Biotin treatment increases insulin sensitivity in type 2 diabetics (T2D)

Biotin is a vitamin that acts as a cofactor of carboxylases, however, evidence is growing about its role in gene expression. Biotin affects the expression of critical regulators of glucose homeostasis. The vitamin increases glu-cokinase and insulin expression, and decreases the expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. These effects suggest that biotin might be used to decrease hyperglycemia. The use of the vitamin as antidiabetic agent has been little explored. In diabetic animals and in one human study in T2D, biotin decreases fasted hyperglycemia. We investigated the effect of pharmacological doses of biotin (15 mg/day) during 14 and 28 days, on glucose and insulin concentrations in oral glucose tolerance test (OGTT), as well as on other metabolites in T2D. In a placebo controlled cross-sectional study (n=10) we found that the vitamin decreased glucose and insulin concentrations in OGTT in patients presenting fasted hyperinsulinemia and exacerbated insulin response to the glucose load (n=5). Insulin sensibility analysis by Composite showed that biotin increased (P<0.05) insulin sensitivity by 51.1±23% and 61.3±22% at 14 and 28 days, respectively. Similar increases were found in HOMA sensibility index. Biotin treatment did not affect either glucose or insulin concentrations in OGTT in patients whose insulin secretion responses to glucose load were normal or decreased. No changes were found in response to placebo. Biotin treatment did not significantly modify triglycerides, cholesterol, or escape enzymes concentrations. No adverse effects were reported in any of the patients. In conclusion, biotin increases insulin sensibility in T2D presenting hyperinsulinemia. These results suggest that biotin treatment can be useful in the treatment of insulin resistance