The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
- Journal
- Nature Communications
In The Last Decade
doi.org/10.1038/ncomms2852 →Countries where authors are citing The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
This map shows the geographic impact of The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43 with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43 more than expected).
Fields of papers citing The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
This network shows the impact of The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.
About The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
This paper, published in 2013, received 1.2k indexed citations . Written by Ikuo Kimura, Kentaro Ozawa, Daisuke Inoue, Takeshi Imamura, Kumi Kimura, Takeshi Maeda, Kazuya Terasawa, Kanako Hirano, Tomoyuki Takahashi and Satoshi Miyauchi covering the research area of Molecular Biology and Physiology. It is primarily cited by scholars working on Molecular Biology (851 citations), Physiology (655 citations) and Endocrinology, Diabetes and Metabolism (189 citations). Published in Nature Communications.
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This paper is also available at doi.org/10.1038/ncomms2852.