Microbiome. 2017 Feb 7;5(1):12. doi: 10.1186/s40168-017-0230-5.
Resistant starch can improve insulin sensitivity independently of the gut microbiota.
Bindels LB1,
Segura Munoz RR1,
Gomes-Neto JC1,
Mutemberezi V2,
Martínez I3,
Salazar N4,
Cody EA1,
Quintero-Villegas MI1,
Kittana H1,
de Los Reyes-Gavilán CG4,
Schmaltz RJ1,
Muccioli GG2,
Walter J3,5,
Ramer-Tait AE6.
Author information
1 Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA.
2 Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, Université catholique de Louvain, Brussels, Belgium.
3 Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.
4 Department of Microbiology and Biochemistry of Dairy Products, Instituto de Productos Lácteos de Asturias-Consejo Superior de Investigaciones Científicas (IPLA-CSIC), Asturias, Spain.
5 Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.
6 Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA.
aramer-tait2@unl.edu.
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.
KEYWORDS:
Adipose tissue macrophages; Gut microbiota; Insulin sensitivity; Resistant starch
PMID: 28166818 PMCID:
PMC5294823 DOI:
10.1186/s40168-017-0230-5
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