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The discovery of adipokines, adipocyte-specific secreted molecules, has highlighted the role of adipose tissue as an active endocrine organ that monitors and alters whole-body metabolism and maintains energy homeostasis. Since its identification in the mid-90’s, the adipokine adiponectin (also known as Acrp30, AdipoQ, and GBP28) has become best known as a regulator of insulin sensitivity. Recently, it was shown that adiponectin is capable of inducing ceramidase activity through its receptors AdipoR1 and AdipoR2, which results in the hydrolysis of ceramide to form sphingosine and free fatty acids.

To gain further insights into the local physiological consequences of adiponectin and AdipoR-induced ceramidase activation, Holland, Xia, and colleagues generated models allowing for AdipoR1 or AdipoR2 to be expressed under the control of a tetracycline response element (TRE- AdipoR1 or TRE-AdipoR2). They used these models to determine which adiponectin receptor may have the most beneficial effects on glucose tolerance and whole body insulin sensitivity and to compare and contrast adiponectin receptor action with a lysosomal ceramidase that does not promote sphingosine 1-phosphate accumulation.

Their data suggest that the lowering of ceramides is a critical player in adiponectin-induced improvements in non-alcoholic fatty liver disease and hepatic insulin resistance in mice with diet-induced obesity. They also demonstrate that the induction of acid ceramidase activity is insufficient to rescue metabolic syndrome in ob/ob mice, while AdipoR2 overexpression is sufficient.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Isa Kolbe, Henrik Oster
University of Lübeck, Germany
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