Retinal Diabetopathy? Sleep Disorders, Retinal Changes, and Insulin Resistance: A Synthesized Systematic Review

Abstract

ABSTRACT Sleep disturbances, particularly prevalent in modern lifestyles, have been increasingly associated with metabolic disorders such as insulin resistance and type 2 diabetes mellitus (DM) (T2DM). Epidemiological evidence underscores the link between impaired sleep and elevated risks of cardiovascular diseases and mortality rates, alongside the emergence of metabolic dysregulation. Notably, conditions such as obstructive sleep apnea syndrome contribute to disrupted sleep architecture and exacerbate insulin resistance through repeated drops in blood oxygen levels during sleep. Furthermore, chronic sleep deprivation, irregular sleep schedules, and shift work disrupt circadian rhythms, amplifying the risk of metabolic disorders. A comprehensive search was conducted in PubMed, Scopus, Web of Science, and Google Scholar for articles from January 2010 to October 2023 using terms such as “sleep disturbances,” “Type 2 Diabetes Mellitus,” and “retinal receptors.” Inclusion criteria covered studies on human and animal participants, comparative analyses, and reviews. Exclusion criteria ruled out nonpeer-reviewed works and those with limited population sizes. Data extraction focused on study design, populations, types of sleep disorders, metabolic effects, and retinal health impacts. Results emphasized the bidirectional relationship among these variables. The critical analytical research and review highlights the bidirectional relationship between retinal receptor dysfunction and DM, emphasizing how metabolic disturbances associated with diabetes impact retinal health, while dysfunctional retinal receptors contribute to the progression of diabetes-related complications. Insights into the role of insulin receptors in the retina and the blood–retinal barrier underscore the mechanisms through which insulin resistance compromises retinal integrity, leading to neuroinflammation, oxidative stress, and photoreceptor damage. The disturbed sleep can also affect the melatonin secretion, thereby affecting insulin resistance. We preliminarily have named the nexus as retinal diabetopathy. By elucidating the impact of intermittent hypoxia and sleep fragmentation on cellular signaling and metabolism, particularly in vital organs such as muscles, liver, fat, and pancreas, the article provides a comprehensive understanding of how prevalent sleep disturbances and retinal changes contribute to the development and progression of T2DM. Overall, this research underscores the importance of addressing sleep disorders in the prevention and management of metabolic disorders.