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10.1161/JAHA.115.003046 http://scihub22266oqcxt.onion/10.1161/JAHA.115.003046 C4889180!4889180 !27151515     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27151515 &cmd=llinks): Failed to open stream: HTTP request failed! 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Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction |pdf=|usr=}}{{27151515 }} gab.com Text Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction JO: J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=27151515 #FOAvip BACKGROUND: Diabetes mellitus (DM) is associated with mitochondrial oxidative stress. We have shown that myocardial oxidative stress leads to diastolic dysfunction in a hypertensive mouse model. Therefore, we hypothesized that diabetes mellitus could cause diastolic dysfunction through mitochondrial oxidative stress and that a mitochondria-targeted antioxidant (MitoTEMPO) could prevent diastolic dysfunction in a diabetic mouse model. METHODS AND RESULTS: C57BL/6J mice were fed either 60 kcal % fat diet (high-fat diet [HFD]) or normal chow (control) for 8 weeks with or without concurrent MitoTEMPO administration, followed by in vivo assessment of diastolic function and ex vivo studies. HFD mice developed impaired glucose tolerance compared with the control (serum glucose=495±45 mg/dL versus 236±30 mg/dL at 60 minutes after intraperitoneal glucose injection, P<0.05). Myocardial tagged cardiac magnetic resonance imaging showed significantly reduced diastolic circumferential strain (Ecc) rate in the HFD mice compared with controls (5.0±0.3 1/s versus 7.4±0.5 1/s, P<0.05), indicating diastolic dysfunction in the HFD mice. Systolic function was comparable in both groups (left ventricular ejection fraction=66.4±1.4% versus 66.7±1.2%, P>0.05). MitoTEMPO-treated HFD mice showed significant reduction in mitochondria reactive oxygen species, S-glutathionylation of cardiac myosin binding protein C, and diastolic dysfunction, comparable to the control. The fasting insulin levels of MitoTEMPO-treated HFD mice were also comparable to the controls (P>0.05). CONCLUSIONS: MitoTEMPO treatment prevented insulin resistance and diastolic dysfunction, suggesting that mitochondrial oxidative stress may be involved in the pathophysiology of both conditions. Twit Text FOAVip Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction ????J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=27151515 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27151515 #FOAvip English Wikipedia <ref>{{Cite pmid|27151515 }}</ref> Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction #MMPMID27151515 Jeong EM ; Chung J ; Liu H ; Go Y ; Gladstein S ; Farzaneh-Far A ; Lewandowski ED ; Dudley SC Jr J Am Heart Assoc 2016[May]; 5 (5 ): ä PMID27151515 show ga BACKGROUND: Diabetes mellitus (DM) is associated with mitochondrial oxidative stress. We have shown that myocardial oxidative stress leads to diastolic dysfunction in a hypertensive mouse model. Therefore, we hypothesized that diabetes mellitus could cause diastolic dysfunction through mitochondrial oxidative stress and that a mitochondria-targeted antioxidant (MitoTEMPO) could prevent diastolic dysfunction in a diabetic mouse model. METHODS AND RESULTS: C57BL/6J mice were fed either 60 kcal % fat diet (high-fat diet [HFD]) or normal chow (control) for 8 weeks with or without concurrent MitoTEMPO administration, followed by in vivo assessment of diastolic function and ex vivo studies. HFD mice developed impaired glucose tolerance compared with the control (serum glucose=495±45 mg/dL versus 236±30 mg/dL at 60 minutes after intraperitoneal glucose injection, P<0.05). Myocardial tagged cardiac magnetic resonance imaging showed significantly reduced diastolic circumferential strain (Ecc) rate in the HFD mice compared with controls (5.0±0.3 1/s versus 7.4±0.5 1/s, P<0.05), indicating diastolic dysfunction in the HFD mice. Systolic function was comparable in both groups (left ventricular ejection fraction=66.4±1.4% versus 66.7±1.2%, P>0.05). MitoTEMPO-treated HFD mice showed significant reduction in mitochondria reactive oxygen species, S-glutathionylation of cardiac myosin binding protein C, and diastolic dysfunction, comparable to the control. The fasting insulin levels of MitoTEMPO-treated HFD mice were also comparable to the controls (P>0.05). CONCLUSIONS: MitoTEMPO treatment prevented insulin resistance and diastolic dysfunction, suggesting that mitochondrial oxidative stress may be involved in the pathophysiology of both conditions. |*Insulin Resistance [MESH] |*Oxidative Stress [MESH] |Animals [MESH] |Biomechanical Phenomena [MESH] |Cardiomyopathies/diagnostic imaging/metabolism [MESH] |Diabetes Mellitus, Experimental/*metabolism [MESH] |Diabetes Mellitus, Type 2/*metabolism [MESH] |Diastole [MESH] |Diet, High-Fat [MESH] |Disease Models, Animal [MESH] |Glucose Intolerance/*metabolism [MESH] |Glucose/*metabolism [MESH] |Heart Failure, Diastolic/diagnostic imaging/*metabolism [MESH] |Hemodynamics [MESH] |Magnetic Resonance Imaging [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Microscopy, Electron, Transmission [MESH] |Mitochondria, Heart/*metabolism [MESH] |Myocardium/metabolism [MESH] |Myocytes, Cardiac/metabolism/ultrastructure [MESH]Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin R(epmc).pdf DeepDyve Pubget Overpricing