Biotin is a water-soluble, sulfur containing B vitamin. At one time, it was referred to as vitamin H.
In foods, biotin is often found bound to proteins or as biocytin (biotin bound to the amino acid lysine). Biotin proteins are rapidly degraded in the digestive tract, releasing biotin, biotinyl peptides, or biocytin. Biocytin and biotinyl peptides are further hydrolyzed by the enzyme biotinidase to release free biotin, which is absorbed. Biocytin is also absorbed, but not as efficiently as free biotin.
The amount of biotin found in foods is much lower than other B vitamins.
Biotin is required for the production and utilization of fats and amino acids in the body.
Biotin is necessary for all organisms but mammals and many plants are unable to synthesize biotin. Bacteria, yeast, other fungi and algae, and certain plant species can produce biotin.
In the human body, bacteria in the large intestine synthesize biotin which may be absorbed.
Avidin (a protein found in raw egg whites) binds tightly to biotin, preventing absorption. Cooking inactivates avidin.
Biotin is a cofactor for five enzymes, called carboxylases, that are essential for metabolism of carbohydrates, fats, and proteins.
The five carboxylase enzymes in mammalian tissue that require biotin are: acetyl coenzyme A (CoA) carboxylase (two forms; required for synthesis of fatty acids), pyruvate carboxylase (critical for synthesis of glucose from amino acids and fats), propionyl CoA carboxylase (essential for matabolism of amino acids, cholesterol, and odd chain fatty acids), and beta-methylcrotonyl CoA carboxylase (involved in synthesis of leucine).
Recent results indicate that gene expression is regulated by biotinylation (attachment of biotin to specific binding sites).
Although clinical deficiency of biotin is rare, it can
occur from prolonged consumption of raw egg whites, which contains the
biotin-binding protein, avidin. Avidin is destroyed by cooking.
Deficiency can also occur from long-term total parenteral nutrition, a genetic defect in the biotin-dependent enzymes, or from malabsorption syndromes such as short-gut syndrome.
Some signs of biotin deficiency are: dry, scaly skin, nausea, anorexia, seborrheic dermatitis, alopecia (hair loss), conjunctivitis, depression, and hallucinations.
No toxic effects of oral biotin have been reported in humans or animals, even at doses up to 10 mg/day. Multivitamin/mineral supplements typically contain between 30 – 60 mcg per daily dose.
Biotin is widely distributed throughout the food supply, but some of the more
concentrated sources of biotin include: egg yolk, soybeans, organ meats (liver, kidney), yeast, cheese, barley, Brewer's yeast, and milk.
Individuals with a carboxylase deficiency are usually treated with pharmacologic doses of biotin. One study showed that high oral doses of biotin were completely absorbed in healthy adults. 2
Anticonvulsants, such as carbamazepine and Phenobarbital, may deplete biotin by competing for absorption in the intestine. Biotin supplementation may be helpful during long-term anticonvulsant therapy. Separating biotin supplements and drug doses by two to three hours prevents this potential competition.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship. 345
Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes.
The efficacy of a combination of 600 mcg chromium picolinate and 2 mg biotin daily for 90 days was evaluated in a recent study. Four hundred forty-seven men and women with poorly controlled type 2 diabetes mellitus participated in the randomized, placebo-controlled, clinical trial. Participants consumed their normal medications throughout the trial, in addition to the supplements or a placebo. At the end of the trial, a significant reduction in hemoglobin A1c (HbA1c) was noted (p=0.03). HbA1c is a measurement of the average glucose levels for the preceding three months. The average reduction in HbA1c for the supplemented group was 0.54%. This reduction was most significant for those with baseline HbA1c of at least 10% (p=0.005). Fastinf glucose was significantly reduced by 9.8 mg/dl for the supplemented group compared to a 0.7 mg/dl increase for the placebo group (p=0.02). The results of this study indicate that a combination of chromium picolinate and biotin can help to improve measurements of glucose metabolism.6
Chromium picolinate and biotin combination reduces atherogenic index of plasma in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial.
