Year-end Sale % OFF 
Abstract
Although hyperglycemia is common in patients with acute myocardial infarction (MI), the underlying mechanisms are largely unknown. Insulin signaling plays a key role in the regulation of glucose homeostasis. In this study, we test the hypothesis that rapid alteration of insulin signaling pathways could be a potential contributor to acute hyperglycemia after MI. Male rats were used to produce MI by ligation of the left anterior descending coronary artery. Plasma glucose and insulin levels were significantly higher in MI rats than those in controls. Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) was reduced significantly in the liver tissue of MI rats compared with controls, followed by decreased attachment of phosphatidylinositol 3-kinase (PI3K) p85 subunit with IRS1 and Akt phosphorylation. However, insulin-stimulated signaling was not altered significantly in skeletal muscle after MI. The relative mRNA levels of phosphoenolpyruvate carboxykinase (PEPCK) and G6Pase were slightly higher in the liver tissue of MI rats than those in controls. Rosiglitazone (ROSI) markedly restored hepatic insulin signaling, inhibited gluconeogenesis and reduced plasma glucose levels in MI rats. Insulin resistance develops rapidly in liver but not skeletal muscle after MI, which contributes to acute hyperglycemia. Therapy aimed at potentiating hepatic insulin signaling may be beneficial for MI-induced hyperglycemia.
Highlights
Hyperglycemia is a common pathological feature in patients with acute myocardial infarction (MI), even in the absence of established diabetes mellitus [1,2]
Our results demonstrated that impaired insulin signaling rapidly developed in liver tissue but not skeletal muscle, which might lead to hyperglycemia through increased hepatic gluconeogenesis after MI
We found that plasma glucose levels were elevated significantly at 5 min of ligation in MI rats (P < 0.01) and increased to 2.2-fold of that in controls at 30 min of ligation (Figure 1C)
Summary
Hyperglycemia is a common pathological feature in patients with acute myocardial infarction (MI), even in the absence of established diabetes mellitus [1,2]. The optimal glucose control level is still inconclusive to date. To resolve these problems in glucose management, it is wise to understand the molecular mechanisms by which acute hyperglycemia develops after MI. Insulin acts as a key regulator of plasma glucose homeostasis, which increases glucose uptake in peripheral tissues such as skeletal muscle and inhibits hepatic glucose production through activating insulin signaling pathways [5,6]. The main pathways stimulated by insulin are the IR/IRSs/ phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways. If impaired, they would result in insulin resistance
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
