Association of apolipoprotein M and sphingosine-1-phosphate with brown adipose tissue after cold exposure in humans

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The HDL-associated apolipoprotein M (apoM) and its ligand sphingosine-1-phosphate (S1P) may control energy metabolism. ApoM deficiency in mice is associated with increased vascular permeability, brown adipose tissue (BAT) mass and activity, and protection against obesity. In the current study, we explored the connection between plasma apoM/S1P levels and parameters of BAT as measured via 18F-FDG PET/CT after cold exposure in humans. Fixed (n = 15) vs personalized (n = 20) short-term cooling protocols decreased and increased apoM (− 8.4%, P = 0.032 vs 15.7%, P < 0.0005) and S1P (− 41.0%, P < 0.0005 vs 19.1%, P < 0.005) plasma levels, respectively. Long-term cooling (n = 44) did not affect plasma apoM or S1P levels. Plasma apoM and S1P did not correlate significantly to BAT volume and activity in the individual studies. However, short-term studies combined, showed that increased changes in plasma apoM correlated with BAT metabolic activity (β: 0.44, 95% CI [0.06–0.81], P = 0.024) after adjusting for study design but not BAT volume (β: 0.39, 95% CI [− 0.01–0.78], P = 0.054). In conclusion, plasma apoM and S1P levels are altered in response to cold exposure and may be linked to changes in BAT metabolic activity but not BAT volume in humans. This contrasts partly with observations in animals and highlights the need for further studies to understand the biological role of apoM/S1P complex in human adipose tissue and lipid metabolism.

OriginalsprogEngelsk
Artikelnummer18753
TidsskriftScientific Reports
Vol/bind12
Udgave nummer1
Antal sider11
ISSN2045-2322
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
The authors would like to thank Charlotte Wandel and Lis Schutt Nielsen for their excellent technical assistance. The project was funded by the Novo Nordisk Foundation Excellence Project (grant NNF13OC0003898 to C.C.), the Department of Biomedical Sciences, the University of Copenhagen (to A.B.), the Fundación Alfonso Martin Escudero (to B.M.T), the Netherlands Cardiovascular Research Initiative: an initiative with the support of the Dutch Heart Foundation (CVON2017-20 GENIUS-II to P.C.N.R) and Dutch Diabetes Research Foundation (Junior Postdoc Fellowship; 2015.81.1808 to M.R.B). Neither of the funding sources was involved in study design, data collection, analysis, interpretation of data, writing or submission of the manuscript.

Funding Information:
The authors would like to thank Charlotte Wandel and Lis Schutt Nielsen for their excellent technical assistance. The project was funded by the Novo Nordisk Foundation Excellence Project (grant NNF13OC0003898 to C.C.), the Department of Biomedical Sciences, the University of Copenhagen (to A.B.), the Fundación Alfonso Martin Escudero (to B.M.T), the Netherlands Cardiovascular Research Initiative: an initiative with the support of the Dutch Heart Foundation (CVON2017-20 GENIUS-II to P.C.N.R) and Dutch Diabetes Research Foundation (Junior Postdoc Fellowship; 2015.81.1808 to M.R.B). Neither of the funding sources was involved in study design, data collection, analysis, interpretation of data, writing or submission of the manuscript.

Publisher Copyright:
© 2022, The Author(s).

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