Dietary Capsaicin Improves Glucose Homeostasis and Alters the Gut Microbiota in Obese Diabetic ob/ob Mice - PubMed (original) (raw)

Dietary Capsaicin Improves Glucose Homeostasis and Alters the Gut Microbiota in Obese Diabetic ob/ob Mice

Jun-Xian Song et al. Front Physiol. 2017.

Abstract

Background: The effects of capsaicin on obesity and glucose homeostasis are still controversial and the mechanisms underlying these effects remain largely unknown. This study aimed to investigate the potential relationship between the regulation of obesity and glucose homeostasis by dietary capsaicin and the alterations of gut microbiota in obese diabetic ob/ob mice. Methods: The ob/ob mice were subjected to a normal, low-capsaicin (0.01%), or high-capsaicin (0.02%) diet for 6 weeks, respectively. Obesity phenotypes, glucose homeostasis, the gut microbiota structure and composition, short-chain fatty acids, gastrointestinal hormones, and pro-inflammatory cytokines were measured. Results: Both the low- and high-capsaicin diets failed to prevent the increase in body weight, adiposity index, and Lee's obesity index. However, dietary capsaicin at both the low and high doses significantly inhibited the increase of fasting blood glucose and insulin levels. These inhibitory effects were comparable between the two groups. Similarly, dietary capsaicin resulted in remarkable improvement in glucose and insulin tolerance. In addition, neither the low- nor high-capsaicin diet could alter the α-diversity and β-diversity of the gut microbiota. Taxonomy-based analysis showed that both the low- and high-capsaicin diets, acting in similar ways, significantly increased the Firmicutes/Bacteroidetes ratio at the phylum level as well as increased the Roseburia abundance and decreased the Bacteroides and Parabacteroides abundances at the genus level. Spearman's correlation analysis revealed that the Roseburia abundance was negatively while the Bacteroides and Parabacteroides abundances were positively correlated to the fasting blood glucose level and area under the curve by the oral glucose tolerance test. Finally, the low- and high-capsaicin diets significantly increased the fecal butyrate and plasma total GLP-1 levels, but decreased plasma total ghrelin, TNF-α, IL-1β, and IL-6 levels as compared with the normal diet. Conclusions: The beneficial effects of dietary capsaicin on glucose homeostasis are likely associated with the alterations of specific bacteria at the genus level. These alterations in bacteria induced by dietary capsaicin contribute to improved glucose homeostasis through increasing short-chain fatty acids, regulating gastrointestinal hormones and inhibiting pro-inflammatory cytokines. However, our results should be interpreted cautiously due to the lower caloric intake at the initial stage after capsaicin diet administration.

Keywords: capsaicin; diabetes; glucose homeostasis; gut microbiota; obesity.

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Figures

Figure 1

Figure 1

Effects of dietary capsaicin on obesity parameters. (A) Body weight; (B) total food intake, expressed as grams per mouse per week; (C) total caloric intake, expressed as kcal per mouse per week; (D) adiposity index, calculated according to the following formula: 100× (mesenteric fat weight + epididymal fat weight + perirenal fat weight)/body weight; (E) Lee's obesity index, calculated according to the following formula: body weight (g)0.33 × 104/naso-anal length (mm). N, normal diet group (n = 5); L, low-capsaicin diet group (n = 5); H, high-capsaicin diet group (n = 5). Data are shown as the mean ± SD; +P < 0.05, analyzed by one-way ANOVA with Tukey's post hoc test.

Figure 2

Figure 2

Effect of dietary capsaicin on glucose homeostasis. (A) Blood glucose; (B) insulin; (C) oral glucose tolerance test (OGTT); (D) area under the curve (AUC) for the OGTT, expressed as a percentage of the normal diet group (%); (E) insulin tolerance test (ITT); (F) area under the curve (AUC) for the ITT, expressed as a percentage of the normal diet group (%). N, normal diet group (n = 5); L, low-capsaicin diet group (n = 5); H, high-capsaicin diet group (n = 5). Data are shown as the mean ± SD; +P < 0.05, analyzed by one-way ANOVA with Tukey's post hoc test.

Figure 3

Figure 3

Rarefaction curves of observed species and Shannon-Wiener diversity for all samples. (A) Rarefaction curves of observed species from fecal samples of individual mice fed with a normal diet (red), low-capsaicin diet (green), or high-capsaicin diet (blue). (B) Rarefaction curves of Shannon-Wiener diversity from fecal samples of individual mice fed with a normal diet (red), low-capsaicin diet (green), or high-capsaicin diet (blue).

Figure 4

Figure 4

Effect of dietary capsaicin on the gut microbiota structure. (A) Ace estimator, (B) Chao estimator, (C) Shannon index, (D) Simpson index, (E) unweighted UniFrac distance-based principal coordinate analysis (PCoA), (F) weighted PCoA. N, normal diet group (n = 5); L, low-capsaicin diet group (n = 5); H, high-capsaicin diet group (n = 5). Data are shown as box and whisker plots. The box indicates the interquartile range (IQR, 75th to 25th percentiles of the data), and the mean value is shown as a line within the box; whiskers extend to the most extreme value within 1.5 × IQR, and outliers are shown as black dots. The results were analyzed by one-way ANOVA with Tukey's post hoc test or the Kruskal–Wallis test.

Figure 5

Figure 5

Effect of dietary capsaicin on the gut microbiota composition. (A) Changes in the taxonomic composition of the gut microbiota at the phylum level; (B) the Firmicutes/Bacteroidetes ratio; (C) the abundance of Roseburia; (D) the abundance of Bacteroides; (E) the abundance of Parabacteroides. N, normal diet group (n = 5); L, low-capsaicin diet group (n = 5); H, high-capsaicin diet group (n = 5). Data are shown as box and whisker plots. The box indicates the interquartile range (IQR, 75th to 25th percentiles of the data), and the mean value is shown as a line within the box; whiskers extend to the most extreme value within 1.5 × IQR, and outliers are shown as crosses. The results were analyzed by one-way ANOVA with Tukey's post hoc test or the Kruskal–Wallis test, +P < 0.05.

Figure 6

Figure 6

Correlations between the glucose parameters and the gut microbiota abundance. (A–C): Correlations of the blood glucose level with the abundance of Roseburia (A), Bacteroides (B), and Parabacteroides (C). (D–F) Correlations of the area under the curve (AUC) for the oral glucose tolerance test (OGTT) with the abundance of Roseburia (D), Bacteroides (E), and Parabacteroides (F). The data were analyzed by Spearman correlation analysis.

Figure 7

Figure 7

Effects of dietary capsaicin on short-chain fatty acids, gastrointestinal hormones, and pro-inflammatory cytokines. (A) Fecal short-chain fatty acid levels; (B) plasma total GLP-l level; (C) plasma total ghrelin level; (D) plasma TNF-α level; (E) plasma IL-1β level; (F) plasma IL-6 level. N, normal diet group (n = 5); L, low-capsaicin diet group (n = 5); H, high-capsaicin diet group (n = 5). Data are shown as the mean ± SD; +P < 0.05. The data analyzed by one-way ANOVA with Tukey's post hoc test.

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References

    1. Allais L., De Smet R., Verschuere S., Talavera K., Cuvelier C. A., Maes T. (2017). Transient receptor potential channels in intestinal inflammation: what is the impact of cigarette smoking? Pathobiology 84, 1–15. 10.1159/000446568 - DOI - PubMed
    1. Baboota R. K., Murtaza N., Jagtap S., Singh D. P., Karmase A., Kaur J., et al. . (2014). Capsaicin-induced transcriptional changes in hypothalamus and alterations in gut microbial count in high fat diet fed mice. J. Nutr. Biochem. 25, 893–902. 10.1016/j.jnutbio.2014.04.004 - DOI - PubMed
    1. Bäckhed F., Ding H., Wang T., Hooper L. V., Koh G. Y., Nagy A., et al. . (2004). The gut microbiota as an environmental factor that regulates fat storage. Proc. Natl. Acad. Sci. U.S.A. 101, 15718–11523. 10.1073/pnas.0407076101 - DOI - PMC - PubMed
    1. Bäckhed F., Manchester J. K., Semenkovich C. F., Gordon J. I. (2007). Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc. Natl. Acad. Sci. U.S.A. 104, 979–984. 10.1073/pnas.0605374104 - DOI - PMC - PubMed
    1. Banner K. H., Igney F., Poll C. (2011). TRP channels: emerging targets for respiratory disease. Pharmacol. Ther. 130, 371–384. 10.1016/j.pharmthera.2011.03.005 - DOI - PubMed

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