High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes
Medical Hypotheses (1999) 52(5): 401-406
M. F. McCarty
Summary Glucokinase (GK), expressed in hepatocyte and pancreatic B cells, has a central regulatory role in glucose metabolism. Efficient GK activity is required for normal glucose-stimulated insulin secretion, postprandial hepatic glucose uptake, and the appropriate suppression of hepatic glucose output and gluconeogenesis by elevated plasma glucose. Hepatic GK activity is subnormal in diabetes, and GK may also be decreased in the B cells of type II diabetics. In supraphysiological concentrations, biotin promotes the transcription and translation of the GK gene in hepatocytes; this effect appears to be mediated by activation of soluble guanylate cyclase. More recent evidence indicates that biotin likewise increases GK activity in islet cells. On the other hand, high-dose biotin suppresses hepatocyte transcription of phosphoenolpyruvate carboxykinase, the rate-limiting enzyme for gluconeogenesis. Administration of high-dose biotin has improved glycemic control in several diabetic animals models, and a recent Japanese clinical study concludes that biotin (3 mg t.i.d. orally) can substantially lower fasting glucose in type II diabetics, without side-effects. The recently demonstrated utility of chromium picolinate in type II diabetes appears to reflect improved peripheral insulin sensitivity - a parameter which is unlikely to be directly influenced by biotin. Thus, the joint administration of supranutritional doses of biotin and chromium picolinate is likely to combat insulin resistance, improve B-cell function, enhance postprandial glucose uptake by both liver and skeletal muscle, and inhibit excessive hepatic glucose production. Conceivably, this safe, convenient, nutritional regimen will constitute a definitive therapy for many type II diabetics, and may likewise be useful in the prevention and management of gestational diabetes. Biotin should also aid glycemic control in type I patients.
Additional note by poster:
The dramatic effects of oral megadose biotin in diabetes have been
largely ignored by medical doctors, perhaps partly because some of the
research papers investigating this effect are not available in medline.
Also biotin is not a patentable drug and so there exists no motivation
for drug companies to promote this as a possible therapy.
Also note that supplemental magnesium (500 mg/day) has also been found
to reduce insulin requirements in type I diabetics. (Magnesium 1988 7:
IMHO - I expect that biotin/chromium picolinate/magnesium supplementation could eliminate the use of insulin by most type II diabetics who try combination. Needless to say, don't expect either drug companies selling insulin, or doctors to recommend this. If you want to try this - you're on your own.
Also note that 16 mg/day biotin has been found to eliminate the need for insulin in some type I diabetics. (Annals of the New York Academy of Sciences June 24 1985 447: 389-392 - note that this citation is not included in medline's database even though other papers from the same issue are)