Published online Sep 15, 2018. doi: 10.4239/wjd.v9.i9.149
Peer-review started: March 27, 2018
First decision: April 23, 2018
Revised: July 3, 2018
Accepted: July 10, 2018
Article in press: July 10, 2018
Published online: September 15, 2018
Processing time: 171 Days and 7.8 Hours
Type 2 diabetes mellitus (T2DM) is associated with an increased risk of myocardial infarction (MI) and poorer prognosis. Recent studies demonstrate that glucagon-like peptide-1 analogs (GLP-1a) possess infarct-limiting effects in experimental settings. However, it is not clear whether GLP-1a have beneficial effects when combined with insulin.
In this study, we intended to compare the cardioprotective effects of GLP-1a therapy with and without concomitant insulin in acute MI in rats with T2DM.
The effects of pre- and post-ischemic GLP-1a and insulin administration on infarct size were studied in the rat model of MI. The effect of a combination of GLP-1a and insulin was assessed in a separate group.
We induced T2DM in Wistar rats with streptozotocin at a dose of 65 mg/kg. Myocardial ischemia was induced by left coronary artery occlusion. Myocardial infarct size was determined histochemically. In addition, we analyzed the number and severity of hypoglycemia episodes in the experimental groups. Animals were treated with either GLP-1a or insulin.
Results of our study show that using GLP-1a before ischemia-reperfusion significantly reduced infarct size. The maximal infarct size reduction was observed in the group treated with GLP-1a prior to ischemia and insulin at reperfusion.
We have shown that insulin infusion before ischemia increased infarct size, while GLP-1a demonstrated cardioprotective effects. Post-ischemic administration of insulin or GLP-1a had no effect on infarct size. Thus, the regimen of GLP-1a and insulin administration is crucial for expression of their cardioprotective effect.
Further studies with larger sample sizes can be conducted in order to develop a clinical trial and introduce new combinations of drugs with antidiabetic activity for MI therapy in patients with T2DM.