Riboflavin and energy metabolism -
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Literature References PubMed ID Title Journal Year Riboflavin metabolism Rivlin, RS N Engl J Med as an event of. Metabolism of water-soluble vitamins and cofactors Homo sapiens. Go Biological Process. riboflavin metabolic process Vitamin B2 riboflavin metabolism Bos taurus.
Vitamin B2 riboflavin metabolism Caenorhabditis elegans. Vitamin B2 riboflavin metabolism Canis familiaris. Vitamin B2 riboflavin metabolism Danio rerio. Vitamin B2 riboflavin metabolism Dictyostelium discoideum. Vitamin B2 riboflavin metabolism Drosophila melanogaster.
Vitamin B2 riboflavin metabolism Gallus gallus. Vitamin B2 riboflavin metabolism Mus musculus. Vitamin B2 riboflavin metabolism Plasmodium falciparum. Vitamin B2 riboflavin metabolism Rattus norvegicus. Flavoproteins are involved in the metabolism of several other vitamins: vitamin B 6 , niacin , vitamin B 12 , and folate.
Therefore, low and deficient riboflavin status can affect several enzyme systems. The conversion of vitamin B 6 to its active coenzyme form in tissues, pyridoxal 5'-phosphate PLP , requires the FMN-dependent enzyme, pyridoxine 5'-phosphate oxidase PPO 7.
Human studies have provided evidence of the metabolic dependency of vitamin B 6 on riboflavin status in older and younger 10 adults. The synthesis of the niacin-containing coenzymes, NAD and NADP, from the amino acid tryptophan, requires the FAD-dependent enzyme, kynurenine 3-monooxygenase.
Severe riboflavin deficiency can thus decrease the conversion of tryptophan to NAD and NADP, increasing the risk of niacin deficiency 3. Methylenetetrahydrofolate reductase MTHFR is an FAD-dependent enzyme that plays a key role in one-carbon metabolism by catalyzing the reduction of 5,10 methyleneTHF to 5 methylTHF.
Once formed, 5 methylTHF is used by methionine synthase for the vitamin B 12 -dependent conversion of homocysteine to methionine and the formation of THF Figure 2.
Both FMN and FAD are coenzymes for the enzyme methionine synthase reductase, which is responsible for the regeneration of methylcobalamin, the biologically active form of vitamin B 12 acting as a coenzyme for methionine synthase Along with other B vitamins folate, vitamin B 12 , and vitamin B 6 , higher dietary riboflavin intakes have been associated with lower plasma concentrations of homocysteine In individuals homozygous for the CT polymorphism in the MTHFR gene , low riboflavin status is associated with elevated plasma homocysteine, and in turn linked with a higher risk of cardiovascular disease and other chronic diseases 13, Furthermore, supplementation with riboflavin results in marked lowering of homocysteine concentrations specifically in individuals with the variant MTHFR TT genotype Such results illustrate that chronic disease risk may be influenced by complex interactions between genetic and dietary factors.
Riboflavin deficiency alters iron metabolism. In humans, low dietary intake of riboflavin has been associated with an increased risk for anemia 17 , and improving riboflavin nutritional status has been found to increase circulating hemoglobin levels Correction of riboflavin deficiency in individuals who are both riboflavin and iron deficient improves the response of iron-deficiency anemia to iron therapy Anemia during pregnancy, a worldwide public health problem, is responsible for considerable perinatal morbidity and mortality 20, The management of maternal anemia typically involves supplementation with iron alone or iron in combination with folic acid It is possible that the inclusion of riboflavin could enhance the effects of iron-folic acid supplementation in treating maternal anemia, but the evidence is limited.
There are, however, randomized , double-blind intervention trials conducted in pregnant women with anemia in Southeast Asia showing that a combination of folic acid, iron, vitamin A , and riboflavin improved hemoglobin levels and decreased anemia prevalence compared to iron-folic acid supplementation alone 23, Ariboflavinosis is the medical name for clinical riboflavin deficiency, which occurs commonly in low- and middle-income countries.
