The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43

Ikuo Kimura (), Kentaro Ozawa, Daisuke Inoue, Takeshi Imamura, Kumi Kimura, Takeshi Maeda, Kazuya Terasawa, Daiji Kashihara, Kanako Hirano, Taeko Tani, Tomoyuki Takahashi, Satoshi Miyauchi, Go Shioi, Hiroshi Inoue and Gozoh Tsujimoto
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Ikuo Kimura: Kyoto University Graduate School of Pharmaceutical Sciences
Kentaro Ozawa: Nara Medical University School of Medicine
Daisuke Inoue: Kyoto University Graduate School of Pharmaceutical Sciences
Takeshi Imamura: Shiga University of Medical Science, Tsukinowa, Seta
Kumi Kimura: Brain/Liver Interface Medicine Research Center, Kanazawa University
Takeshi Maeda: Kyoto University Graduate School of Pharmaceutical Sciences
Kazuya Terasawa: Kyoto University Graduate School of Pharmaceutical Sciences
Daiji Kashihara: Kyoto University Graduate School of Pharmaceutical Sciences
Kanako Hirano: Kyoto University Graduate School of Pharmaceutical Sciences
Taeko Tani: Kyoto University Graduate School of Pharmaceutical Sciences
Tomoyuki Takahashi: Kyoto University Graduate School of Pharmaceutical Sciences
Satoshi Miyauchi: Kyoto University Graduate School of Pharmaceutical Sciences
Go Shioi: Laboratory for Animal Resources and Genetic Engineering, Riken Center for Developmental Biology
Hiroshi Inoue: Brain/Liver Interface Medicine Research Center, Kanazawa University
Gozoh Tsujimoto: Kyoto University Graduate School of Pharmaceutical Sciences

Nature Communications, 2013, vol. 4, issue 1, 1-12

Abstract: Abstract The gut microbiota affects nutrient acquisition and energy regulation of the host, and can influence the development of obesity, insulin resistance, and diabetes. During feeding, gut microbes produce short-chain fatty acids, which are important energy sources for the host. Here we show that the short-chain fatty acid receptor GPR43 links the metabolic activity of the gut microbiota with host body energy homoeostasis. We demonstrate that GPR43-deficient mice are obese on a normal diet, whereas mice overexpressing GPR43 specifically in adipose tissue remain lean even when fed a high-fat diet. Raised under germ-free conditions or after treatment with antibiotics, both types of mice have a normal phenotype. We further show that short-chain fatty acid-mediated activation of GPR43 suppresses insulin signalling in adipocytes, which inhibits fat accumulation in adipose tissue and promotes the metabolism of unincorporated lipids and glucose in other tissues. These findings establish GPR43 as a sensor for excessive dietary energy, thereby controlling body energy utilization while maintaining metabolic homoeostasis.

Date: 2013
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DOI: 10.1038/ncomms2852

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