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Annual Review of Nutrition Aug 2023Riboflavin, in its cofactor forms flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), plays fundamental roles in energy metabolism, cellular antioxidant... (Review)
Review
Riboflavin, in its cofactor forms flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), plays fundamental roles in energy metabolism, cellular antioxidant potential, and metabolic interactions with other micronutrients, including iron, vitamin B, and folate. Severe riboflavin deficiency, largely confined to low-income countries, clinically manifests as cheilosis, angular stomatitis, glossitis, seborrheic dermatitis, and severe anemia with erythroid hypoplasia. Subclinical deficiency may be much more widespread, including in high-income countries, but typically goes undetected because riboflavin biomarkers are rarely measured in human studies. There are adverse health consequences of low and deficient riboflavin status throughout the life cycle, including anemia and hypertension, that could contribute substantially to the global burden of disease. This review considers the available evidence on causes, detection, and consequences of riboflavin deficiency, ranging from clinical deficiency signs to manifestations associated with less severe deficiency, and the related research, public health, and policy priorities.
Topics: Humans; Riboflavin Deficiency; Riboflavin; Causality; Antioxidants; Bone Marrow Failure Disorders; Disease Progression; Lip Diseases
PubMed: 37603429
DOI: 10.1146/annurev-nutr-061121-084407 -
Progress in Clinical and Biological... 1990
Review
Topics: Animals; Humans; Liver; Mitochondria, Liver; Riboflavin; Riboflavin Deficiency; Structure-Activity Relationship
PubMed: 2183235
DOI: No ID Found -
Advances in Nutrition (Bethesda, Md.) Sep 2016
Topics: Diet; Dietary Supplements; Dose-Response Relationship, Drug; Humans; Nutrition Surveys; Recommended Dietary Allowances; Riboflavin; Riboflavin Deficiency
PubMed: 27633112
DOI: 10.3945/an.116.012716 -
Critical Reviews in Food Science and... Nov 2017There has lately been a renewed interest in Riboflavin owing to insight into its recognition as an essential component of cellular biochemistry. The knowledge of the... (Review)
Review
There has lately been a renewed interest in Riboflavin owing to insight into its recognition as an essential component of cellular biochemistry. The knowledge of the mechanisms and regulation of intestinal absorption of riboflavin and its health implications has significantly been expanded in recent years. The purpose of this review is to provide an overview of the importance of riboflavin, its absorption and metabolism in health and diseased conditions, its deficiency and its association with various health diseases, and metabolic disorders. Efforts have been made to review the available information in literature on the relationship between riboflavin and various clinical abnormalities. The role of riboflavin has also been dealt in the prevention of a wide array of health diseases like migraine, anemia, cancer, hyperglycemia, hypertension, diabetes mellitus, and oxidative stress directly or indirectly. The riboflavin deficiency has profound effect on iron absorption, metabolism of tryptophan, mitochondrial dysfunction, gastrointestinal tract, brain dysfunction, and metabolism of other vitamins as well as is associated with skin disorders. Toxicological and photosensitizing properties of riboflavin make it suitable for biological use, such as virus inactivation, excellent photosensitizer, and promising adjuvant in chemo radiotherapy in cancer treatment. A number of recent studies have indicated and highlighted the cellular processes and biological effects associated with riboflavin supplementation in metabolic diseases. Overall, a deeper understanding of these emerging roles of riboflavin intake is essential to design better therapies for future.