Riboflavin deficiency is rarely found in isolation; it typically occurs in combination with deficiencies of other water-soluble vitamins. Clinical signs of riboflavin deficiency include sore throat, redness and swelling of the lining of the mouth and throat, cracks or sores on the outsides of the lips cheliosis and at the corners of the mouth angular stomatitis , inflammation and redness of the tongue magenta tongue , and a moist, scaly skin inflammation seborrheic dermatitis.
Other signs may involve the formation of blood vessels in the clear covering of the eye vascularization of the cornea and decreased red blood cell count in which the existing red blood cells contain normal levels of hemoglobin and are of normal size normochromic normocytic anemia 1, 3.
Subclinical deficiency low status of riboflavin without clinical signs may be widespread, including in high-income countries, but usually goes undetected because riboflavin biomarkers are very rarely measured in human studies.
Low or deficient riboflavin status may result in decreased conversion of vitamin B 6 to its active coenzyme form PLP and decreased conversion of tryptophan to niacin see Nutrient interactions. Preeclampsia is defined as the presence of elevated blood pressure, protein in the urine, and edema significant swelling during pregnancy.
Eclampsia is characterized by seizures, in addition to high blood pressure and increased risk of hemorrhage severe bleeding A study in pregnant women at increased risk of preeclampsia found that those who were riboflavin deficient were 4. The cause of preeclampsia-eclampsia is not known.
Decreased intracellular levels of flavocoenzymes could cause mitochondrial dysfunction, increase oxidative stress , and interfere with nitric oxide release and thus blood vessel dilation — all of these changes have been associated with preeclampsia A meta-analysis of 54 case-control studies found that the MTHFR CT polymorphism was associated with an increased risk of preeclampsia, especially in Caucasian and Asian populations The reduction in the flavoprotein MTHFR activity observed in individuals with the variant MTHFR TT genotype leads to an increase in plasma homocysteine 14 ; higher homocysteine concentrations have been associated with preeclampsia One small randomized controlled trial in pregnant women in West Africa, without specified MTHFR genotype but at high risk for preeclampsia, found that supplementation with 15 mg of riboflavin daily was not effective in preventing the condition 29 , but the study was likely underpowered to detect a significant effect.
Further studies are needed to assess the potential benefit of riboflavin supplementation in reducing perinatal complications generally and specifically in preeclamptic women with the MTHFR TT genotype.
Interestingly, the elevated blood homocysteine concentrations associated with riboflavin deficiency rapidly decline during alcohol withdrawal Additionally, people with anorexia rarely consume adequate dietary riboflavin, and those who are lactose intolerant are unlikely to meet requirements due to the avoidance of dairy products, the major dietary sources of riboflavin.
The conversion of riboflavin into the active cofactor forms FAD and FMN is impaired in hypothyroidism and adrenal insufficiency 3, 4.
Further, people who are very active physically athletes, laborers may have slightly increased riboflavin requirements. However, riboflavin supplementation has not generally been found to increase exercise tolerance or performance 31 unless the individuals are riboflavin deficient The RDA for riboflavin, revised in , is based on the prevention of deficiency Table 1.
Clinical signs of deficiency in humans appear at intakes of less than 0. Age-related cataracts are the leading cause of visual disability in the US and other developed countries. Research has focused on the role of nutritional antioxidants because of evidence that light-induced oxidative damage of lens proteins may lead to the development of age-related cataracts.
Another case-control study reported that individuals in the highest quintile of riboflavin status , as measured by red blood cell glutathione reductase activity, had approximately one-half the occurrence of age-related cataract as those in the lowest quintile of riboflavin status, though the results were not statistically significant A prospective cohort study of more than 50, women did not observe a difference between rates of cataract extraction between women in the highest quintile of riboflavin intake median of 1.