A small, placebo-controlled, double-blind, randomized clinical trial investigated the affect of chromium picolinate and biotin supplements on measures of cardiovascular disease risk. Thirty-six moderately obese men and women with poorly controlled type 2 diabetes mellitus participated in the study. Subjects were randomly assigned to receive 600 mg chromium picolinate plus 2 mg biotin or a placebo for four weeks. At the end of the study, the supplemented group demonstrated a significant reduction in the atherogenic index of plasma (P<0.05). Triglycerides (P<0.02) and the LDL to HDL ratio (P<0.05) were also significantly reduced in the supplemented group after four weeks. In the supplemented group, glucose concentration at one and two hours and the are under the curve were significantly reduced; fructosamine concentration was also reduced. These data suggest that chromium picolinate, in combination with biotin, significantly improve measures of cardiovascular disease risk and glucose control in people with type 2 diabetes mellitus. 7
The effect of chromium picolinate and biotin supplementation on glycemic control in poorly controlled patients with type 2 diabetes mellitus: a placebo-controlled, double-blind, randomized trial.
This pilot study investigated the effect of chromium picolinate and biotin on glycemic control in people with poorly controlled type 2 diabetes mellitus. Previous studies have suggested that glucose uptake by skeletal muscle cells and glucose disposal are enhanced by a combination of chromium picolinate and biotin. Forty-three men and women aged 18 to 65 years with impaired glycemic control enrolled in the study and were randomized to receive 600 mcg chromium picolinate and 2 mg biotin daily or a placebo for four weeks. Glycemic control and blood lipids were monitored at baseline and at the end of the study. Glucose tolerance was significantly improved (P<0.03) in the supplemented group relative to the placebo group. Reductions in fructosamine (P<0.03), triglycerides (P<0.02), and triglyceride:high-density lipoprotein cholesterol ratio (P<0.05) were also noted in the supplemented group. The results of this pilot study indicate that chromium picolinate with biotin may improve glycemic control and lipid metabolism in people with poorly controlled type 2 diabetes mellitus. 8
Biotin supplementation reduces plasma triacylglycerol and VLDL in type 2 diabetic patients and in nondiabetic subjects with hypertriglyceridemia.
The affect of biotin supplementation on blood lipid profiles, glucose concentration, and insulin were investigated in a small study. Eighteen people with type 2 diabetes and 15 nondiabetic people participated in the study. Ages ranged from 30 to 65 years. Participants were randomized to receive either 15 mg biotin or a placebo daily for 28 days. Plasma samples were analyzed at baseline and 28 days for total triglyceride, cholesterol, very low density lipoprotein (VLDL), glucose, and insulin. In both the diabetic and nondiabetic subjects, biotin supplementation significantly reduced plasma triacylglycerol (P=0.005) and VLDL (P=0.005) concentrations. Cholesterol, glucose, and insulin were not significantly altered in any group. These results suggest that biotin may improve hypertriglyceridemia. 9
Effects of biotin on pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and markers for glucose and lipid homeostasis in type 2 diabetic patients and nondiabetic subjects.
Biotin is essential for function of the biotin-dependent carboxylase enzymes necessary for normal metabolism. A small study investigated the affect of biotin supplementation (15 mg/day) versus placebo on the function of pyruvate carboxylase, acetyl-CoA carboxylase, and propionyl carboxylase. Additionally, markers of glucose and lipid homeostasis were monitored. Twenty-four people with type 2 diabetes and 30 people without diabetes aged 33 to 70 years enrolled in the study. Both men and women were included. Participants were randomized to receive either 15 mg biotin daily or a placebo. Plasma and lymphocytes were collected at baseline, on day 14, and on day 28 for analysis. Activity of all three carboxylase enzymes monitored was significantly increased by biotin supplementation at 14 and 28 days (P<0.05 for each enzyme). Diabetic state did not alter the effect of biotin supplementation. The results of this study indicate that biotin supplementation increases activity of carboxylase enzymes. A larger trial is currently being conducted to investigate the clinical effects of this increased activity. 10
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