The influence of obese insulin-resistance on the outcome of the ischemia/reperfusion insult to the heart

• Main Authors: Krekwit Shinlapawittayatorn, Siriporn C. Chattipakorn, Nipon Chattipakorn
• Format: Journal
• Published: 2018
• Subjects: Biochemistry, Genetics and Molecular Biology; Pharmacology, Toxicology and Pharmaceutics
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85048887896&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/56782
• Institution: Chiang Mai University

© 2018 Bentham Science Publishers. Background: Obese insulin-resistance is one of the most important risk factor for cardiovascular diseases including ischemic heart disease (IHD). Growing evidences suggest that the susceptibility to myocardial ischemia-reperfusion (I/R) injury is increased in an obese insulin-resistance condition. Based on the currently available evidence from human and animal studies, this review mainly focuses on the influence of obese insulinresistance on the outcome of the I/R insult to the heart. Moreover, we have discussed whether improving insulin sensitivity by pharmacological interventions could ameliorate reperfusion induced myocardial injury. Methods: The electronic database Pubmed was used as the source of selected peerreviewed research articles published in English. Both pre-clinical studies and clinical trials were obtained using obesity, insulin resistance, ischemia-reperfusion injury and myocardial infarction as keywords. Results: Twenty-seven pre-clinical studies were obtained using obesity, insulin resistance, and cardiac ischemia-reperfusion injury as keywords, and five clinical trials were obtained using obesity, insulin resistance, and myocardial infarction as keywords. The underlying mechanisms responsible for the exacerbation of I/R injury in obese insulinresistance were the main subject of our review. Conclusion: The findings of this review suggest that the susceptibility to I/R injury is increased in an obese insulin-resistance condition. However, the underlying mechanisms responsible for the exacerbation of I/R injury in obese insulin-resistance have not been fully elucidated, but increased basal oxidative stress, the impairment of anti-oxidant capacities, insulin signaling and pro-survival signaling and increased inflammation, likely play an important role.