However, the range between the highest and lowest quintiles was small, and median intake levels for both quintiles were above the RDA for riboflavin. A study in women found that higher dietary intakes of riboflavin were inversely associated with a five-year change in lens opacification Of note is that the results of this trial are somewhat conflicting, and the study design does not allow the effects of riboflavin and niacin to be differentiated.
In summary, there is some evidence predominantly from observational studies , that suggests higher riboflavin status might be beneficial; however, more evidence from well-designed, randomized controlled trials is needed to confirm a role for riboflavin in the prevention of cataracts.
The flavoprotein, methylenetetrahydrofolate reductase MTHFR , plays a pivotal role in folate-mediated one-carbon metabolism. MTHFR converts 5,methylenetetrahydrofolate to 5-methyltetrahydrofolate, the cofactor form necessary for the re-methylation of homocysteine to methionine see Figure 2 above.
The conversion of homocysteine to methionine is of importance for homocysteine detoxification and for the production of S-adenosylmethionine SAM , the methyl donor for the methylation of DNA and histones. Folate deficiency and elevated homocysteine concentrations may increase cancer risk see the article on Folate.
Aberrant methylation changes are also known to alter the structure and function of DNA and histones during cancer development Since MTHFR controls the detoxification of homocysteine and the supply of methyl groups for SAM synthesis, a reduction in its activity can affect homocysteine metabolism and disturb cellular methylation processes.
The substitution of a cytosine by a thymine in position c. Subjects homozygous for this mutation MTHFR TT genotype exhibit reduced MTHFR activity and increased risk for a wide variety of cancers , but the evidence of an association between this polymorphism and cancer is inconsistent, with some reports suggesting a reduction in colorectal cancer risk with the T allele As mentioned above see B-complex vitamins , riboflavin intake is a determinant of homocysteine concentration.
This suggests that riboflavin status can influence MTHFR activity and the metabolism of folate, thereby affecting cancer risk These interventions significantly improved folate and riboflavin status in vitamin - supplemented individuals compared to those taking the placebo.
Interestingly, riboflavin enhanced the effect of μg folic acid on circulating 5-methyltetrahydrofolate 5-MTHF specifically in the polyp patients with the CT genetic variant This suggests that riboflavin may improve the response to folic acid supplementation in individuals with a reduced MTHFR activity.
The subjects in this study were not prescreened to identify those with the variant MTHFR TT genotype, and the association between this polymorphism and colorectal cancer remains unclear, with some reports suggesting a reduction in cancer risk with the T allele Two meta-analyses have found inverse associations between riboflavin intake and risk of colorectal cancer 47, The most recent of these was a dose-response meta-analysis that pooled results from five prospective cohort studies, nine case-control studies , and two studies reporting blood concentrations of riboflavin.
Associations between riboflavin intake and cancer risk have also been evaluated in other types of cancer. A seven-year intervention study evaluated the use of riboflavin-fortified salt in 22, individuals at high risk for esophageal cancer in China.
Riboflavin status and esophageal pathology percent normal, dysplastic, and cancerous tissues improved in the intervention group compared to the control group, but the lower incidence of esophageal cancer found in the intervention group was not statistically significant Additionally, a year follow up of an intervention trial in patients at high risk for gastric cancer found that dietary supplementation with riboflavin 3.
In the Melbourne Collaborative Cohort Study, which followed 41, men and women over a year period, weak inverse associations were found between riboflavin intake and lung cancer 51 and breast cancer 52 ; no association of riboflavin intake with prostate cancer was observed in this cohort Further, studies to date have not found riboflavin intake or measures of riboflavin status to be associated with renal cell carcinoma, as reviewed in a recent meta-analysis Some evidence indicates that impaired mitochondrial oxygen metabolism in the brain may play a role in the pathology of migraine headaches.
