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Impairment of pancreatic β‐cell function by chronic intermittent hypoxia

•  What is the central question of this study? Periodic decreases in arterial blood O2 or chronic intermittent hypoxia (CIH) is a hallmark feature of sleep apnoea patients. Despite a large body of clinical evidence linking sleep‐disordered breathing with apnoeas to diabetes, the causal relationships between CIH and β‐cell function and the underlying molecular mechanisms have not been established. •  What is the main finding and its importance? In a rodent model, we show that mitochondrial oxidative stress generated by CIH leads to pancreatic β‐cell dysfunction manifested by augmented basal insulin secretion, insulin resistance, defective proinsulin processing and impaired glucose‐stimulated insulin secretion. The results of the present study provide evidence for direct effects of CIH on β‐cell function, which may be an underlying molecular mechanism contributing to the development of type 2 diabetes among sleep apnoea patients.