Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796
The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones. However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have ide...
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| Veröffentlicht in: | Cell research 2023-04, Vol.33 (4), p.273-287 |
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| creator | Long, Aijun Liu, Yang Fang, Xinlei Jia, Liangjie Li, Zhiyuan Hu, Jiang Wu, Shuang Chen, Chao Huang, Ping Wang, Yiguo |
| description | The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones. However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting. Mechanistically, famsin is shed from a single-pass transmembrane protein, Gm11437, during fasting and then binds OLFR796, an olfactory receptor, to activate intracellular calcium mobilization. This famsin-OLFR796 signaling axis promotes gluconeogenesis and ketogenesis for energy mobilization, and torpor for energy conservation during fasting. In addition, neutralization of famsin by an antibody improves blood glucose profiles in diabetic models, which identifies famsin as a potential therapeutic target for treating diabetes. Therefore, our results demonstrate that communication between the intestine and other organs by a famsin-OLFR796 signaling axis is critical for metabolic adaptations to fasting. |
| doi_str_mv | 10.1038/s41422-023-00782-7 |
| format | Article |
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However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting. Mechanistically, famsin is shed from a single-pass transmembrane protein, Gm11437, during fasting and then binds OLFR796, an olfactory receptor, to activate intracellular calcium mobilization. This famsin-OLFR796 signaling axis promotes gluconeogenesis and ketogenesis for energy mobilization, and torpor for energy conservation during fasting. In addition, neutralization of famsin by an antibody improves blood glucose profiles in diabetic models, which identifies famsin as a potential therapeutic target for treating diabetes. Therefore, our results demonstrate that communication between the intestine and other organs by a famsin-OLFR796 signaling axis is critical for metabolic adaptations to fasting.</description><identifier>ISSN: 1748-7838</identifier><identifier>ISSN: 1001-0602</identifier><identifier>EISSN: 1748-7838</identifier><identifier>DOI: 10.1038/s41422-023-00782-7</identifier><identifier>PMID: 36806353</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>13/1 ; 13/106 ; 13/109 ; 13/31 ; 631/80/304 ; 631/80/86 ; 64/60 ; 82/58 ; 82/83 ; Adaptation ; Antibodies ; Biomedical and Life Sciences ; Blood Glucose - metabolism ; Calcium (intracellular) ; Calcium signalling ; Cell Biology ; Chemical communication ; Diabetes mellitus ; Energy conservation ; Fasting ; Fasting - physiology ; Gluconeogenesis ; Gluconeogenesis - physiology ; Hormones ; Hormones - metabolism ; Intestine ; Intracellular signalling ; Ketogenesis ; Ketone Bodies - metabolism ; Life Sciences ; Liver - metabolism ; Metabolism ; Neutralization ; Odorant receptors ; Organs ; Receptors ; Signaling ; Therapeutic targets ; Torpor</subject><ispartof>Cell research, 2023-04, Vol.33 (4), p.273-287</ispartof><rights>The Author(s) under exclusive licence to Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s) under exclusive licence to Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences.</rights><rights>The Author(s) under exclusive licence to Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-6d0d0e9c457e0cec2e3239e0bd5b02a4004d15ee9fd331a45257fe6c1b3ad4343</citedby><cites>FETCH-LOGICAL-c431t-6d0d0e9c457e0cec2e3239e0bd5b02a4004d15ee9fd331a45257fe6c1b3ad4343</cites><orcidid>0000-0003-1458-9234</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10066382/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10066382/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,41488,42557,51319,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36806353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Long, Aijun</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Fang, Xinlei</creatorcontrib><creatorcontrib>Jia, Liangjie</creatorcontrib><creatorcontrib>Li, Zhiyuan</creatorcontrib><creatorcontrib>Hu, Jiang</creatorcontrib><creatorcontrib>Wu, Shuang</creatorcontrib><creatorcontrib>Chen, Chao</creatorcontrib><creatorcontrib>Huang, Ping</creatorcontrib><creatorcontrib>Wang, Yiguo</creatorcontrib><title>Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796</title><title>Cell research</title><addtitle>Cell Res</addtitle><addtitle>Cell Res</addtitle><description>The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones. However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting. Mechanistically, famsin is shed from a single-pass transmembrane protein, Gm11437, during fasting and then binds OLFR796, an olfactory receptor, to activate intracellular calcium mobilization. This famsin-OLFR796 signaling axis promotes gluconeogenesis and ketogenesis for energy mobilization, and torpor for energy conservation during fasting. In addition, neutralization of famsin by an antibody improves blood glucose profiles in diabetic models, which identifies famsin as a potential therapeutic target for treating diabetes. 