“…The pathophysiology of the cardiometabolic complications in OSA is still incompletely understood; however, intermittent hypoxia (IH) as observed in OSA, and characterized by repetitive short cycles of oxyhemoglobin desaturation and reoxygenation, likely plays a pivotal role. Furthermore, emerging evidence of a relationship between OSA and metabolic perturbations, and in particular with alterations in glucose metabolism such as insulin resistance (IR) and type 2 diabetes (T2D) has been reproducibly reported across a multitude of studies [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ], including in healthy volunteers [ 16 , 17 , 18 ]. To elucidate the potential mechanisms implicated in such metabolic derangements, murine models have been developed that traditionally include one of the major perturbations of OSA, namely IH [ 1 , 19 , 20 ].…”