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The Cardioprotective Effects of Adiponectin in the ZDF Heart Following Ischemia Are Associated with a Significant Attenuation of Myocardial ICAM‐1 Expression
Author(s) -
Choi JiEun,
DavisGorman Grace,
Tsao TsuShuen,
McDonagh Paul
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.594.6
Subject(s) - adiponectin , medicine , cardioprotection , myocardial infarction , type 2 diabetes , cardiology , inflammation , diabetes mellitus , endocrinology , insulin resistance
Ischemic heart disease (IHD) is significantly enhanced in type 2 diabetes (T2D) and inflammation is associated with IHD and T2D. The adipocytokine, adiponectin (APN), which has anti‐inflammatory actions, is chronically reduced in type 2 diabetes. APN may link inflammation, T2D and IHD. We examined if a globular form of adiponectin was cardioprotective in the Zucker Diabetic Fatty (ZDF) rodent model of T2D and if the cardioprotection was associated with myocardial expression of ICAM‐1, a key adhesion molecule and marker of coronary microvascular dysfunction. ZDF (n=14) rats and their lean controls ZLC (n=13) were subjected to 30 minutes of LAD occlusion and 120 minutes of reperfusion. Animals were treated with either PBS or recombinant globular adiponectin (1.0 μg/g). At R120, the extent of myocardial infarction was measured. Myocardial ICAM‐1 expression was also quantified immunohistochemically. We found that adiponectin treatment significantly attenuated the enhanced myocardial infarction in the ZDF model of T2D (p<0.05). The reduced infarction was associated with a significant reduction in myocardial ICAM‐1 expression (p<0.05). These findings suggest that adiponectin treatment protects against I/R injury in the T2D heart. The cardioprotective action may be related to reduced coronary microvascular inflammation enhancing PMN sequestration and PMN‐mediated tissue injury. Supported by NIH HL 58859.