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Published on: August 7, 2017
Abnormal Growth and Feeding Behavior in Upper Airway Obstruction in Rats
Ariel Tarasiuk1,2, Yael Segev3
1Sleep-Wake Disorders Unit, Soroka University Medical Center, Beer-Sheva, Israel.
Insights
Pediatric obstructive sleep apnea (OSA) can lead to growth issues and obesity, even after treatment. Studies show airway obstruction removal may not fully restore normal growth patterns in animal models.
Area of Science:
- Pediatric Sleep Medicine
- Endocrinology
- Metabolic Syndrome
Background:
- Pediatric obstructive sleep apnea (OSA) causes snoring and breathing issues, impacting sleep and potentially leading to growth problems, obesity, and metabolic syndrome.
- Adenotonsillectomy, a common OSA treatment, often fails to fully resolve obesity risk, suggesting mechanisms beyond breathing restoration.
- The link between upper airway obstruction (AO) and persistent changes in feeding, metabolism, and growth remains poorly understood.
Purpose of the Study:
- To investigate persistent endocrine regulation abnormalities in feeding and growth following chronic upper airway obstruction removal in rats.
- To explore metabolic regulation aspects unrelated to intermittent hypoxia in an animal model mimicking pediatric OSA.
Main Methods:
- Utilized a rat model to simulate chronic upper airway obstruction (AO) and its removal.
- Focused on analyzing endocrine regulation of feeding and growth, distinguishing effects from intermittent hypoxia.
Main Results:
- Evidence indicates persistent abnormalities in endocrine regulation of feeding and growth after chronic AO removal.
- Findings highlight metabolic regulation issues not solely attributable to intermittent hypoxia.
- The animal model replicated key clinical features of pediatric OSA.
Conclusions:
- Obstruction removal in OSA may not be sufficient to prevent a post-treatment tendency for abnormal growth.
- Further research is needed to understand and address persistent metabolic and growth dysregulation in pediatric OSA.
Abstract:
Pediatric obstructive sleep apnea (OSA) is a syndrome manifesting with snoring and increased respiratory effort due to increased upper airway resistance. In addition to cause the abnormal sleep, this syndrome has been shown to elicit either growth retardation or metabolic syndrome and obesity. Treating OSA by adenotonsillectomy is usually associated with increased risk for obesity, despite near complete restoration of breathing and sleep. However, the underlying mechanism linking upper airways obstruction (AO) to persistent change in food intake, metabolism, and growth remains unclear. Rodent models have examined the impact of intermittent hypoxia on metabolism. However, an additional defining feature of OSA that is not related to intermittent hypoxia is enhanced respiratory loading leading to increased respiratory effort and abnormal sleep. The focus of this mini review is on recent evidence indicating the persistent abnormalities in endocrine regulation of feeding and growth that are not fully restored by the chronic upper AO removal in rats. Here, we highlight important aspects related to abnormal regulation of metabolism that are not related to intermittent hypoxia per se, in an animal model that mimics many of the clinical features of pediatric OSA. Our evidence from the AO model indicates that obstruction removal may not be sufficient to prevent the post-removal tendency for abnormal growth.
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