Impact of conditioning hyperglycemic on myocardial infarction rats: Cardiac cell survival factors

Abstract

in diabetic animals leads to increased capillary density before myocardial infarction. Despite poor prognostic in the long-term, all these results suggest that diabetes mellitus and consequently hyperglycemia may indeed play a cardioprotective role against myocardial infarction in the short term.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Conditioned hyperglycemia; Diabetes mellitus; Myocardial infarction; Cardioprotection; Survival factors Core tip: Hyperglycemia or diabetes triggers a conditioned state that may protect the heart against ischemic injury and associated detrimental effects. These beneficial effects are present in short term diabetes and/ or moderate hyperglycemia. The increase in glucose availability, the preferred energy substrate of the heart in stress condition, is likely to be one of the main cardioprotector mechanisms of hyperglycemia. However, other cardioprotective mechanisms seem to be involved, such as the release of cellular survival factors, ions preventing overload and angiogenesis. A fuller understanding of the mechanisms underlying conditioned hyperglycemia is then critical for the development of effective therapeutic strategies against ischemic heart disease. AbstractWhile clinical data have suggested that the diabetic heart is more susceptible to ischemic heart disease (IHD), animal data have so far pointed to a lower probability of IHD. Thus, the aim of this present review is to look at these conflicting results and discuss the protective mechanisms that conditioned hyperglycemia may confer to the heart against ischemic injury. Several mechanisms have been proposed to explain the cardioprotective action of high glucose exposure, namely, upregulation of anti-apoptotic factor Bcl-2, inactivation of pro-apoptotic factor bad, and activation of pro-survival factors such as protein kinase B (Akt), vascular endothelial growth factor (VEGF), hypoxia inducible factor-1α and protein kinase C-ε. Indeed, cytosolic increase in Ca 2+ concentration, the mitochondrial permeability transition pore, plays a key role in the genesis of ischemic injury. Previous studies have shown that the diabetic heart decreased Na + /Ca 2+ and Na + /H + exchanger activity and as such it accumulates less Ca 2+ in cardiomyocyte, thus preventing cardiac injury and the associated heart dysfunctions. In addition, the expression of VEGF TOPIC HIGHLIGHTSubmit a

Glucose and fatty acid metabolism in infarcted heart from streptozotocin-induced diabetic rats after 2 weeks of tissue remodeling

“…Malfitano et al [ 40 ] and Egorova et al [ 41 ] have found that the increase in glucose availability, the preferred energetic substrate for the heart in stress condition, is likely to play a key cardioprotective role under ischemia. Diabetes promotes a marked increase in plasma glucose and free fatty acid levels, thus increasing the availability of these metabolites to tissues and organs, including the heart.…”

Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats

“…Accordingly, capillary density may effectively contribute to the reduction of ischemic injury and cardiac fibrosis in diabetic animals. These alterations might play an important role in improving heart function and increasing glucose transporter type 1 expression, which in turn may be critical for glucose uptake in ischemic conditions in diabetic infarcted rats [ 41 ].…”

Mild Type 2 Diabetes Mellitus Reduces the Susceptibility of the Heart to Ischemia/Reperfusion Injury: Identification of Underlying Gene Expression Changes

“…Evidence suggests that the ischemic hearts from the mildly diabetic animals are resistant to ischemia [ 8 ], and the severely diabetic hearts are more prone to ischemic injury [ 9 ]. Several mechanisms have been proposed to explain the cardioprotective property of a high glucose exposure, by an increase in survival pathways, such as antiapoptotic factor Bcl-2, and prosurvival factors such as protein kinase B (Akt), the inactivation of the proapoptotic factor bad, inappropriate expression of proangiogenic vascular endothelial growth factor (VEGF), hypoxia inducible factor 1 α , and protein kinase C- ε [ 10 ].…”