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Mild Type 2 Diabetes Mellitus Reduces the Susceptibility of the Heart to Ischemia/Reperfusion Injury: Identification of Underlying Gene Expression Changes
- Source :
- Journal of Diabetes Research, Vol 2015 (2015)
- Publication Year :
- 2015
- Publisher :
- Hindawi Limited, 2015.
-
Abstract
- Despite clinical studies indicating that diabetic hearts are more sensitive to ischemia/reperfusion injury, experimental data is contradictory. Although mild diabetes prior to ischemia/reperfusion may induce a myocardial adaptation, further research is still needed. Nondiabetic Wistar (W) and type 2 diabetic Goto-Kakizaki (GK) rats (16-week-old) underwent 45 min occlusion of the left anterior descending coronary artery and 24 h reperfusion. The plasma glucose level was significantly higher in diabetic rats compared to the nondiabetics. Diabetes mellitus was associated with ventricular hypertrophy and increased interstitial fibrosis. Inducing myocardial infarction increased the glucose levels in diabetic compared to nondiabetic rats. Furthermore, the infarct size was smaller in GK rats than in the control group. Systolic and diastolic functions were impaired in W + MI and did not reach statistical significance in GK + MI animals compared to the corresponding controls. Among the 125 genes surveyed, 35 genes showed a significant change in expression in GK + MI compared to W + MI rats. Short-term diabetes promotes compensatory mechanisms that may provide cardioprotection against ischemia/reperfusion injury, at least in part, by increased antioxidants and the upregulation of the prosurvival PI3K/Akt pathway, by the downregulation of apoptotic genes, proinflammatory cytokine TNF-α, profibrogenic TGF-β, and hypertrophic marker α-actin-1.
- Subjects :
- Diseases of the endocrine glands. Clinical endocrinology
RC648-665
Subjects
Details
- Language :
- English
- ISSN :
- 23146745 and 23146753
- Volume :
- 2015
- Database :
- Directory of Open Access Journals
- Journal :
- Journal of Diabetes Research
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.77bb4dc71b784d93b193a11f89d6c298
- Document Type :
- article
- Full Text :
- https://doi.org/10.1155/2015/396414