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Senyilmaz-Tiebe, D.* ; Pfaff, D.H.* ; Virtue, S.* ; Schwarz, K.V.* ; Fleming, T. ; Altamura, S.* ; Muckenthaler, M.U.* ; Okun, J.G.* ; Vidal-Puig, A.* ; Nawroth, P.P. ; Teleman, A.A.*

Dietary stearic acid regulates mitochondria in vivo in humans.

Nat. Commun. 9:3129 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Since modern foods are unnaturally enriched in single metabolites, it is important to understand which metabolites are sensed by the human body and which are not. We previously showed that the fatty acid stearic acid (C18:0) signals via a dedicated pathway to regulate mitofusin activity and thereby mitochondrial morphology and function in cell culture. Whether this pathway is poised to sense changes in dietary intake of C18:0 in humans is not known. We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion. C18:0 intake also causes a drop in circulating long-chain acylcarnitines, suggesting increased fatty acid beta-oxidation in vivo. This work thereby identifies C18:0 as a dietary metabolite that is sensed by our bodies to control our mitochondria. This could explain part of the epidemiological differences between C16:0 and C18:0, whereby C16:0 increases cardiovascular and cancer risk whereas C18:0 decreases both.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cancer Risk; Plasma; Cholesterol; Absorption; Ingestion; Fructose; Disease; Glucose
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 9, Heft: , Seiten: , Artikelnummer: 3129 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-251
DOI 10.1038/s41467-018-05614-6
WOS ID WOS:000440981600006
PubMed ID 30087348
Erfassungsdatum 2018-09-07
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