Since riboflavin is the precursor of the two flavocoenzymes FAD and FMN required by the flavoproteins of the mitochondrial electron transport chain , supplemental riboflavin has been investigated as a treatment for migraine. Riboflavin compared to placebo reduced attack frequency and the number of headache days, though the beneficial effect was most pronounced during the third month of treatment A small study in 23 patients reported a reduction in median migraine attack frequency after supplementation with mg of riboflavin daily for three months Riboflavin elicited significantly fewer adverse effects compared to the drug Thus, although the available trials have been small and short term, most studies to date suggest that high-dose riboflavin supplementation might be a useful adjunct therapy in adults with migraine headaches.
A few randomized controlled trials have investigated the effect of riboflavin supplementation on the frequency and severity of headache attacks in children with migraines. Neither study showed differences in the frequency, duration, or intensity of migraines between treatments.
Retrospective studies of children and adolescents suffering from migraine have also suggested some benefit associated with supplemental riboflavin Thus, studies to date are somewhat conflicting, and more research is needed to understand whether riboflavin supplementation might have utility in the treatment of childhood migraine and the most effective dose required for any beneficial effects.
Increasing evidence from case reports indicates that patients with autosomal recessive disorders caused by defective FAD-dependent enzymes could benefit from riboflavin supplementation. MADD, also known as type II glutaric aciduria or acidemia , is a fatty acid metabolism disorder characterized by the accumulation of short-, medium-, and long-chain acyl- carnitines in various tissues.
MADD is classified into three separate types based on age of onset and clinical symptoms: type I MADD is evident in the neonatal period and is characterized by the presence of congenital anomalies ; type II MADD is present in the neonatal period but lacks congenital defects; and type III is characterized by late onset, from infancy through adulthood 68 , and even as late as the seventh decade of life Clinical symptoms of type I and II MADD present shortly after birth and include hypoglycemia, hyperammonemia, metabolic acidosis, hepatomegaly, and respiratory distress 68 , 70 ; these forms of MADD are often fatal in infancy, even if treated.
Type III MADD usually presents later in life and includes milder symptoms, varying from periodic vomiting, rhabdomyolysis, muscle pain and weakness, and exercise intolerance 68 , Peripheral neuropathy has also recently been reported as a symptom of adult-onset MADD Deficiencies in these enzymes ETF or ETFDH lead to a decrease in oxidized FAD, which becomes unavailable for FAD-dependent dehydrogenation reactions, including the first step in β-oxidation — a major fatty acid catabolic process that takes place in the mitochondria.
A defect in fatty acid β-oxidation causes lipid accumulation in skeletal muscles, leading to lipid storage myopathy characterized by muscle pain and weakness and exercise intolerance.
Together with a low-fat, high-carbohydrate diet, riboflavin supplementation has led to significant clinical improvements in patients with ETFDH mutations. Additionally, the report of a year-old man with riboflavin-responsive MADD failed to find mutations in ETF and ETFDH genes, suggesting that other sites of mutation should not be excluded Finally, secondary deficiencies in the respiratory chain are observed in MADD and appear to respond favorably to riboflavin supplementation 72 , Acyl-CoA dehydrogenase family member 9 ACAD9 is an FAD-dependent enzyme with important roles in both the electron transport chain and β-oxidation of fatty acids in the mitochondria.
Recessive mutations in the ACAD9 gene coding for ACAD9 have been found in patients with mitochondrial complex I deficiency, a respiratory chain disorder Complex I carries electrons from NADH to coenzyme Q 10 in the electron transport chain. Defective oxidative phosphorylation ATP synthesis by the respiratory chain due to complex I deficiency has been linked to a broad variety of clinical manifestations, from neonatal death to late-onset neurodegenerative diseases.
The clinical symptoms of complex I deficiency due to ACAD9 mutations typically include muscle weakness, exercise intolerance, lactic acidosis, and hypertrophic cardiomyopathy However, symptoms can be of varying severity, likely due to the remaining functional activity of ACAD9.
For example, affected patients have been reported to exhibit a spectrum of cardiac deficits, including isolated, mild ventricular hypertrophy to severe hypertrophic cardiomyopathy Improvements in muscle strength and exercise tolerance have also been associated with riboflavin supplementation A review of cases of ACAD9 deficiency presenting in infancy i.
