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Review Article Open Access
Volume 1 | Issue 4 | DOI: https://doi.org/10.33696/Signaling.1.025

Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1

  • 1Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
  • 2Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
  • 3Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, New Haven, Connecticut 06520, USA
  • 4Department of Biological Sciences, University of Alabama in Huntsville, