We are pleased to announce the release of the new Soluble Leptin Receptor (sLEP-R) ELISA suitable for serum or plasma.

The adipokine leptin realizes signal transduction via four different leptin receptor (LEP-R) isoforms. The amount of functionally active LEP-R, however, is affected by constitutive shedding of the extracellular domain. The product of the cleavage process, the so-called soluble leptin receptor (sLEP-R, soluble Leptin receptor), is the main binding protein for leptin in human blood and modulates its bioavailability.

Concentrations of sLEP-R are differentially regulated in metabolic disorders, such as type 1 diabetes mellitus or obesity and can therefore enhance or reduce leptin sensitivity.

Lipotoxicity and apoptosis increase LEP-R cleavage via ADAM10-dependent mechanisms. 

In contrast, although increased sLEP-R concentrations seem directly to inhibit leptin effects, reduced amounts of sLEP-R may reflect decreased membrane expression of LEP-R. These findings, in part, explain alterations of leptin sensitivity that are associated with changes in serum sLEP-R concentrations seen in metabolic disorders.

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