SLC52A1 , SLC52A2 , and SLC52A3 genes code for the human riboflavin transporters RFVT1, RFVT2, and RFVT3, respectively. Mutations in these genes lead to riboflavin transporter deficiency, a rare neurodegenerative condition with variable age of onset, from infancy to early stages of adulthood.
Autosomal recessive mutations in SLC52A2 or SLC52A3 respectively cause disorders known as riboflavin transporter deficiency type 2 RFVT2 deficiency and riboflavin transporter deficiency type 3 RFVT3 deficiency.
These genetic disorders were formerly called Brown-Vialetto-Van Laere syndrome and Fazio-Londe syndrome Riboflavin transporter deficiency caused by mutation of SLC52A1 is exceedingly rare and has been reported in only three cases reviewed in Clinical features of riboflavin transporter deficiency can include muscle weakness in the arms and legs, sensory ataxia , bulbar palsy with hypotonia and facial weakness, sensorineural deafness, and respiratory insufficiency 83, High-dose, oral supplementation with riboflavin improves many of these symptoms in the majority of affected patients; such treatment should be given at the time of suspected riboflavin transporter deficiency for a better prognosis Primary trimethylaminuria is caused by defective oxidation of trimethylamine by a liver flavoprotein called flavin containing mono-oxygenase 3 FMO3.
Individuals with FMO3 deficiency have increased levels of trimethylamine in urine, sweat, and breath This socially distressing condition is known as "fish odor syndrome" due to the fishy odor and volatile nature of trimethylamine.
FMO3 gene mutations are usually associated with mild or intermittent trimethylaminuria; the condition is sometimes limited to peri-menstrual periods in female subjects or to the consumption of trimethylamine-rich food. The clinical management of the condition includes dietary restriction of trimethylamine and its precursors , such as foods rich in choline and seafood, as well as cruciferous vegetables that contain both trimethylamine precursors and FMO3 antagonists The use of riboflavin supplements was reported in a year-old female patient affected by pyridoxine non-responsive homocystinuria The disease was initially treated with betaine a choline derivative , which caused body odor secondary to FMO3 deficiency.
Similar effects were seen with riboflavin supplementation in two pediatric patients The data suggest that riboflavin might help maximize residual FMO3 enzyme activity in patients with primary trimethylaminuria.
Moreover, a recent case report in a year-old male with HIV described supplemental riboflavin as an effective treatment for secondary trimethylaminuria caused by antiretroviral therapy Hypertension in adulthood is recognized as the leading risk factor contributing to mortality worldwide primarily from cardiovascular disease , while hypertension in pregnancy leads to serious adverse fetal and maternal outcomes.
A number of risk factors are recognized to contribute to the development of hypertension. In recent years, evidence has emerged from genetic and clinical studies pointing to the role of one-carbon metabolism in blood pressure The common MTHFR CT polymorphism , affecting 1 in 10 adults globally, is associated with higher blood pressure, although this is much less well recognized compared with the phenotype of elevated homocysteine concentrations that was established at the time of discovery of this polymorphism and its link with cardiovascular disease The MTHFR CT polymorphism is also associated with a significantly higher risk of hypertension in pregnancy 93 and with preeclampsia Since FAD is required as a cofactor for the MTHFR enzyme and the MTHFR CT polymorphism results in decreased MTHFR activity, studies have investigated whether affected individuals may benefit from riboflavin supplementation.
In an initial randomized controlled trial in 77 healthy young adults stratified by MTHFR genotype , riboflavin supplementation at dietary levels 1. Three randomized controlled trials subsequently investigated the effect of riboflavin on blood pressure in patients with hypertension with or without overt cardiovascular disease 91 , 94, The results of these trials showed that supplementation with low-dose riboflavin 1.
The trial findings therefore suggest that the excess risk of hypertension linked to this genetic polymorphism can be overcome by low-dose riboflavin supplementation. Also, analysis of plasma samples from individuals participating in these trials showed lower concentrations of S-adenosylmethionine SAM , an important methyl group donor for methylation reactions, in those with the MTHFR TT genotype versus the CC genotype However, riboflavin supplementation 1.
