Dietary stearic acid regulates mitochondria in vivo in humans

Deniz Senyilmaz-Tiebe, Daniel H. Pfaff, Sam Virtue, Kathrin V. Schwarz, Thomas Fleming, Sandro Altamura, Martina U. Muckenthaler, Jürgen G. Okun, Antonio Vidal-Puig, Peter Nawroth and Aurelio A. Teleman ()
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Deniz Senyilmaz-Tiebe: German Cancer Research Center (DKFZ)
Daniel H. Pfaff: German Cancer Research Center (DKFZ)
Sam Virtue: Wellcome Trust-MRC Institute of Metabolic Science
Kathrin V. Schwarz: University Hospital Heidelberg
Thomas Fleming: Heidelberg University Hospital
Sandro Altamura: University of Heidelberg
Martina U. Muckenthaler: University of Heidelberg
Jürgen G. Okun: University Hospital Heidelberg
Antonio Vidal-Puig: Wellcome Trust-MRC Institute of Metabolic Science
Peter Nawroth: Heidelberg University Hospital
Aurelio A. Teleman: German Cancer Research Center (DKFZ)

Nature Communications, 2018, vol. 9, issue 1, 1-10

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-05614-6

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