title: Adiponectin alleviates genioglossal mitochondrial dysfunction in rats exposed to intermittent hypoxia.
abstract: BACKGROUND
  Genioglossal dysfunction is involved in the pathophysiology of obstructive sleep apnea hypoxia syndrome (OSAHS) characterized by nocturnal chronic intermittent hypoxia (CIH). The pathophysiology of genioglossal dysfunction and possible targeted pharmacotherapy for alleviation of genioglossal injury in CIH require further investigation.
  
  
  RESULTS
  Rats in the control group were exposed to normal air, while rats in the CIH group and CIH+adiponectin (AD) group were exposed to the same CIH condition (CIH 8 hr/day for 5 successive weeks). Furthermore, rats in CIH+AD group were administrated intravenous AD supplementation at the dosage of 10 µg, twice a week for 5 consecutive weeks. We found that CIH-induced genioglossus (GG) injury was correlated with mitochondrial dysfunction, reduction in the numbers of mitochondrias, impaired mitochondrial ultrastructure, and a reduction in type I fibers. Compared with the CIH group, impaired mitochondrial structure and function was significantly improved and a percentage of type I fiber was elevated in the CIH+AD group. Moreover, compared with the control group, the rats' GG in the CIH group showed a significant decrease in phosphorylation of LKB1, AMPK, and PGC1-α, whereas there was significant rescue of such reduction in phosphorylation within the CIH+AD group.
  
  
  CONCLUSIONS
  CIH exposure reduces mitochondrial biogenesis and impairs mitochondrial function in GG, while AD supplementation increases mitochondrial contents and alleviates CIH-induced mitochondrial dysfunction possibly through the AMPK pathway.
authors.affiliation: Department of Respirology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
authors.forename: Hanpeng
authors.initials: H
authors.lastname: Huang
authors.affiliation: Department of Respirology, Nanjing Medical University affiliated Wuxi People's Hospital, Wuxi, China.
authors.forename: Xiufeng
authors.initials: X
authors.lastname: Jiang
authors.affiliation: Department of Respirology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
authors.forename: Yanbin
authors.initials: Y
authors.lastname: Dong
authors.affiliation: Department of Respirology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Respirology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Ding
authors.affiliation: Department of Respiratory Diseases, Jangsu Geriatric Hospital, Nanjing, China.
authors.forename: Jiannan
authors.initials: J
authors.lastname: Liu
authors.affiliation: Morsani College of Medicine, Tampa, FL, United States of America.
authors.forename: Sean Z
authors.initials: SZ
authors.lastname: Hutchinson
authors.affiliation: Department of Respiratory Diseases, Jangsu Geriatric Hospital, Nanjing, China.
authors.forename: Gan
authors.initials: G
authors.lastname: Lu
authors.affiliation: Department of Respirology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
authors.forename: Xilong
authors.initials: X
authors.lastname: Zhang
mesh_terms: D052242:Adiponectin / Q000494:pharmacology*; D000818:Animals; D000860:Hypoxia / Q000150:complications*; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D009132:Muscles / Q000473:pathology*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D052242:Adiponectin