Supplementation of 1-Kestose Modulates the Gut Microbiota Composition to Ameliorate Glucose Metabolism in Obesity-Prone Hosts

Laboratory of Nutritional Biochemistry, Department of Applied Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya 464-8601, Aichi, Japan

Department of Gastroenterology and Hepatology, Fujita Health University, Toyoake 470-1192, Aichi, Japan

B Food Science Co., Ltd., Chita 478-0046, Aichi, Japan

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Healthcare Systems Co., Ltd., Nagoya 466-0058, Aichi, Japan

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Preventive Medical Center, Shin Oyama City Hospital, Oyama 323-0827, Tochigi, Japan

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Metabologenomics, Inc., Tsuruoka 997-0052, Yamagata, Japan

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Department of Food, Aroma and Cosmetic Chemistry, Faculty of Bioindustry, Tokyo University of Agriculture, Abashiri 099-2493, Hokkaido, Japan

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Department of Food and Nutritional Sciences, College of Bioscience and Biotechnology, Chubu University, Kasugai 487-8501, Aichi, Japan

Author to whom correspondence should be addressed.

Academic Editor: Oliver Chen

Nutrients 2021, 13(9), 2983; https://doi.org/10.3390/nu13092983

Received: 1 August 2021 / Revised: 24 August 2021 / Accepted: 26 August 2021 / Published: 27 August 2021

(This article belongs to the Section Prebiotics and Probiotics)

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Abstract

Insulin resistance leads to the onset of medical conditions such as type 2 diabetes, and its development is associated with the alteration in the gut microbiota. Although it has been demonstrated that supplementation with prebiotics modulates the gut microbiota, limited evidence is available for effects of prebiotics on insulin resistance, especially for humans. We investigated the prebiotic effect of 1-kestose supplementation on fasting insulin concentration in obesity-prone humans and rats. In the preliminary study using rats, the hyperinsulinemia induced by high-fat diet was suppressed by intake of water with 2% (w/v) 1-kestose. In the clinical study using obese-prone volunteers, the fasting serum insulin level was significantly reduced from 6.5 µU/mL (95% CI, 5.5–7.6) to 5.3 (4.6–6.0) by the 12-week intervention with supplementation of 10 g 1-kestose/day, whereas it was not changed by the intervention with placebo (6.2 µU/mL (5.4–7.1) and 6.5 (5.5–7.6) before and after intervention, respectively). The relative abundance of fecal Bifidobacterium was significantly increased to 0.3244 (SD, 0.1526) in 1-kestose-supplemented participants compared to that in control participants (0.1971 (0.1158)). These results suggest that prebiotic intervention using 1–kestose may potentially ameliorate insulin resistance in overweight humans via the modulation of the gut microbiota. UMIN 000028824. View Full-Text

Keywords: insulin resistance; obesity; prebiotics; gut microbiota; Bifidobacterium

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MDPI and ACS Style

Watanabe, A.; Tochio, T.; Kadota, Y.; Takahashi, M.; Kitaura, Y.; Ishikawa, H.; Yasutake, T.; Nakano, M.; Shinohara, H.; Kudo, T.; Nishimoto, Y.; Mizuguchi, Y.; Endo, A.; Shimomura, Y. Supplementation of 1-Kestose Modulates the Gut Microbiota Composition to Ameliorate Glucose Metabolism in Obesity-Prone Hosts. Nutrients 2021, 13, 2983. https://doi.org/10.3390/nu13092983

AMA Style

Watanabe A, Tochio T, Kadota Y, Takahashi M, Kitaura Y, Ishikawa H, Yasutake T, Nakano M, Shinohara H, Kudo T, Nishimoto Y, Mizuguchi Y, Endo A, Shimomura Y. Supplementation of 1-Kestose Modulates the Gut Microbiota Composition to Ameliorate Glucose Metabolism in Obesity-Prone Hosts. Nutrients. 2021; 13(9):2983. https://doi.org/10.3390/nu13092983

Chicago/Turabian Style

Watanabe, Ayako, Takumi Tochio, Yoshihiro Kadota, Motoki Takahashi, Yasuyuki Kitaura, Hirohito Ishikawa, Takanori Yasutake, Masahiro Nakano, Hiroe Shinohara, Toru Kudo, Yuichiro Nishimoto, Yoshinori Mizuguchi, Akihito Endo, and Yoshiharu Shimomura. 2021. "Supplementation of 1-Kestose Modulates the Gut Microbiota Composition to Ameliorate Glucose Metabolism in Obesity-Prone Hosts" Nutrients 13, no. 9: 2983. https://doi.org/10.3390/nu13092983

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Supplementation of 1-Kestose Modulates the Gut Microbiota Composition to Ameliorate Glucose Metabolism in Obesity-Prone Hosts

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