Intermittent Hypoxia Induces Leptin Signalling in the Carotid Body

Abstract

Glomus cells in the carotid body are responsible for detecting changes in blood PO2. These glomus cells have recently been found to express leptin receptors and are activated by intermittent hypoxia (IH) and systemic leptin injections, although the function of leptin within the carotid body remains unknown. The present study was done to investigate whether IH activates leptin signalling pathways within leptin‐expressing carotid body glomus cells. Rats were subjected to IH (120s normoxia, 80s hypoxia for 8 h) or normoxia (8h). Exposure to IH increased plasma leptin levels almost 6‐fold compared to normoxic controls. Additionally, IH was found to increase leptin, ERK1/2 and Fra‐1/2 immunoreactivity within glomus cells. Systemic leptin injections evoked similar effects on leptin, ERK1/2 and Fra‐1/2 immunoreactivity within the glomus cells. Furthermore, using Western blot analysis, IH was found to increase protein expression of leptin, the short form of the leptin receptor (Ob‐R100 kDa), pSTAT3 and SOCS3. On the other hand, IH induced a decrease in Ob‐Rb protein expression. Taken together, these data suggest that the increased levels of leptin within the circulation and those within the glomus cells induced by IH may function within the carotid body to alter the sensitivity of chemoreceptors to hypoxic stimuli.Supported by Heart and Stroke Foundation of Ontario