Topics: Chronic Disease; Diabetes Mellitus; Diet; Health Status; Humans; Hyperglycemia; Nutritional Requirements; Oxidative Stress; Riboflavin; Riboflavin Deficiency; Vitamins
PubMed: 27029320
DOI: 10.1080/10408398.2016.1145104 -
The American Journal of Clinical... Dec 2022
Topics: Adult; Humans; Riboflavin Deficiency; Vitamin B 6; Riboflavin; Pyridoxine; Genotype; Vitamins; Methylenetetrahydrofolate Reductase (NADPH2)
PubMed: 36264295
DOI: 10.1093/ajcn/nqac269 -
Journal of Inherited Metabolic Disease Jul 2016Riboflavin (vitamin B2) is absorbed in the small intestine by the human riboflavin transporters RFVT1 and RFVT3. A third riboflavin transporter (RFVT2) is expressed in... (Review)
Review
INTRODUCTION
Riboflavin (vitamin B2) is absorbed in the small intestine by the human riboflavin transporters RFVT1 and RFVT3. A third riboflavin transporter (RFVT2) is expressed in the brain. In 2010 it was demonstrated that mutations in the riboflavin transporter genes SLC52A2 (coding for RFVT2) and SLC52A3 (coding for RFVT3) cause a neurodegenerative disorder formerly known as Brown-Vialetto-Van Laere (BVVL) syndrome, now renamed to riboflavin transporter deficiency. Five years after the diagnosis of the first patient we performed a review of the literature to study the presentation, treatment and outcome of patients with a molecularly confirmed diagnosis of a riboflavin transporter deficiency.
METHOD
A search was performed in Medline, Pubmed using the search terms 'Brown-Vialetto-Van Laere syndrome' and 'riboflavin transporter' and articles were screened for case reports of patients with a molecular diagnosis of a riboflavin transporter deficiency.
RESULTS
Reports on a total of 70 patients with a molecular diagnosis of a RFVT2 or RTVT3 deficiency were retrieved. The riboflavin transporter deficiencies present with weakness, cranial nerve deficits including hearing loss, sensory symptoms including sensory ataxia, feeding difficulties and respiratory difficulties which are caused by a sensorimotor axonal neuropathy and cranial neuropathy. Biochemical abnormalities may be absent and the diagnosis can only be made or rejected by molecular analysis of all genes. Treatment with oral supplementation of riboflavin is lifesaving. Therefore, if a riboflavin transporter deficiency is suspected, treatment must be started immediately without first awaiting the results of molecular diagnostics.
Topics: Bulbar Palsy, Progressive; Diagnosis, Differential; Hearing Loss, Sensorineural; Humans; Membrane Transport Proteins; Molecular Diagnostic Techniques; Mutation; Prognosis; Riboflavin Deficiency
PubMed: 26973221
DOI: 10.1007/s10545-016-9924-2 -
International Journal For Vitamin and... Jun 2021Riboflavin deficiency led to lower blood cholesterol level and higher content of hepatic cholesterol in rats and the mechanisms are not clarified yet. We hypothesized...
Riboflavin deficiency led to lower blood cholesterol level and higher content of hepatic cholesterol in rats and the mechanisms are not clarified yet. We hypothesized that riboflavin deficiency might alter cholesterol homeostasis via apolipoprotein B100, one of the important proteins in cholesterol transport. To test this hypothesis, HepG2 cells were cultured in riboflavin-deficient media for 4 days to develop riboflavin deficiency. Compared to riboflavin-sufficient cells, the mRNA (0. 37 ± 0.04 1.03 ± 0.29 relative expression level, n = 3) and protein expressions of apolipoprotein B100 (intracellular: 173.7 ± 14.4 254.8 ± 47.2 μg/mg protein; extracellular: 93.8 ± 31.1 161.6 ± 23.9 μg/mg protein; n = 3) were significantly reduced in riboflavin-deficient cells ( < 0.05). Endoplasmic reticulum oxidoreductin 1 and protein disulfide isomerase, two enzymes involved in the oxidative folding of apolipoprotein B100, were also lower remarkably in expression at both mRNA and protein levels. Meanwhile, intracellular cholesterol was increased (256.3 ± 17.1 μM/g protein 181.4 ± 23.9 μM/g protein, n = 4) and extracellular cholesterol decreased (110.0 ± 23.2 μM/g protein 166.2 ± 34.6 μM/g protein, n = 4) significantly in riboflavin-deficient cells ( < 0.05). Very low-density lipoprotein was also diminished (29.0 ± 6.1 μM/g protein 67.0 ± 11.0 μM/g protein, n = 4) in the culture media ( < 0.05). These findings suggest that riboflavin deficiency alters cholesterol homeostasis partly by reducing apolipoprotein B100 synthesis in HepG2 cells.
