Purpose of review
To focus on state-of-the-art knowledge on the apolipoprotein M (ApoM) physiology and physiopathology regarding metabolism.
In humans, the ApoM was recently described as secreted by adipocytes. Obesity, metabolic syndrome and type 2 diabetes are associated with low circulating ApoM and adipose tissue APOM
expression. Dieting-induced weight loss enhances adipose tissue expression and secretion, and exercise training increases plasma ApoM. The ApoM is a chaperone for the bioactive sphingolipid, sphingosine-1-phosphate
(S1P), which has a specific role in inflammation
. Its association with S1P in the inhibition of brown adipose tissue activity and subsequent insulin sensitivity was reported with the model of ApoM-deficient mouse.
The adipose tissue is an endocrine organ responsible for obesity-related comorbidities. Obesity and dieting impact the adipose tissue secretory profile. The recent demonstration of ApoM being secreted by healthy adipocytes questions about the possible role of this adipose production in metabolic diseases. Low-circulating ApoM is associated with unhealthy metabolic phenotype. The lower circulating apoM during metabolic syndrome might be a cause of obesity-related comorbidities. Lifestyle interventions enhance ApoM production. Whether it acts in combination to S1P or other small lipidic molecules deserves further investigations.