title: Chronic intermittent hypobaric hypoxia prevents cardiac dysfunction through enhancing antioxidation in fructose-fed rats.
abstract: High-fructose intake induces metabolic syndrome and cardiac dysfunction. Chronic intermittent hypobaric hypoxia (CIHH) preserves cardiac function during ischemia. We hypothesized that CIHH restores the impaired cardiac function in fructose-fed rats. Sprague-Dawley rats were randomly subject to treatment with fructose (10% fructose in drinking water for 6 weeks), CIHH (simulated 5000 m altitude, 6 h/day for 6 weeks in a hypobaric chamber), and CIHH plus fructose groups. In addition to an increase in blood pressure, fructose feeding caused elevated serum levels of glucose, fasting insulin and insulin C peptide, triglyceride, cholesterol, and mass ratio of heart to body. CIHH treatment decreased the arterial blood pressure, serum levels of biochemical markers, and cardiac hypertrophy in fructose-fed rats. Furthermore, CIHH treatment improved the recovery of left ventricular function after ischemia-reperfusion procedure (30 min global no-flow ischemia followed by 60 min of reperfusion) in rats with or without fructose feeding. In addition, CIHH treatment caused a significant increase in superoxide dismutase (SOD) activity and decrease in malondialdehyde level in cardiac myocardium experiencing ischemia-reperfusion in control and fructose-fed rats. Collectively, these data suggest that CIHH improve impaired cardiac function in fructose-fed rats through enhancing antioxidation in the myocardium.
authors: Department of Physiology, Hebei Medical University, Hebei Key Laboratory of Medical Biotechnology, Hebei 050017, People's Republic of China.
authors: Jing-Jing
authors: JJ
authors: Zhou
authors: Yan
authors: Y
authors: Wei
authors: Li
authors: L
authors: Zhang
authors: Jiao
authors: J
authors: Zhang
authors: Lan-Ying
authors: LY
authors: Guo
authors: Chao
authors: C
authors: Gao
authors: De-Pei
authors: DP
authors: Li
authors: Yi
authors: Y
authors: Zhang
mesh_terms: D000821:Animal Feed; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002096:C-Peptide / Q000097:blood; D002784:Cholesterol / Q000097:blood; D005632:Fructose / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D000860:Hypoxia / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D014280:Triglycerides; D005632:Fructose; D008315:Malondialdehyde; D002784:Cholesterol; D013482:Superoxide Dismutase