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Old 05-16-2019, 05:03 AM
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rss IGF - Suppression of cardiac autophagy by hyperinsulinemia in insulin receptors defic

Suppression of cardiac autophagy by hyperinsulinemia in insulin receptors deficient hearts is mediated by insulin-like growth factor receptor signaling.

Antioxid Redox Signal. 2019 May 15;:

Authors: Pires KM, Torres N, Buffolo M, Gunville RG, Schaaf CI, Davis K, Selzman CH, Gottlieb RA, Boudina S

Abstract
AIMS: Autophagy is a catabolic process required for the maintenance of cardiac health. Insulin and insulin-like growth factor 1 (IGF-1) are potent inhibitors of autophagy and as such, one would predict that autophagy will be increased in the insulin resistant/diabetic heart. However, autophagy is rather decreased in the hearts of diabetic/insulin resistant mice. The aim of this study is determine the contribution IGF-1 receptors signaling to autophagy suppression in insulin receptors deficient hearts.
RESULTS: Absence of insulin receptors (IRs) in the heart was associated with reduced autophagic flux and further inhibition of autophagosomes clearance reduced survival, impaired contractile function and enhanced myocyte loss. Contrary to the in vivo setting, isolated cardiomyocytes from IRs deficient hearts exhibited unrestrained autophagy in the absence of insulin, whereas addition of insulin was able to suppress autophagy. To investigate the mechanisms involved in the maintenance of the responsiveness to insulin in IRs deficient hearts, we generated mice lacking both IRs and one copy of the IGF-1R in cardiac cells and showed that these mice had increased autophagy. Innovation and Conclusion: This study unveils a new mechanism by which insulin receptors deficient hearts can still respond to insulin to suppress autophagy in part through activation of IGF-1R signaling. This is a highly significant observation because it is the first to show that systemic hyperinsulinemia can suppress autophagy in IR deficient hearts through IGF-1R signaling.


PMID: 31088290 [PubMed - as supplied by publisher]



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