Effects of chronic intermittent hypoxia on glucose transporter 4 expression in rat skeletal muscles.
- Author:
Jian TAN
1
;
Hailan MO
;
Jie LI
;
Yingling WU
;
Xiaoli HE
;
Bing LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blood Glucose; Glucose Transporter Type 4; metabolism; Hypoxia; Insulin; blood; Insulin Resistance; Interleukin-6; Male; Muscle, Skeletal; metabolism; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha; blood
- From: Journal of Southern Medical University 2014;34(7):1061-1064
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of chronic intermittent hypoxia-induced inflammatory cytokines and reoxygenation on glucose transporter 4 (GLUT-4) expression in rat skeletal muscles.
METHODSTwenty-four male Sprague-Dawley rats were randomly assigned to blank control group, chronic intermittent hypoxia (CIH) group, and reoxygenation group. At the end of the experiment, fasting blood glucose (FBG), fasting blood insulin (FINS) and serum inflammatory cytokine levels were measured with glucose oxidase-peroxidase, insulin radioimmunoassay and ELISA, respectively. Homeostasis model assessment (IRI) was used to evaluate insulin resistance in the rats, and GLUT-4 protein expression in the skeletal muscles was measured with Western blotting.
RESULTSCompared with the blank control group, CIH resulted in significantly increased fasting blood glucose, blood insulin levels and insulin resistance index (IRI) (P<0.05); fasting blood glucose was significantly elevated in reoxygenation group (P<0.05). Inflammatory cytokines levels (IL-6 and TNF-α) were significantly higher in CIH group than in the blank control and reoxygenation groups (P<0.05), and were higher in reoxygenation group than in the blank control group. GLUT-4 expression in the skeletal muscles was significantly reduced after CIH (P<0.05) but increased after subsequent reoxygenation (P<0.05).
CONCLUSIONCIH can cause increased release of inflammatory cytokines to lower GLUT-4 protein expression in the skeletal muscles, which contributes to insulin resistance in adult rats.