Document Detail


The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis.
MedLine Citation:
PMID:  18202171     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: nocturnal sustained hypoxia during sleeping time has been reported in severe obesity, but no information regarding the cardiac molecular mechanism in the coexistence of nocturnal sustained hypoxia and obesity is available. This study evaluates whether the coexistence of nocturnal sustained hypoxia and obesity will increase cardiac Fas death receptor and mitochondrial-dependent apoptotic pathway.
METHODS: 32 lean and 32 obese 5- to 6-mo-old rats with or without nocturnal sustained hypoxia were studied and assigned to one of four subgroups: normoxia lean (NL), normoxia obese (NO), hypoxia lean (HL, 12% O(2) for 8 h and 21% O(2) 16 h/day, 1 wk), and hypoxia obese (HO). The heart weight index, tail cuff plethysmography, echocardiography, hematoxylin-eosin staining, TUNEL assays, Western blotting, and RT-PCR were performed.
RESULTS: systolic and diastolic blood pressures in HO were higher than those in NL, and fractional shortening in HO was reduced compared with others. The whole heart weight, the left ventricular weight, the abnormal myocardial architecture, and TUNEL-positive apoptotic cells, as well as the activity of cardiac Fas-dependent and mitochondrial-dependent apoptotic pathway, were significantly increased in obese group or nocturnal sustained hypoxia group and were further increased when obesity and nocturnal sustained hypoxia coexisted, the evidence for which is based on decreases in an anti-apoptotic protein Bcl2 level and Bid and increases in Fas, FADD, pro-apoptotic Bad, BNIP3, cytosolic cytochrome c, activated caspase-8, activated caspase-9, and activated caspase-3.
CONCLUSIONS: The cardiac Fas receptor- and mitochondrial-dependent apoptotic pathways were more activated in obesity with coexistent nocturnal sustained hypoxia, which may represent one possible apoptotic mechanism for the development of heart failure in obesity with nocturnal sustained hypoxia.
Authors:
Shin-Da Lee; Wei-Wen Kuo; Da-Tian Bau; Fu-Yang Ko; Fong-Li Wu; Chia-Hua Kuo; Fuu-Jen Tsai; Paulus S Wang; Min-Chi Lu; Chih-Yang Huang
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-17
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  104     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-03     Completed Date:  2008-06-17     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1144-53     Citation Subset:  IM    
Affiliation:
Graduate Institute of Chinese Medical Science and Institute of Medical Science, China Medical Univ., No. 91, Hsueh-Shih Road, Taichung, 404, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / complications,  pathology*
Antigens, CD95 / metabolism
Apoptosis / physiology*
Blood Pressure / physiology
Blotting, Western
Body Weight / physiology
Caspases / metabolism
Cytochromes c / biosynthesis,  genetics
Cytosol / metabolism
Echocardiography
Electrophoresis, Polyacrylamide Gel
In Situ Nick-End Labeling
Membrane Proteins / biosynthesis
Mitochondria, Heart / physiology
Myocardium / pathology*
Obesity / complications,  pathology*
Organ Size / physiology
Plethysmography
Proto-Oncogene Proteins / biosynthesis
RNA / biosynthesis,  genetics
Rats
Rats, Zucker
Reverse Transcriptase Polymerase Chain Reaction
Sleep Apnea, Obstructive / complications,  pathology*
Ventricular Function, Left / physiology
Chemical
Reg. No./Substance:
0/Antigens, CD95; 0/BNIP3 protein, rat; 0/Membrane Proteins; 0/Proto-Oncogene Proteins; 63231-63-0/RNA; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspases

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