Cuiping Fu1, Liyan Jiang2, Fen Zhu1, Zilong Liu1, Wenjing Li1, Hong Jiang1, Hongying Ye3, Clete A Kushida4, Shanqun Li5,6. 1. Department of Respiratory Medicine, Clinical Center for Sleep Breathing Disorder and Snoring, Zhongshan Hospital, Fudan University, Shanghai, China. 2. Department of Respiratory Medicine, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, China. jiang_liyan@126.com. 3. Division of Endocrinology, Hua Shan Hospital, Fudan University, Shanghai, China. dryehongying@hotmail.com. 4. Stanford University Sleep Clinic and Center for Human Sleep Research, Redwood City, CA, USA. clete@stanford.edu. 5. Department of Respiratory Medicine, Clinical Center for Sleep Breathing Disorder and Snoring, Zhongshan Hospital, Fudan University, Shanghai, China. lsq18616880856@163.com. 6. Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Fenglin Road 180, Xuhui District, Shanghai, 200032, People's Republic of China. lsq18616880856@163.com.
Abstract
BACKGROUND AND OBJECTIVES: The aim of this study was to determine whether chronic intermittent hypoxia (CIH) could affect the secretion of adipokines, such as resistin, leptin, and adiponectin, in non-obese rats and to investigate the potential mechanisms. METHODS: An established rodent model of CIH was utilized, in which rats were exposed to varying oxygen levels (7-21 %) respectively over a period of 5 weeks. The area under the curve (AUCG) and the insulin resistance index (homeostasis model of assessment for insulin resistance index, HOMA-IR) were calculated. The levels of several secretory factors in the blood were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression in adipose tissues was measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Glucose tolerance and the levels of adiponectin in non-obese rats were decreased in the CIH group both in the serum and adipose tissue compared with the controls, while the insulin resistance index and the levels of resistin and leptin were increased. Moreover, the expressions of hypoxia inducible factor-1α and lactate dehydrogenase A were significantly higher in chronic intermittent hypoxia rats than in control rats, suggesting the presence of adipose tissue hypoxia. CONCLUSIONS: These results show that CIH leads to insulin resistance (IR) and impaired glucose tolerance (IGT) in a non-obese rodent model of obstructive sleep apnea-hypopnea syndrome, and these effects may be due to the dysregulation of adiponectin, resistin, and leptin.
BACKGROUND AND OBJECTIVES: The aim of this study was to determine whether chronic intermittent hypoxia (CIH) could affect the secretion of adipokines, such as resistin, leptin, and adiponectin, in non-obeserats and to investigate the potential mechanisms. METHODS: An established rodent model of CIH was utilized, in which rats were exposed to varying oxygen levels (7-21 %) respectively over a period of 5 weeks. The area under the curve (AUCG) and the insulin resistance index (homeostasis model of assessment for insulin resistance index, HOMA-IR) were calculated. The levels of several secretory factors in the blood were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression in adipose tissues was measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS:Glucose tolerance and the levels of adiponectin in non-obeserats were decreased in the CIH group both in the serum and adipose tissue compared with the controls, while the insulin resistance index and the levels of resistin and leptin were increased. Moreover, the expressions of hypoxia inducible factor-1α and lactate dehydrogenase A were significantly higher in chronic intermittent hypoxiarats than in control rats, suggesting the presence of adipose tissue hypoxia. CONCLUSIONS: These results show that CIH leads to insulin resistance (IR) and impaired glucose tolerance (IGT) in a non-obese rodent model of obstructive sleep apnea-hypopnea syndrome, and these effects may be due to the dysregulation of adiponectin, resistin, and leptin.
Authors: Mary S M Ip; Bing Lam; Matthew M T Ng; Wah Kit Lam; Kenneth W T Tsang; Karen S L Lam Journal: Am J Respir Crit Care Med Date: 2002-03-01 Impact factor: 21.405
Authors: Joseph G Yu; Sandrine Javorschi; Andrea L Hevener; Yolanta T Kruszynska; Rodney A Norman; Madhur Sinha; Jerrold M Olefsky Journal: Diabetes Date: 2002-10 Impact factor: 9.461
Authors: R V Considine; M K Sinha; M L Heiman; A Kriauciunas; T W Stephens; M R Nyce; J P Ohannesian; C C Marco; L J McKee; T L Bauer Journal: N Engl J Med Date: 1996-02-01 Impact factor: 91.245