Correlation of Urinary Excretion of Riboflavin with Dietary Intake and Symptoms of Ariboflavinosis

Horwitt, M. K.; Harvey, C. C.; Hills, O. W.; Liebert, Erich

doi:10.1093/jn/41.2.247

Cited by 74 publications

(39 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The fall in riboflavin content of the urine after institution of the riboflavin-deficient diet is in keeping with the observations of others (72). An immediate increase in riboflavin excretion to levels many times above intake of the vitamin occurred simultaneously with galactoflavin therapy.…”

Section: Discussionsupporting

confidence: 88%

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

Lane¹,

Alfrey²,

Mengel³

et al. 1964

J. Clin. Invest.

View full text Add to dashboard Cite

Signs of riboflavin deficiency require many months to develop in patients placed on riboflavinrestricted diets (1-6). The demonstrations that riboflavin deficiency induced by dietary restriction or riboflavin antagonists resulted in regression of rodent tumors (7-13) prompted several efforts in this laboratory to produce riboflavin deficiency in patients with neoplastic disease (14, 15). Riboflavin antagonists were used in these studies with the objective of producing the deficiency state rapidly, since a regimen requiring many months of dietary restriction would not lend itself to therapeutic evaluation in patients with metastatic cancer. These earlier investigations did not result in the production of clinical evidences of riboflavin deficiency or in objective demonstrations of tumor regression. The administered riboflavin antagonists, selected on the basis of their effectiveness in rats, were shown to be metabolized differently in man. The most active of these agents against rat tumors, 6,7-dimethyl-9-(2'-acetoxyethyl) -isoalloxazine, was rapidly and almost completely hydrolyzed in man, although a significant amount of the absorbed drug was excreted unchanged by rats. With the objective of producing human riboflavin deficiency, an analog was sought that would be an effective riboflavin antagonist in rodents and would be metabolized similarly in rodents and in man.The present paper describes studies with 1O-Ddulcityl -7,8-dimethyl-isoalloxazine, galactoflavin,

show abstract

Section: Discussionsupporting

confidence: 88%

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

Lane¹,

Alfrey²,

Mengel³

et al. 1964

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…The slope of urinary riboflavin excretion rose sharply when dietary intake reached 1.1 mg per day, which is the identical level at which the slope of the riboflavin-excretion curve changed in a classic study of younger adults (243). Thus, despite lower energy expenditure in older people, riboflavin requirements appear to be the same as for younger people.…”

Section: Riboflavinmentioning

confidence: 68%

The prevalence and risk factors for age-related macular degeneration in rural–urban India, Sankara Nethralaya Rural–Urban Age-related Macular degeneration study, Report No. 1

Raman

Pal

Ganesan

et al. 2016

Eye

View full text Add to dashboard Cite

“…Riboflavin excretion is reduced to 40 µg/24 h during deficiency compared with 120 µg/24 h when optimal status is achieved (49) . A number of studies have used biological samples particularly plasma and erythrocytes to measure riboflavin status directly but the results are inconsistent (50,51) .…”

Section: Assessment Of Biomarker Status Of Riboflavinmentioning

confidence: 99%

Riboflavin status, MTHFR genotype and blood pressure: current evidence and implications for personalised nutrition

et al. 2016

View full text Add to dashboard Cite

Clinical deficiency of the B-vitamin riboflavin (vitamin B 2 ) is largely confined to developing countries; however accumulating evidence indicates that suboptimal riboflavin status is a widespread problem across the developed world. Few international data are available on riboflavin status as measured by the functional biomarker, erythrocyte glutathione reductase activation coefficient, considered to be the gold standard index. One important role of riboflavin in the form of flavin dinucleotide is as a co-factor for the folate-metabolising enzyme methylenetetrahydrofolate reductase (MTHFR). Homozygosity for the common C677T polymorphism in MTHFR, affecting over 10 % of the UK and Irish populations and up to 32 % of other populations worldwide, has been associated with an increased risk of CVD, and more recently with hypertension. This review will explore available studies reporting riboflavin status worldwide, the interaction of riboflavin with the MTHFR C677T polymorphism and the potential role of riboflavin in personalised nutrition. Evidence is accumulating for a novel role of riboflavin as an important modulator of blood pressure (BP) specifically in individuals with the MTHFR 677TT genotype, with results from a number of recent randomised controlled trials demonstrating that riboflavin supplementation can significantly reduce systolic BP by 5-13 mmHg in these genetically at risk adults. Studies are however required to investigate the BP-lowering effect of riboflavin in different populations and in response to doses higher than 1·6 mg/d. Furthermore, work focusing on the translation of this research to health professionals and patients is also required.Riboflavin: Methylenetetrahydrofolate reductase: MTHFR C677T: Blood pressure:Personalised nutrition Riboflavin (vitamin B 2 ) is a water-soluble B-vitamin defined chemically as 7,8-dimethyl-10-1′-D-ribityl isoalloxazine. It acts as a precursor for FMN and FAD (1) . Clinical riboflavin deficiency is not generally considered to be a problem in the developed world but in recent years evidence has shown that sub-optimal status may be more widespread than generally perceived based on studies reporting the functional biomarker, erythrocyte glutathione reductase activation coefficient (EGRac) generally considered as the gold standard index of status. Few international data are however available based on EGRac and reports on riboflavin status are more commonly based solely on dietary intake data. Although riboflavin is required for numerous metabolic reactions its role (in the form of FAD) as a cofactor for the folatemetabolising enzyme, methylenetetrahydrofolate reductase (MTHFR) has recently received particular attention. Homozygosity (MTHFR 677TT genotype) for a common polymorphism in MTHFR, affecting over 10 % of the UK and Irish populations and up to 32 % of other populations worldwide (2) , has been associated with an increased risk of CVD (3) and more recently with hypertension (4) . Emerging evidence from intervention trials supports a novel role for riboflav...

show abstract

Correlation of Urinary Excretion of Riboflavin with Dietary Intake and Symptoms of Ariboflavinosis

Cited by 74 publications

References 7 publications

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

The prevalence and risk factors for age-related macular degeneration in rural–urban India, Sankara Nethralaya Rural–Urban Age-related Macular degeneration study, Report No. 1

Riboflavin status, MTHFR genotype and blood pressure: current evidence and implications for personalised nutrition

Contact Info

Product

Resources

About