Resistant starch can improve insulin sensitivity independently of the gut microbiota

Authors

Laure B. Bindels, University of Nebraska-Lincoln
Rafael R. Segura Munoz, University of Nebraska-LincolnFollow
João Carlos Gomes-Neto, University of Nebraska-LincolnFollow
Valentin Mutemberezi, Université catholique de Louvain
Inés Martínez, University of Alberta
Nuria Salazar, Instituto de Productos Lácteos de Asturias-Consejo Superior de Investigaciones Científicas (IPLA-CSIC)
Elizabeth A. Cody, University of Nebraska-Lincoln
Maria I. Quintero-Villegas, University of Nebraska-Lincoln
Hatem Kittana, University of Nebraska-Lincoln
Clara G de los Reyes-Gavilán, Instituto de Productos Lácteos de Asturias-Consejo Superior de Investigaciones Científicas (IPLA-CSIC)
Robert J. Schmaltz, University of Nebraska-LincolnFollow
Giulio G. Muccioli, Université catholique de Louvain
Jens Walter, University of AlbertaFollow
Amanda E. Ramer-Tait, University of Nebraska-LincolnFollow

Date of this Version

2017

Citation

Bindels et al. Microbiome (2017) 5:12, DOI 10.1186/s40168-017-0230-5.

Comments

© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License. Used by permission.

Abstract

Background: Obesity-related diseases, including type 2 diabetes and cardiovascular disease, have reached epidemic proportions in industrialized nations, and dietary interventions for their prevention are therefore important. Resistant starches (RS) improve insulin sensitivity in clinical trials, but the mechanisms underlying this health benefit remain poorly understood. Because RS fermentation by the gut microbiota results in the formation of physiologically active metabolites, we chose to specifically determine the role of the gut microbiota in mediating the metabolic benefits of RS. To achieve this goal, we determined the effects of RS when added to a Western diet on host metabolism in mice with and without a microbiota.

Results: RS feeding of conventionalized mice improved insulin sensitivity and redressed some of the Western diet-induced changes in microbiome composition. However, parallel experiments in germ-free littermates revealed that RS-mediated improvements in insulin levels also occurred in the absence of a microbiota. RS reduced gene expression of adipose tissue macrophage markers and altered cecal concentrations of several bile acids in both germ-free and conventionalized mice; these effects were strongly correlated with the metabolic benefits, providing a potential microbiota-independent mechanism to explain the physiological effects of RS.

Conclusions: This study demonstrated that some metabolic benefits exerted by dietary RS, especially improvements in insulin levels, occur independently of the microbiota and could involve alterations in the bile acid cycle and adipose tissue immune modulation. This work also sets a precedent for future mechanistic studies aimed at establishing the causative role of the gut microbiota in mediating the benefits of bioactive compounds and functional foods.