Role of dietary beta‐glucans in the prevention of the metabolic syndrome

The present review examines the evidence regarding the effect of β‐glucan on variables linked to the metabolic syndrome (MetS), including appetite control, glucose control, hypertension, and gut microbiota composition. Appetite control can indirectly influence MetS by inducing a decreased energy int...

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Published inNutrition reviews Vol. 70; no. 8; pp. 444 - 458
Main Authors Cloetens, Lieselotte, Ulmius, Matilda, Johansson‐Persson, Anna, Åkesson, Björn, Önning, Gunilla
Format Journal Article
LanguageEnglish
Published Malden, USA Blackwell Publishing Inc 01.08.2012
Wiley
Oxford University Press
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Summary:The present review examines the evidence regarding the effect of β‐glucan on variables linked to the metabolic syndrome (MetS), including appetite control, glucose control, hypertension, and gut microbiota composition. Appetite control can indirectly influence MetS by inducing a decreased energy intake, and promising results for a β‐glucan intake to decrease appetite have been found using gut hormone responses and subjective appetite indicators. Beta‐glucan also improves the glycemic index of meals and beneficially influences glucose metabolism in patients with type 2 diabetes or MetS, as well as in healthy subjects. Furthermore, a blood‐pressure‐lowering effect of β‐glucan in hypertensive subjects seems fairly well substantiated. The gut microbiota composition might be an interesting target to prevent MetS, and preliminary results indicate the prebiotic potential of β‐glucan. The evidence that β‐glucan influences appetite control and gut microbiota in a positive way is still insufficient or difficult to interpret, and additional studies are needed in this field. Still, much evidence indicates that increased β‐glucan intake could prevent MetS. Such evidence should encourage increased efforts toward the development of β‐glucan‐containing functional foods and promote the intake of β‐glucan‐rich foods, with the aim of reducing healthcare costs and disease prevalence.
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ISSN:0029-6643
1753-4887
1753-4887
DOI:10.1111/j.1753-4887.2012.00494.x