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metabolism</subject><subject>Life Sciences</subject><subject>Liver - metabolism</subject><subject>Metabolism</subject><subject>Neutralization</subject><subject>Odorant receptors</subject><subject>Organs</subject><subject>Receptors</subject><subject>Signaling</subject><subject>Therapeutic targets</subject><subject>Torpor</subject><issn>1748-7838</issn><issn>1001-0602</issn><issn>1748-7838</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kV9rFDEUxQdRbK1-AR8k4IsPHb35M5PMk5TiqrBQEH0OmeTuNmUmWZPMQr-92W6t1Qefcsn53ZMcTtO8pvCeAlcfsqCCsRYYbwGkYq180pxSKVQrFVdPH80nzYucbwBYJzr6vDnhvYKed_y0uV2ZOftwTgwJcY8T2S6lzWgTFnTkOqY5BjwnNoaS_LgUzKREMmMxY5y8JcaZXTHFx3AnbEwuPmzJ3hsy-uAOc732JZOEFnclJnK1Xn2TQ_-yebYxU8ZX9-dZ82P16fvll3Z99fnr5cW6tYLT0vYOHOBgRScRLFqGnPEBYXTdCMwIAOFohzhsHOfUiI51coO9pSM3TnDBz5qPR9_dMs7oLNYkZtK75GeTbnU0Xv-tBH-tt3GvKUDfc8Wqw7t7hxR_LpiLnn22OE0mYFyyZlKqQQEMB_TtP-hNXFKo-So1cNarntNKsSNlU8w54ebhNxT0oVp9rFbXavVdtVrWpTePczys_O6yAvwI5CqFLaY_b__H9hehgbBy</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Long, Aijun</creator><creator>Liu, Yang</creator><creator>Fang, Xinlei</creator><creator>Jia, Liangjie</creator><creator>Li, Zhiyuan</creator><creator>Hu, Jiang</creator><creator>Wu, Shuang</creator><creator>Chen, Chao</creator><creator>Huang, Ping</creator><creator>Wang, Yiguo</creator><general>Springer Nature Singapore</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1458-9234</orcidid></search><sort><creationdate>20230401</creationdate><title>Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796</title><author>Long, Aijun ; Liu, Yang ; Fang, Xinlei ; Jia, Liangjie ; Li, Zhiyuan ; Hu, Jiang ; Wu, Shuang ; Chen, Chao ; Huang, Ping ; Wang, Yiguo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-6d0d0e9c457e0cec2e3239e0bd5b02a4004d15ee9fd331a45257fe6c1b3ad4343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>13/1</topic><topic>13/106</topic><topic>13/109</topic><topic>13/31</topic><topic>631/80/304</topic><topic>631/80/86</topic><topic>64/60</topic><topic>82/58</topic><topic>82/83</topic><topic>Adaptation</topic><topic>Antibodies</topic><topic>Biomedical and Life Sciences</topic><topic>Blood Glucose - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Long, Aijun</au><au>Liu, Yang</au><au>Fang, Xinlei</au><au>Jia, Liangjie</au><au>Li, Zhiyuan</au><au>Hu, Jiang</au><au>Wu, Shuang</au><au>Chen, Chao</au><au>Huang, Ping</au><au>Wang, Yiguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796</atitle><jtitle>Cell research</jtitle><stitle>Cell Res</stitle><addtitle>Cell Res</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>33</volume><issue>4</issue><spage>273</spage><epage>287</epage><pages>273-287</pages><issn>1748-7838</issn><issn>1001-0602</issn><eissn>1748-7838</eissn><abstract>The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones. However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting. Mechanistically, famsin is shed from a single-pass transmembrane protein, Gm11437, during fasting and then binds OLFR796, an olfactory receptor, to activate intracellular calcium mobilization. This famsin-OLFR796 signaling axis promotes gluconeogenesis and ketogenesis for energy mobilization, and torpor for energy conservation during fasting. In addition, neutralization of famsin by an antibody improves blood glucose profiles in diabetic models, which identifies famsin as a potential therapeutic target for treating diabetes. Therefore, our results demonstrate that communication between the intestine and other organs by a famsin-OLFR796 signaling axis is critical for metabolic adaptations to fasting.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><pmid>36806353</pmid><doi>10.1038/s41422-023-00782-7</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-1458-9234</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/106 13/109 13/31 631/80/304 631/80/86 64/60 82/58 82/83 Adaptation Antibodies Biomedical and Life Sciences Blood Glucose - metabolism Calcium (intracellular) Calcium signalling Cell Biology Chemical communication Diabetes mellitus Energy conservation Fasting Fasting - physiology Gluconeogenesis Gluconeogenesis - physiology Hormones Hormones - metabolism Intestine Intracellular signalling Ketogenesis Ketone Bodies - metabolism Life Sciences Liver - metabolism Metabolism Neutralization Odorant receptors Organs Receptors Signaling Therapeutic targets Torpor |
| title | Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796 |
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