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Randomized Controlled Trial
. 2010 Apr;27(4):391-7.
doi: 10.1111/j.1464-5491.2010.02923.x.

Resistant starch improves insulin sensitivity in metabolic syndrome

Affiliations
Randomized Controlled Trial

Resistant starch improves insulin sensitivity in metabolic syndrome

K L Johnston et al. Diabet Med. 2010 Apr.

Erratum in

  • Corrigendum.
    [No authors listed] [No authors listed] Diabet Med. 2015 Feb;32(2):288. doi: 10.1111/dme.12623. Diabet Med. 2015. PMID: 26892904 No abstract available.

Abstract

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.

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