The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity

Christina Christoffersen; Christine K Federspiel; Anna Borup; Pernille M Christensen; Andreas N Madsen; Markus Heine; Carsten H Nielsen; Andreas Kjaer; Birgitte Holst; Joerg Heeren; Lars B Nielsen

doi:10.1016/j.celrep.2017.12.029

The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity

Christina Christoffersen, Christine K Federspiel, Anna Borup, Pernille M Christensen, Andreas N Madsen, Markus Heine, Carsten H Nielsen, Andreas Kjaer, Birgitte Holst, Joerg Heeren, Lars B Nielsen

54 Citationer (Scopus)

Abstract

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 S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.

Originalsprog	Engelsk
Tidsskrift	Cell Reports
Vol/bind	22
Udgave nummer	1
Sider (fra-til)	175-188
Antal sider	14
DOI	https://doi.org/10.1016/j.celrep.2017.12.029
Status	Udgivet - 2 jan. 2018

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10.1016/j.celrep.2017.12.029

Citationsformater

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title = "The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity",

abstract = "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 S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.",

author = "Christina Christoffersen and Federspiel, {Christine K} and Anna Borup and Christensen, {Pernille M} and Madsen, {Andreas N} and Markus Heine and Nielsen, {Carsten H} and Andreas Kjaer and Birgitte Holst and Joerg Heeren and Nielsen, {Lars B}",

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doi = "10.1016/j.celrep.2017.12.029",

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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

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 S1P1 stimulation. 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 S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.

U2 - 10.1016/j.celrep.2017.12.029

DO - 10.1016/j.celrep.2017.12.029

M3 - Journal article

C2 - 29298420

SN - 2211-1247

VL - 22

SP - 175

EP - 188

JO - Cell Reports

JF - Cell Reports

IS - 1

ER -

The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity

Abstract

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