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

Publication date: 2 January 2018
Source:Cell Reports, Volume 22, Issue 1
Author(s): 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
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.

Graphical abstract

Teaser

Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in lipoproteins. Christoffersen et al. show that lack of apoM in mice increases the amount of brown adipose tissue, accelerates the turnover of fat, and protects against obesity. The results reveal a link between the apoM/S1P axis and energy metabolism.


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