The Influence of Obese Insulin-Resistance on the Outcome of the Ischemia/Reperfusion Insult to the Heart

• Published in: Current medicinal chemistry Vol. 25; no. 13; p. 1501
• Main Authors: Shinlapawittayatorn, Krekwit, Chattipakorn, Siriporn C, Chattipakorn, Nipon
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2018
• Subjects: Animals; Heart; Humans; Insulin - metabolism; Insulin Resistance - physiology; Myocardial Ischemia - prevention & control; Myocardial Reperfusion Injury - prevention & control; Obesity - metabolism; Oxidative Stress - physiology; Signal Transduction; ischemia/reperfusion; Obese insulin-resistance; heart; obesity; ishemic heart disease; myocardial infarction
• ISSN: 1875-533X
• DOI: 10.2174/0929867324666170616105639

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. 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. 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. 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.