Open AccessThe Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity
Author(s) -
Christina Christoffersen,
Christine K. Federspiel,
Anna Borup,
Pernille M. Christensen,
Andreas Nygaard Madsen,
Markus Heine,
Carsten H. Nielsen,
Andreas Kjær,
Birgitte Holst,
Jöerg Heeren,
Lars B. Nielsen
Publication year - 2018
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2017.12.029
Subject(s) - endocrinology , medicine , sphingosine , apolipoprotein b , postprandial , stimulation , lipid metabolism , brown adipose tissue , triglyceride , receptor , metabolism , adipose tissue , biology , phenotype , cholesterol , chemistry , biochemistry , insulin , gene
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 (S1P 1-5 ). 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 β 3 -adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P 1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.
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