Chronic intermittent hypoxia from pedo-stage decreases glucose transporter 4 expression in adipose tissue and causes insulin resistance

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 kg(-1) min(-1) vs (13.34 +/- 1.54) mg kg(-1) 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 Chin Med J 2010;123(4):463-470