Silke Ryan1,2. 1. Pulmonary and Sleep Disorders Unit, St. Vincent's University Hospital. 2. School of Medicine, University College Dublin, Dublin, Ireland.
Abstract
PURPOSE OF REVIEW: Abnormal sleep duration, including short and long sleep, and sleep disorders, in particular obstructive sleep apnea (OSA), have evolved as major public health concerns attributed to their high prevalence and significant links with mortality and comorbid conditions. There is compelling evidence of an independent association of such sleep disturbances with the development, control, and progression of disorders affecting glucose metabolism such as type 2 diabetes (T2D). However, little is known of the underlying pathophysiological mechanisms and the potential interactions of these sleep disturbances in this process. The present review explores emerging evidence in this field. RECENT FINDINGS: Cross-sectional and longitudinal analyses of large cohorts support the association of abnormal sleep duration and T2D. However, significant methodological limitations hinder the conclusive interpretation of the data. OSA is a fast-emerging risk factor for the development and control of T2D. Experimental studies support a key role of intermittent hypoxia as the hallmark feature of OSA in the pathophysiology. SUMMARY: The present review highlights the need for large-scale, multicenter, prospective studies in order to determine the causative role of sleep disturbances in diabetes. There is also a clear demand of a greater understanding of the detailed pathophysiological mechanisms.
PURPOSE OF REVIEW: Abnormal sleep duration, including short and long sleep, and sleep disorders, in particular obstructive sleep apnea (OSA), have evolved as major public health concerns attributed to their high prevalence and significant links with mortality and comorbid conditions. There is compelling evidence of an independent association of such sleep disturbances with the development, control, and progression of disorders affecting glucose metabolism such as type 2 diabetes (T2D). However, little is known of the underlying pathophysiological mechanisms and the potential interactions of these sleep disturbances in this process. The present review explores emerging evidence in this field. RECENT FINDINGS: Cross-sectional and longitudinal analyses of large cohorts support the association of abnormal sleep duration and T2D. However, significant methodological limitations hinder the conclusive interpretation of the data. OSA is a fast-emerging risk factor for the development and control of T2D. Experimental studies support a key role of intermittent hypoxia as the hallmark feature of OSA in the pathophysiology. SUMMARY: The present review highlights the need for large-scale, multicenter, prospective studies in order to determine the causative role of sleep disturbances in diabetes. There is also a clear demand of a greater understanding of the detailed pathophysiological mechanisms.