What is vitamin B7?Vitamin B7 (biotin), also known as vitamin H or coenzyme R, is an essential micronutrient. Vitamin B7 is one of the water-soluble B-complex group of vitamins.
AdvertisementsBiotin is essential for gluconeogenesis, synthesis of fatty acids, metabolism of fatty acids and amino acids, production of antibodies and digestive enzymes and in niacin (vitamin B3) metabolism.
Biotin deficiency is a rare nutritional disease which can become serious when not properly treated. Vitamin B7 is available in several food sources. Intestinal fauna synthesizes fair amounts of this nutrient. Low circulating levels of the vitamin B7 occurs in certain specific health conditions. Biotin inadequacy can result in delayed development, respiratory problems, neuropsychological impairment, neuropathy, behavioral problems, dermatological manifestations, alopecia and reduced immune function.
Biotin food sourcesVitamin B7 is available in several food sources of both animal and plant origins.
Absorption and excretion of vitamin B7Biotin bioavailability is variable, dependent on the type of diet. Dietary vitamin B7 is available as protein-bound form, biocytin and free biotin. Proteolysis by protease enzyme is required for breaking down biotin-protein and biocytin for absorption. Being water-soluble, excess of this micronutrient is excreted in the urine.
Functions of BiotinBiotin is a cofactor for carboxylase enzymes including, pyruvate carboxylase, acetyl CoA carboxylase and propionyl CoA carboxylase. The biotin-dependent carboxylase enzymes add carbon dioxide to substrates, making use of a covalently-linked biotin prosthetic group. All the biotin-dependent carboxylase reactions require ATP hydrolysis to generate carboxybiotin.
- Pyruvate carboxylase is involved in gluconeogenesis, an anabolic process by which glucose is generated from non-carbohydrate precursors.
- Acetyl CoA carboxylase is involved in fatty acid synthesis, a cycle of reactions in which an oxidized two-carbon fragment is attached to a growing fatty acyl chain.
- Propionyl CoA carboxylase is involved in fatty acid oxidation, the metabolic pathway by which fatty acids are broken down to produce energy.
Biotinylation of histones with biotin plays a role in cell proliferation, gene silencing and cellular response to DNA damage.
Biotin deficiency causesThe primary dietary insufficiency of the biotin is very rare. The secondary inadequacy arises in to several situations.
- Severe malnutrition due to poverty, ketogenic diet or eating foods very low in the vitamin may cause low levels of the vitamin B7 in the plasma.
- Regular consumption of raw egg whites can cause binding of vitamin B7 to avidin present in the egg-white rendering it unabsorbable.
- Prolonged total parenteral nutrition without supplementation of vitamin B7 can lead to low biotin blood levels.
- Some anticonvulsants (except valproic acid) inhibit vitamin B7 transport across the intestinal mucosa as well as catabolize the vitamin, rendering it unavailable for its important functions.
- Prolonged oral antibiotic use eliminates and alters the biotin-synthesizing bacteria in the gut.
- Smoking, especially in women, leads to low blood levels of the vitamin B7 due to increased catabolism.
- Alcoholism and related malnutrition may cause dietary inadequacy and/or poor absorption of micronutrients.
- Pregnancy and lactation increases the demand for the vitamin in the body, sometimes causing reduced biotin plasma levels.
- Malabsorption diseases including, short bowel syndrome, coeliac disease, Crohn's disease, cystic fibrosis, chronic diarrhea, multiple food allergy and ulcerative colitis can cause deficiency of biotin in the body.
- Burn patients, epileptics, elderly individuals, people suffering from chronic diseases and athletes are prone to develop biotin inadequacy.
- Certain inherited genetic mutations cause metabolic impairments in activities of biotin-dependent carboxylases leading to several severe symptoms in children.
Biotin deficiency symptomsSeveral neuropsychological, respiratory, gastrointestinal and dermal symptoms are observed in association with severe vitamin B7 deficiency. Some of the associated symptoms are:
- behavioral problems,
- lack of coordination,
- learning disabilities,
- hearing loss,
- optic atrophy,
- hair loss,
- seborrhoeic dermatitis and
- reduced immune function.
Vitamin B7 deficiency diseasesDermatological diseases caused by low levels of the vitamin biotin include seborrheic dermatitis, hair loss and also a characteristic scaly, erythematous dermatitis distributed around body orifices including the eyes, ears, nose, mouth, anus and genital area. Neuropsychological diseases include depression, lethargy, hallucination, behavioral problems, seizures and numbness and tingling of the extremities. Anorexia, dyspepsia, anemia, heart abnormalities, fungal infections, conjunctivitis and developmental delays are the other connected diseases.
Inherited biotin metabolic disordersCertain inborn errors of metabolism render the body being unable to use the vitamin biotin effectively.
Multiple carboxylase deficiency (MCD) describes inborn errors of biotin metabolism characterized by reduced activities of biotin-dependent enzymes, biotinidase and holocarboxylase synthetase.
Biotinidase deficiency (BTD)BTD is an autosomal recessive disease of vitamin B7 metabolism caused by mutations in the BTD gene (3p25) resulting in reduced BTD activity or its absence. Biotinidase recycles free, non-protein bound, biotin for several metabolic reactions. There are more than 150 known mutations of the BTD gene that cause BTD. It is a late-onset form of MCD and the symptoms typically appear within the first few months of life. BTD symptoms include, seizures, dermatitis, respiratory difficulties, hypotonia, hair loss, hearing loss, ataxia, reduced immune function and developmental delay. The symptoms can be kept under control by lifelong vitamin B7 supplementation.
Holocarboxylase synthetase deficiency (HCSD)HCSD is an autosomal recessive disease of biotin metabolism caused by mutations in the HLCS gene (21q22.1) resulting in reduced holocarboxylase synthetase activity. It is a life-threatening form of MCD and its clinical onset is usually within hours or days of birth. Holocarboxylase synthetase is required in covalent binding of biotin to the various biotin-dependent carboxylases. Failure of the various biotin-dependent carboxylases activity can lead to accumulation of various, specific abnormal organic acids.
Affected children may usually show symptoms like poor appetite, vomiting, tachypnea, hypotonia, irritability, lethargy, exfoliative dermatitis and seizures. The HCSD may progress into intractable seizures, cerebral edema and coma. The symptoms can be kept under control by life long vitamin B7 supplementation. The morbidity and recovery depends on how early the vitamin B7 supplementation started and the degree of metabolic damage repair.
Biotin deficiency treatmentWhatever is the cause of low levels of vitamin B7, the primary method of treatment is supplementation with biotin.
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