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Updated: Jan 19, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Relationship Between Intermittent Hypoxia and Type 2 Diabetes in Sleep Apnea Syndrome
Hiroyo Ota1, Yukio Fujita2, Motoo Yamauchi3
1Second Department of Internal Medicine, Nara Medical University, Kashihara, Nara 634-8522, Japan. hiroyon@naramed-u.ac.jp.
Abstract:
Sleep apnea syndrome (SAS) is a very common disease involving intermittent hypoxia (IH), recurrent symptoms of deoxygenation during sleep, strong daytime sleepiness, and significant loss of quality of life. A number of epidemiological researches have shown that SAS is an important risk factor for insulin resistance and type 2 diabetes mellitus (DM), which is associated with SAS regardless of age, gender, or body habitus. IH, hallmark of SAS, plays an important role in the pathogenesis of SAS and experimental studies with animal and cellular models indicate that IH leads to attenuation of glucose-induced insulin secretion from pancreatic β cells and to enhancement of insulin resistance in peripheral tissues and cells, such as liver (hepatocytes), adipose tissue (adipocytes), and skeletal muscles (myocytes). In this review, we focus on IH-induced dysfunction in glucose metabolism and its underlying molecular mechanisms in several cells and tissues related to glucose homeostasis.
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