Thus, studies to date indicate that riboflavin supplementation may have benefits in lowering blood pressure and reducing hypertension in individuals and sub-populations affected by the common MTHFR CT polymorphism.
However, the mechanisms explaining the blood pressure phenotype and its responsiveness to riboflavin remain unclear. Future studies examining the effects of riboflavin supplementation on one-carbon metabolism may help to elucidate the biological mechanisms involved.
Interestingly, a recent randomized controlled trial found that riboflavin supplementation in those with the variant MTHFR TT genotype resulted in altered DNA methylation of certain genes known to be involved in blood pressure regulation Anticancer agents often display various side effects that may force patients to limit the dose or to discontinue the treatment.
This supplementation effectively prevented the oxidative stress associated with tamoxifen treatment Riboflavin can also act as a photosensitizer, and this property may have value in photodynamic therapy of cancer. A mouse model was used to assess the effect of riboflavin in combination with cisplatin, one of the most effective anticancer agents.
Under light exposure, riboflavin administration reduced cisplatin-induced DNA damage in the liver and kidneys These results are promising, but human studies are needed to examine whether riboflavin is an effective adjunct to chemotherapy. Corneal ectasia is an eye condition characterized by irregularities of the cornea that affect vision.
Corneal cross-linking — a fairly new procedure used by professionals to limit the progression of corneal damage —involves the use of topical riboflavin in conjunction with ultraviolet-A irradiation.
Riboflavin functions as a photosensitizer in the reaction. Cross-linking modifies the properties of the cornea and strengthens its architecture , Multiple sclerosis MS is an autoimmune disease of unknown etiology that is characterized by the progressive destruction of myelin and nerve fibers in the central nervous system , causing neurological symptoms in affected individuals Riboflavin appears to have a role in the formation of myelin , and oxidative stress has been implicated in the pathogenesis of MS; thus, riboflavin may be helpful in treatment of the disease.
A strong inverse association between dietary riboflavin intake and risk for MS was initially observed in a case-control study In a mouse model of MS i.
Large-scale randomized, placebo-controlled trials are needed to determine whether riboflavin supplementation has a beneficial effect in the treatment of MS. Most plant- and animal-derived foods contain at least small quantities of riboflavin. In the US, wheat flour and bread have been enriched with riboflavin as well as thiamin , niacin , and iron since Data from a US national survey indicate that the average dietary intake of riboflavin is 2.
Surveys of adults of ages 70 years or older showed similar intakes: 2. Riboflavin is heat-stable, but it is easily destroyed upon exposure to light. Nationally representative surveys from the US, Ireland, and the UK showed that milk and other dairy products were the main dietary contributors to riboflavin intake, followed by meat and ready-to-eat breakfast cereals Some foods with substantial amounts of riboflavin are listed in Table 2 , along with their riboflavin content in milligrams mg.
For more information on the nutrient content of food, search USDA's FoodData Central. Limited data exist for the relative bioavailability of riboflavin from different food sources, however a cross-over study in healthy women using stable isotopes and kinetic modeling did not find significant differences in riboflavin absorption from milk and spinach The most common forms of riboflavin available in supplements are riboflavin and riboflavin 5'-monophosphate.
Riboflavin is commonly found in multivitamin and vitamin B-complex preparations No toxic or adverse effects of high riboflavin intake in humans are known. Studies in cell culture indicate that excess riboflavin may increase the risk of DNA strand breaks in the presence of chromium VI , a known carcinogen This may be of concern to workers exposed to chrome, yet no data in humans are available.
High-dose riboflavin therapy has been found to intensify urine color to a bright yellow flavinuria , but this is a harmless side effect. The Food and Nutrition Board did not establish a tolerable upper intake level UL when the RDA was revised in 1.
Several early reports indicated that women taking high-dose oral contraceptives had diminished riboflavin biomarker status.
