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Chronic intermittent hypoxia from pedo-stage decreases glucose transporter 4 expression in adipose tissue and causes
Lin Chen1, Zhao-long Cao, Fang Han
1Department of Pneumology, Peking University People's Hospital, Beijing 100044, China.
Insights
Chronic intermittent hypoxia in young rats induced insulin resistance by affecting glucose transporters. This highlights the need for early detection of insulin insensitivity in childhood obstructive sleep apnea.
Area of Science:
- Physiology
- Endocrinology
- Sleep Medicine
Background:
- Persistent sleep-disordered breathing symptoms after surgery are common in children with obstructive sleep apnea (OSA).
- Chronic intermittent hypoxia (CIH) during early development may impact glucose metabolism and contribute to insulin resistance.
- Investigating glucose transporter (GLUT) disturbances in adipose tissue offers insight into persistent OSA symptoms.
Purpose of the Study:
- To test if CIH in young rats disrupts glucose transporters (GLUTs) in intraabdominal adipose tissue.
- To determine if these GLUT disturbances contribute to peripheral insulin resistance.
- To explore the link between GLUT changes and persistent SDB in children with OSA.
Main Methods:
- 30 Sprague-Dawley rats were exposed to CIH, chronic continuous hypoxia (CCH), or normal oxygen for 40 days.
- Measurements included weight, fasting blood glucose/insulin, and insulin resistance via hyperinsulinemic-euglycemic clamp.
- GLUT mRNA and protein expression in intraabdominal adipose tissue were analyzed using qPCR and Western blotting.
Main Results:
- CIH significantly increased fasting insulin levels and decreased glucose infusion rate, indicating insulin resistance.
- GLUT-4 mRNA and protein expression were significantly reduced in the CIH group compared to controls.
- These findings suggest CIH adversely affects glycometabolism and GLUT expression.
Conclusions:
- CIH in young rats induces insulin resistance through impaired glycometabolism.
- Adverse effects on GLUTs in adipose tissue are implicated in CIH-induced insulin resistance.
- Early detection and treatment of insulin insensitivity are crucial for obese children with OSA.
Background:
The persistence of sleep disordered breathing (SDB) symptoms after tonsil and/or adenoid (T&A) surgery are common in children with obstructive sleep apnea (OSA). We tested the hypothesis that disturbances of glucose transporters (GLUTs) in intraabdominal adipose tissue caused by chronic intermittent hypoxia (CIH) from the pedo-period could facilitate the appearance of periphery insulin resistance in Sprague-Dawley (SD) rats. We tested the hypothesis that the changes of GLUTs in adipose tissue may be one of the reasons for persistent SDB among clinical OSA children after T&A surgery.
Methods:
Thirty 21-day-old SD rats were randomly divided into a CIH group, a chronic continuous hypoxia (CCH) group, and a normal oxygen group (control group) and exposed for 40 days. The changes of weight, fasting blood glucose and fasting blood insulin levels were measured. Hyperinsulinemic-euglycemic clamp techniques were used to measure insulin resistance in each animal. Real-time quantitative PCR and Western blotting were used to measure GLUT mRNA and proteins in intraabdominal adipose tissue. Additional intraabdomial white adipose tissue (WAT) was also processed into paraffin sections and directly observed for GLUTs1-4 expression.
Results:
When compared with control group, CIH increased blood fasting insulin levels, (245.07 +/- 53.89) pg/ml vs. (168.63 +/- 38.70) pg/ml, P = 0.038, and decreased the mean glucose infusion rate (GIR), (7.25 +/- 1.29) mg x kg(-1) x min(-1) vs. (13.34 +/- 1.54) mg x kg(-1) x min(-1), P < 0.001. GLUT-4 mRNA and protein expression was significantly reduced after CIH compared with CCH or normal oxygen rats, 0.002 +/- 0.002 vs. 0.039 +/- 0.009, P < 0.001; 0.642 +/- 0.073 vs. 1.000 +/- 0.103, P = 0.035.
Conclusions:
CIH in young rats could induce insulin resistance via adverse effects on glycometabolism. These findings emphasize the importance of early detection and treatment of insulin insensitivity in obese childhood OSA.
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