Association of apolipoprotein M and sphingosine-1-phosphate with brown adipose tissue after cold exposure in humans
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Association of apolipoprotein M and sphingosine-1-phosphate with brown adipose tissue after cold exposure in humans. / Borup, Anna; Donkin, Ida; Boon, Mariëtte R.; Frydland, Martin; Martinez-Tellez, Borja; Loft, Annika; Keller, Sune H.; Kjaer, Andreas; Kjaergaard, Jesper; Hassager, Christian; Barrès, Romain; Rensen, Patrick C.N.; Christoffersen, Christina.
In: Scientific Reports, Vol. 12, No. 1, 18753, 2022.Research output: Contribution to journal › Journal article › peer-review
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TY - JOUR
T1 - Association of apolipoprotein M and sphingosine-1-phosphate with brown adipose tissue after cold exposure in humans
AU - Borup, Anna
AU - Donkin, Ida
AU - Boon, Mariëtte R.
AU - Frydland, Martin
AU - Martinez-Tellez, Borja
AU - Loft, Annika
AU - Keller, Sune H.
AU - Kjaer, Andreas
AU - Kjaergaard, Jesper
AU - Hassager, Christian
AU - Barrès, Romain
AU - Rensen, Patrick C.N.
AU - Christoffersen, Christina
N1 - Publisher Copyright: © 2022, The Author(s).
PY - 2022
Y1 - 2022
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85141397816&partnerID=8YFLogxK
U2 - 10.1038/s41598-022-21938-2
DO - 10.1038/s41598-022-21938-2
M3 - Journal article
C2 - 36335116
AN - SCOPUS:85141397816
VL - 12
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
IS - 1
M1 - 18753
ER -
ID: 327058745