP Team at: wrap@warwick.ac.uk

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“…Beriberi, classically categorized as dry or wet, is present in populations relying on diet constituting predominantly of polished rice (very low thiamine content). Wet beriberi (also known as thiamine deficiency with cardiopathy) affects primarily heart and can lead to a congestive heart failure with peripheral oedemas, tachycardia, dyspnoea and weakness [15] . Patients with dry form usually suffer from peripheral neuropathy leading to paralysis, weakness, leg paraesthesia, wasting of muscle and various other symptoms.…”

Section: Thiamine Deficiencymentioning

confidence: 99%

“…Thiamine effect expresses the increase of TKT activity after addition of saturating amount of thiamine to the reaction. The increase up to 15% is considered as normal thiamine status, higher increase is an indicator of mild (up to 25%) or severe (more than 25%) thiamine deficiency [15] . Plasma thiamine levels can also be measured although they predominantly reflect thiamine intake rather than cellular levels.…”

Section: Laboratory Test Used For Estimation Of Thiamine Statusmentioning

confidence: 99%

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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Thiamin status, diuretic medications and the management of congestive heart failure

Cited by 22 publications

References 0 publications

Prevention of Incipient Diabetic Nephropathy by High-Dose Thiamine and Benfotiamine

Prevention of Incipient Diabetic Nephropathy by High-Dose Thiamine and Benfotiamine

The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity

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

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