Anorexigenic Effects of Intermittent Hypoxia on the Gut-Brain Axis in Sleep Apnea Syndrome

• Published in: International journal of molecular sciences Vol. 23; no. 1; p. 364
• Main Authors: Shobatake, Ryogo, Ota, Hiroyo, Takahashi, Nobuyuki, Ueno, Satoshi, Sugie, Kazuma, Takasawa, Shin
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 29.12.2021; MDPI
• Subjects: Adipocytes; Adipose tissue; Airway management; Amphetamines; Animal models; Animals; Anorexia - pathology; Apnea; Appetite; Attenuation; Beta cells; Binding sites; Body mass index; Brain-Gut Axis; Cocaine; Cocaine- and amphetamine-regulated transcript protein; enteroendocrine cells; Enzymes; Epidemiology; Feeding behavior; Food; Gene expression; Glucagon; Glucagon-like peptide 1; Glucose; Glucose - metabolism; Hepatocytes; Humans; Hypertension; Hypothalamus; Hypoxia; Hypoxia - complications; Hypoxia - genetics; Insulin; Insulin resistance; Insulin secretion; intermittent hypoxia; Molecular modelling; Muscles; Myocytes; neuronal cells; Neurotensin; Obesity; Proopiomelanocortin; Review; Risk factors; Signal transduction; Skeletal muscle; Sleep apnea; sleep apnea syndrome; Sleep Apnea Syndromes - complications; Sleep disorders; Transcription; enteroendocrine cells; neurotensin; cocaine- and amphetamine-regulated transcript; glucagon-like peptide-1; sleep apnea syndrome; neuronal cells; proopiomelanocortin; appetite; peptide YY; intermittent hypoxia
• DOI: 10.3390/ijms23010364
• ISSN: 1422-0067; 1661-6596

Sleep apnea syndrome (SAS) is a breathing disorder characterized by recurrent episodes of upper-airway collapse, resulting in intermittent hypoxia (IH) during sleep. Experimental studies with animals and cellular models have indicated 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 the liver (hepatocytes), adipose tissue (adipocytes), and skeletal muscles (myocytes), both of which could lead to obesity. Although obesity is widely recognized as a major factor in SAS, it is controversial whether the development of SAS could contribute directly to obesity, and the effect of IH on the expression of appetite regulatory genes remains elusive. Appetite is regulated appropriately by both the hypothalamus and the gut as a gut-brain axis driven by differential neural and hormonal signals. In this review, we summarized the recent epidemiological findings on the relationship between SAS and feeding behavior and focused on the anorexigenic effects of IH on the gut-brain axis by the IH-induced up-regulation of proopiomelanocortin and cocaine- and amphetamine-regulated transcript in neuronal cells and the IH-induced up-regulation of peptide YY, glucagon-like peptide-1 and neurotensin in enteroendocrine cells and their molecular mechanisms.