Topics: Animals; Apolipoprotein B-100; Cholesterol; Hep G2 Cells; Homeostasis; Rats; Riboflavin Deficiency
PubMed: 31656126
DOI: 10.1024/0300-9831/a000610 -
Advances in Experimental Medicine and... 1986Riboflavin deficiency diminishes the rate of growth of spontaneous tumors in experimental animals but enhances the carcinogenicity of specific drugs such as the azo...
Riboflavin deficiency diminishes the rate of growth of spontaneous tumors in experimental animals but enhances the carcinogenicity of specific drugs such as the azo dyes, which are degraded by a microsomal hydroxylase system requiring riboflavin. Human esophageal cancer has been epidemiologically associated with riboflavin deficiency, but the precise role of riboflavin in this tumor remains to be defined. Riboflavin nutriture influences epithelial integrity, tissue flavin concentrations, rates of prostaglandin biosynthesis, and glutathione metabolism, each of which may have implications for carcinogenesis.
Topics: Animals; Carcinogens; Esophageal Neoplasms; Humans; Neoplasms; Neoplasms, Experimental; Riboflavin; Riboflavin Deficiency; Vitamins
PubMed: 3591527
DOI: 10.1007/978-1-4613-1835-4_26 -
Redox Biology Aug 2022Ariboflavinosis is a pathological condition occurring as a result of riboflavin deficiency. This condition is treatable if detected early enough, but it lacks timely...
Ariboflavinosis is a pathological condition occurring as a result of riboflavin deficiency. This condition is treatable if detected early enough, but it lacks timely diagnosis. Critical symptoms of ariboflavinosis include neurological and visual manifestations, yet the effects of flavin deficiency on the retina are not well investigated. Here, using a diet induced mouse model of riboflavin deficiency, we provide the first evidence of how retinal function and metabolism are closely intertwined with riboflavin homeostasis. We find that diet induced riboflavin deficiency causes severe decreases in retinal function accompanied by structural changes in the neural retina and retinal pigment epithelium (RPE). This is preceded by increased signs of cellular oxidative stress and metabolic disorder, in particular dysregulation in lipid metabolism, which is essential for both photoreceptors and the RPE. Though many of these deleterious phenotypes can be ameliorated by riboflavin supplementation, our data suggests that some patients may continue to suffer from multiple pathologies at later ages. These studies provide an essential cellular and mechanistic foundation linking defects in cellular flavin levels with the manifestation of functional deficiencies in the visual system and paves the way for a more in-depth understanding of the cellular consequences of ariboflavinosis.
Topics: Animals; Homeostasis; Mice; Retina; Retinal Pigment Epithelium; Riboflavin; Riboflavin Deficiency
PubMed: 35738087
DOI: 10.1016/j.redox.2022.102375 -
Seminars in Dermatology Dec 1991Mucocutaneous lesions are present in both acute and chronic riboflavin deficiency. The distribution of the lesions varies with the age and gender of the patient. Lesions... (Review)
Review
Mucocutaneous lesions are present in both acute and chronic riboflavin deficiency. The distribution of the lesions varies with the age and gender of the patient. Lesions of acute riboflavin deficiency are similar to those observed in protein-energy malnutrition of the kwashiorkor type. In chronic riboflavin deficiency the cutaneous lesions resemble monilial intertrigo and the mucous membrane lesions include a characteristic glossitis. Prompt resolution of lesions after therapeutic doses of the vitamin are given confirms the diagnosis. Biochemical changes caused by riboflavin deficiency, which explain the dermatoses and mucous membrane lesions, have not as yet been determined. Lack of information in this area is explained by the difficulty of separating cutaneous changes caused by the deficiency from those caused by trauma or other proximate etiologic agents.
Topics: Acute Disease; Adult; Child; Chronic Disease; Humans; Middle Aged; Mouth Diseases; Riboflavin Deficiency; Skin Diseases
PubMed: 1764356
DOI: No ID Found