Berberine Lowers Glucose Levels in Type 2 Diabetics

Study examines how Berberine affects insulin receptor expression in diabetic patients.

By Steve Austin, ND

Printer Friendly PagePrinter Friendly Page

Reference

Zhang H, Wei J, Xue R, et al. Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Metabolism 2010;59:285-292
 

Design

This randomized, blinded intervention trial compared the effect of berberine against that of 2 conventional hypoglycemic drugs. For ethical reasons, no patients were assigned to placebo.
 

Participants

97 patients with type 2 diabetes with a fasting blood glucose ≥126 mg/dL or a postprandial level of ≥200 mg/dL
 

Study Medication and Dosage

Patients were randomly assigned to take berberine (500 mg twice per day) in the form of berberine HCl, 1.5 gram per day metformin, or 4 mg per day rosiglitazone for 2 months.
 

Main Outcome Measures

Blood glucose, glycosylated hemoglobin (HgbA1c), and serum triglycerides (TG)
 

Key Findings

Fasting blood glucose fell 48 mg/dL or 26% (P<0.001 versus baseline), a decrease similar to (and statistically nonsignificantly different from) the 30% and 18% declines observed in the metformin and rosiglitazone groups respectively. In the presence of declining glucose levels, serum insulin declined 28% in those given berberine (P<0.01), further confirming an improvement in glucose tolerance in that group. (Before-and-after insulin levels in the other 2 groups were not provided.)
 
HgbA1c fell 18% in those assigned to berberine (P<0.001 versus baseline), compared with similar declines in the other 2 groups (-23% and -18% in the metformin and rosiglitazone groups respectively).
 
TG levels declined 18% in those assigned to berberine (P<0.01 versus baseline), compared with 6% and 16% declines in the metformin and rosiglitazone groups respectively.
 

Practice Implications

Berberine has previously been reported to increase insulin receptor expression and improve parameters of glucose tolerance in rodents and in human cell lines. The findings of this report suggest that for type 2 diabetic patients, 1 gram per day berberine is approximately as effective as the use of first-line prescription hypoglycemic drugs. The effect appears to have been a function of up-regulating insulin receptor activity.
The report of improved glucose tolerance in humans mirrors recent findings from other trials conducted by the same and other research groups.
 The report of improved glucose tolerance in humans mirrors recent findings from other trials conducted by the same1 and other research groups.2
 
Although liver enzymes of the diabetic patients were normal before the trial began, those assigned to berberine experienced a 26% decline in alanine aminotransferase (ALT) levels (P<0.01) and a 34% decline in gamma-glutamyl transferase (GGT) levels (P<0.01) by the end of the 2-month trial. In contrast, both hypoglycemic drugs are contraindicated in patients with liver disease. As a result of the impressive effects of berberine on hepatic health, an additional 35 patients with glucose intolerance or type 2 diabetes who were also suffering from hepatitis B or C were given berberine to see whether similar reductions in liver enzyme levels would occur.
 
Improvements in glucose tolerance also appeared in this set of patients, and those changes essentially mirrored the improvements reported for other diabetic patients discussed above. For these hepatitis patients, ALT levels declined 29%–50%, with similar declines in AST levels. All changes in enzyme levels were highly statistically significant.
 
Despite the current report’s finding that berberine “always shows [a] convincing safety record in patients,” some cautions should be considered in using this botanical extract. Berberine has been reported to interfere with bilirubin metabolism in infants,3 thus hypothetically exacerbating neonatal jaundice and potentially providing argument against use in pregnancy and lactation. Also, while berberine has lowered cholesterol, it has recently been reported to promote foam cell formation in animals.4 Whether the trade-off would favor protection against or cause progression of heart disease is unknown, though the cholesterol-lowering effect has recently been duplicated in humans.5

About the Author

Steve Austin, ND, is a naturopathic physician and co-author of the A-Z Guide to Drug-Herb-Vitamin Interactions; Breast Cancer: What You Should Know (But May Not Be Told) About Prevention, Diagnosis, and Treatment and The Natural Pharmacy, now in its second edition. Dr. Austin was the founding Chief Science Officer for the Healthnotes team of writers. He is also former Professor of Nutrition at National College of Naturopathic Medicine, in Portland, Oregon. Previously, Dr. Austin headed the nutrition departments at Bastyr University in Seattle and Western States Chiropractic College in Portland, and has been on the faculties of four of the five naturopathic colleges in North America. He is a contributor to the Textbook of Natural Medicine, and was nutrition editor of the Quarterly Review of Natural Medicine and the Healthnotes Review of Natural Medicine. Dr. Austin is also an international lecturer on topics related to clinical nutrition.

References

1. Zhang Y, Li X, Zou D, et al. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. J Clin Endocrinol Metab. 2008;93:2559-2565.
2. Yin J, Xing H, Ye J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism. 2008;57(5):712-717.
3. Chan, E. Displacement of bilirubin from albumin by berberine. Biol Neonate. 1993;63(4):201-208.
4. Li K, Yao W, Zheng X, Liao K. Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage. Cell Res. 2009;19(8):1006-1017.
5. Yin J, Xing H, Ye J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism. 2008;57(5):712-717.

Copyright © 2010 by the Natural Medicine Journal All rights reserved. No part of this article may be reproduced in any form without the written permission of the publisher.