Resistant starch improves insulin sensitivity in metabolic syndrome
Article first published online: 7 APR 2010
© 2010 The Authors. Journal compilation © 2010 Diabetes UK
Volume 27, Issue 4, pages 391–397, April 2010
How to Cite
Johnston, K. L., Thomas, E. L., Bell, J. D., Frost, G. S. and Robertson, M. D. (2010), Resistant starch improves insulin sensitivity in metabolic syndrome. Diabetic Medicine, 27: 391–397. doi: 10.1111/j.1464-5491.2010.02923.x
- Issue published online: 7 APR 2010
- Article first published online: 7 APR 2010
- Accepted 27 November 2009
- magnetic resonance spectroscopy;
- pulse wave velocity
Diabet. Med. 27, 391–397 (2010)
Aims Diets rich in non-viscous fibre are linked to a reduced risk of both diabetes and cardiovascular disease; however, the mechanism of action remains unclear. This study was undertaken to assess whether chronic consumption of this type of fibre in individuals with the metabolic syndrome would improve insulin sensitivity via changes in ectopic fat storage.
Methods The study was a single-blind, randomized, parallel nutritional intervention where 20 insulin resistant subjects consumed either the fibre supplement (resistant starch) (40 g/day) or placebo supplement (0 g/day) for 12 weeks. Insulin sensitivity was measured by euglycaemic–hyperinsulinaemic clamp and ectopic fat storage measured by whole-body magnetic resonance spectroscopy.
Results Resistant starch consumption did not significantly affect body weight, fat storage in muscle, liver or visceral depots. There was also no change with resistant starch feeding on vascular function or markers of inflammation. However, in subjects randomized to consume the resistant starch, insulin sensitivity improved compared with the placebo group (P = 0.023). Insulin sensitivity correlated significantly with changes in waist circumference and fat storage in tibialis muscle and to a lesser extent to visceral-to-subcutaneous abdominal adipose tissue ratio.
Conclusion Consumption of resistant starch improves insulin sensitivity in subjects with the metabolic syndrome. Unlike in animal models, diabetes prevention does not appear to be directly related to changes in body adiposity, blood lipids or inflammatory markers. Further research to elucidate the mechanisms behind this change in insulin sensitivity in human subjects is required.