Send to

Choose Destination
Br J Nutr. 2000 Jul;84(1):57-61.

Acarbose raises serum butyrate in human subjects with impaired glucose tolerance.

Author information

Department of Nutritional Sciences and Medicine, University of Toronto, Ontario, Canada.


The fermentation of starch in vitro produces a higher proportion of butyrate than the fermentation of most other substrates. The alpha-glucosidase inhibitor acarbose increases the amount of starch entering the colon, and has been shown to increase faecal butyrate in humans. It is generally considered that colonic butyrate is quantitatively removed by the colonic mucosa and liver and does not appear in peripheral blood. However, studies in animals suggest that a small proportion of colonic butyrate reaches peripheral blood. Thus, we hypothesised that an increase in colonic butyrate production would result in a rise in serum butyrate in human subjects. To test this, subjects with impaired glucose tolerance were randomly treated in a double-blind fashion with placebo (n 11) or acarbose (n 11) (100 mg three times per day). Serum short-chain fatty acid concentrations were measured twelve times over 12 h with subjects eating a standard diet before randomization and after 4 months of therapy. At baseline, 12 h mean serum butyrate concentrations were similar in the placebo and acarbose groups (2.8 (SE 0.7) and 3.3 (SE 0.6) microM, respectively). After 4 months on placebo, mean serum butyrate (2.6 (SE 0.5) microM) was no different from baseline. However, after 4 months on acarbose, serum butyrate had increased to 4.2 (SE 1.0) microM, a value which differed significantly from both the baseline value in the acarbose group and the treatment value in the placebo group. We conclude that acarbose increased serum butyrate in subjects with impaired glucose tolerance. These results support the hypothesis that increased colonic butyrate production in human subjects can be detected by an increase in serum butyrate.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Cambridge University Press
Loading ...
Support Center