It is unclear whether the cardiac hypertrophy and hypertrophy-related regulators will be enhanced by long-term intermittent hypoxia in obese Zucker Twelve obese Zucker rats and twelve age-matched lean Zucker rats were divided into four groups including normoxia in lean group, normoxia in obese group，hypoxia in lean group, and hypoxia in obese group. The hypoxia group were housed in a hypoxic chamber (12% O2, 88% N2 ), 8 hour per day for 7 days. The ratio of whole heart weight and left ventricular weight to tibia length and body weight was compared, The myocardial architecture and key components of hypertrophic pathway, IL-6-MEK5-ERK-5 in the excised left ventricle from rats were measured by histological analysis and western blotting. The ratio of whole heart weight and left ventricular weight to tibia length and body weight and myocardial morphological changes were increased in the obse group, and were further augmented by Long term intermittent hypoxia with eccentric cardiac hypertrophy and cardiomyocyte disarray. The activity levels of IL-6-MEK5-ERK5 hypertrophic pathway, were increased in lean rat heart after long-term intermittent hypoxia. The activity levels of IL-6-MEK5-ERK5 hypertrophic pathway, were increased in obese rat hearts, compared with lean rat heart and further increased after long-term intermittent hypoxia in obese rat hearts, compared with either lean in hypoxia group or obese in normoxia group. Long term intermittent hypoxia and obesity itself would make additively deleterious effects on cardiac tissues in obese Zucker Rat. Our findings imply that intermittent hypoxia and obesity itself will additively increases cardiac hypertrophy through IL6-MEK5-ERK5 pathway.?
