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.
|Controls||2 controls, lyophilized|
|Sample Types||Serum or plasma|
|Sample Volume||30 µL single determination / 50 µL double determination|
|Standards||8 standards, lyophilized|
|Standard Range||0 / 3.125 - 150 ng/mL|
|Incubation Time||5 hours total incubation time|
|FDA Status||Research Use Only|