Effects of intermittent hypoxia on leptin signalling in the carotid body

Glomus cells in the carotid body are responsible for detecting changes in the partial pressure of blood oxygen (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 (120-s normoxia, 80-s hypoxia for 8 h) or normoxia (8 h). Exposure to IH increased plasma leptin levels almost sixfold 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) and suppressor of cytokine signalling 3. On the other hand, IH induced a decrease in long form of leptin receptors (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 alter carotid bodies chemosensitivity to hypoxic stimuli.

► Carotid bodies express leptin, and long and short forms leptin receptors.
► Intermittent hypoxia (IH) in conscious rat increases plasma levels of leptin.
► IH induces leptin, Fra, Ob-R100, pSTAT3, ERK and SOCS3 reduces Ob-Rb in carotid body.
► Injections of leptin induces leptin and Fra expression in carotid body.
► Leptin during IH modulates the sensitivity of carotid bodies to hypoxic stimulation.