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Sökning: WFRF:(Shilkova O) > (2021) > Orphan GPR116 media...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003475naa a2200697 4500
001oai:prod.swepub.kib.ki.se:146789714
003SwePub
008240913s2021 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1467897142 URI
024a https://doi.org/10.1038/s41467-021-22579-12 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Georgiadi, A4 aut
2451 0a Orphan GPR116 mediates the insulin sensitizing effects of the hepatokine FNDC4 in adipose tissue
264 c 2021-05-20
264 1b Springer Science and Business Media LLC,c 2021
520 a The proper functional interaction between different tissues represents a key component in systemic metabolic control. Indeed, disruption of endocrine inter-tissue communication is a hallmark of severe metabolic dysfunction in obesity and diabetes. Here, we show that the FNDC4-GPR116, liver-white adipose tissue endocrine axis controls glucose homeostasis. We found that the liver primarily controlled the circulating levels of soluble FNDC4 (sFNDC4) and lowering of the hepatokine FNDC4 led to prediabetes in mice. Further, we identified the orphan adhesion GPCR GPR116 as a receptor of sFNDC4 in the white adipose tissue. Upon direct and high affinity binding of sFNDC4 to GPR116, sFNDC4 promoted insulin signaling and insulin-mediated glucose uptake in white adipocytes. Indeed, supplementation with FcsFNDC4 in prediabetic mice improved glucose tolerance and inflammatory markers in a white-adipocyte selective and GPR116-dependent manner. Of note, the sFNDC4-GPR116, liver-adipose tissue axis was dampened in (pre) diabetic human patients. Thus our findings will now allow for harnessing this endocrine circuit for alternative therapeutic strategies in obesity-related pre-diabetes.
700a Lopez-Salazar, V4 aut
700a El-Merahbi, R4 aut
700a Karikari, RA4 aut
700a Ma, XC4 aut
700a Mouraeo, A4 aut
700a Klepac, K4 aut
700a Buehler, L4 aut
700a Alfaro, AJ4 aut
700a Kaczmarek, I4 aut
700a Linford, A4 aut
700a Bosma, M4 aut
700a Shilkova, Ou Karolinska Institutet4 aut
700a Ritvos, O4 aut
700a Nakamura, N4 aut
700a Hirose, S4 aut
700a Lassi, M4 aut
700a Teperino, R4 aut
700a Machado, J4 aut
700a Scheideler, M4 aut
700a Dietrich, A4 aut
700a Geerlof, A4 aut
700a Feuchtinger, A4 aut
700a Blutke, A4 aut
700a Fischer, K4 aut
700a Mueller, TD4 aut
700a Kessler, K4 aut
700a Schoeneberg, T4 aut
700a Thor, D4 aut
700a Hornemann, S4 aut
700a Kruse, M4 aut
700a Nawroth, P4 aut
700a Pivovarova-Ramich, O4 aut
700a Pfeiffer, AFH4 aut
700a Sattler, M4 aut
700a Blueher, M4 aut
700a Herzig, S4 aut
710a Karolinska Institutet4 org
773t Nature communicationsd : Springer Science and Business Media LLCg 12:1, s. 2999-q 12:1<2999-x 2041-1723
856u https://www.nature.com/articles/s41467-021-22579-1.pdf
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:146789714
8564 8u https://doi.org/10.1038/s41467-021-22579-1

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