LEP and obstructive sleep apnea syndrome: We have shown that intracerebroventricular administration of leptin did not affect breathing in Leprb-deficient db/db mice, which hypoventilate during sleep and have elevated PaCO2, and the respiratory effects of leptin were restored upon selective expression of LEPRb in the DMH.47 We hypothesize that LEPRb+ neurons in the DMH regulate both metabolism and breathing and that stimulation of these neurons relieves OHS and OSA.