Communication Between Autophagy and Insulin Action: At the Crux of Insulin Action-Insulin Resistance?

Scott Frendo-Cumbo; Victoria L Tokarz; Philip J Bilan; John H Brumell; Amira Klip

doi:10.3389/fcell.2021.708431

Communication Between Autophagy and Insulin Action: At the Crux of Insulin Action-Insulin Resistance?

Front Cell Dev Biol. 2021 Jul 15:9:708431. doi: 10.3389/fcell.2021.708431. eCollection 2021.

Authors

Scott Frendo-Cumbo^{1

2}, Victoria L Tokarz^{1

2}, Philip J Bilan¹, John H Brumell^{1

3

4

5}, Amira Klip^{1

2

6}

Affiliations

¹ Cell Biology Program, Hospital for Sick Children, Toronto, ON, Canada.
² Department of Physiology, University of Toronto, Toronto, ON, Canada.
³ Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
⁴ Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
⁵ SickKids Inflammatory Bowel Disease (IBD) Centre, Hospital for Sick Children, Toronto, ON, Canada.
⁶ Department of Biochemistry, University of Toronto, Toronto, ON, Canada.

Abstract

Insulin is a paramount anabolic hormone that promotes energy-storage in adipose tissue, skeletal muscle and liver, and these responses are significantly attenuated in insulin resistance leading to type 2 diabetes. Contrasting with insulin's function, macroautophagy/autophagy is a physiological mechanism geared to the degradation of intracellular components for the purpose of energy production, building-block recycling or tissue remodeling. Given that both insulin action and autophagy are dynamic phenomena susceptible to the influence of nutrient availability, it is perhaps not surprising that there is significant interaction between these two major regulatory mechanisms. This review examines the crosstalk between autophagy and insulin action, with specific focus on dysregulated autophagy as a cause or consequence of insulin resistance.

Keywords: adipose tissue; autophagy; insulin action; insulin resistance; liver; obesity; skeletal muscle; type 2 diabetes.

Publication types

Review