However, when investigators controlled for dietary riboflavin intake, no differences between users of oral contraceptives and non-users were found 1.
Phenothiazine derivatives like the anti-psychotic medication, chlorpromazine Thorazine , and tricyclic antidepressants inhibit the conversion of riboflavin to FAD and FMN, as do the anti-malarial medication, quinacrine, and the cancer chemotherapy agent, adriamycin 4.
Long-term use of the anticonvulsant, phenobarbitol, may increase destruction of riboflavin by liver enzymes , increasing the risk of deficiency 3. Additionally, chronic alcohol consumption has been associated with riboflavin deficiency. In rats chronically fed alcohol, the inhibition of riboflavin transporters caused impairment in intestinal absorption and renal re-uptake of the vitamin The RDA for riboflavin 1.
Consuming a varied diet should supply 1. Some experts in nutrition and aging feel that the RDA 1. Epidemiological studies of cataract prevalence indicate that riboflavin intakes of 1.
Additionally, older people suffering from acute ischemic stroke were found to be deficient for riboflavin , and riboflavin deficiency has been linked to a higher risk of fracture in postmenopausal women with the MTHFR T variant Originally written in by: Jane Higdon, Ph.
Linus Pauling Institute Oregon State University. Updated in September by: Jane Higdon, Ph. Updated in June by: Victoria J. Drake, Ph. Updated in July by: Barbara Delage, Ph. Updated in August by: Victoria J. Reviewed in July by: Kristina Pentieva, MD, Ph.
and Helene McNulty, RD, Ph. Nutrition Innovation Centre for Food and Health NICHE Ulster University, Coleraine, Northern Ireland. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B-6, Vitamin B, Pantothenic Acid, Biotin, and Choline.
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Ruboflavin, known as vitamin B2, a metabolksm Riboflavin and energy metabolism, Riboflavij an essential nutrient in Your ultimate thirst solution, hence adequate Riboflavin and energy metabolism intake is imperative. Riboflavin plays a role in a variety of metabolic pathways, serving primarily as an integral component of its crucial biologically active forms, the metaboliwm flavin adenine dinucleotide Riboflavin and energy metabolism flavin mononucleotide. These flavocoenzymes ensure the functionality of numerous flavoproteins including dehydrogenases, oxidases, monooxygenases, and reductases, which play pivotal roles in mitochondrial electron transport chain, β-oxidation of fatty acids, redox homeostasis, citric acid cycle, branched-chain amino acid catabolism, chromatin remodeling, DNA repair, protein folding, and apoptosis. Unsurprisingly, impairment of flavin homeostasis in humans has been linked to various diseases including neuromuscular and neurological disorders, abnormal fetal development, and cardiovascular diseases. This review presents an overview of riboflavin metabolism, its role in mitochondrial function, primary and secondary flavocoenzyme defects associated with mitochondrial dysfunction, and the role of riboflavin supplementation in these conditions. Vitamin African Mango Complex, commonly called riboflavin, is Ribofalvin of Ribofpavin water-soluble B vitamins. Like its close relative vitamin B1 Riboflavin and energy metabolismriboflavin plays Rihoflavin crucial role Riboflaavin certain metabolic reactions, Metzbolism the conversion of carbohydrates enrgy sugar, which is "burned" to produce energy. Together, the eight B vitamins, often Annd to as Eenergy complex vitamins, are also essential in the breakdown of fats and protein. In addition, B complex vitamins play an important role in maintaining muscle tone along the lining of the digestive tract and promoting the health of the nervous system, skin, hair, eyes, mouth, and liver. Riboflavin is important to energy metabolism processing nutrients like protein, fat, carbohydrate and alcohol that have calories to a form of energy that the body can use - ATPnormal eyesight and healthy skin. Foods high in riboflavin are milk, yogurt, cheeses, meat, leafy green vegetables, whole and enriched grains. Riboflavin is an essential vitamin and is easily destroyed by light.
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