The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity
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The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity. / Christoffersen, Christina; Federspiel, Christine K; Borup, Anna; Christensen, Pernille M; Madsen, Andreas N; Heine, Markus; Nielsen, Carsten H; Kjaer, Andreas; Holst, Birgitte; Heeren, Joerg; Nielsen, Lars B.
In: CELL REP, Vol. 22, No. 1, 02.01.2018, p. 175-188.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity
AU - Christoffersen, Christina
AU - Federspiel, Christine K
AU - Borup, Anna
AU - Christensen, Pernille M
AU - Madsen, Andreas N
AU - Heine, Markus
AU - Nielsen, Carsten H
AU - Kjaer, Andreas
AU - Holst, Birgitte
AU - Heeren, Joerg
AU - Nielsen, Lars B
N1 - Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.
PY - 2018/1/2
Y1 - 2018/1/2
N2 - Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in plasma high-density lipoproteins. S1P is a bioactive lipid interacting with five receptors (S1P1-5). We show that lack of apoM in mice increases the amount of brown adipose tissue (BAT), accelerates the clearance of postprandial triglycerides, and protects against diet-induced obesity (i.e., a phenotype similar to that induced by cold exposure or β3-adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P1stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.
AB - Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in plasma high-density lipoproteins. S1P is a bioactive lipid interacting with five receptors (S1P1-5). We show that lack of apoM in mice increases the amount of brown adipose tissue (BAT), accelerates the clearance of postprandial triglycerides, and protects against diet-induced obesity (i.e., a phenotype similar to that induced by cold exposure or β3-adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P1stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.
KW - Journal Article
U2 - 10.1016/j.celrep.2017.12.029
DO - 10.1016/j.celrep.2017.12.029
M3 - SCORING: Journal article
C2 - 29298420
VL - 22
SP - 175
EP - 188
JO - CELL REP
JF - CELL REP
SN - 2211-1247
IS - 1
ER -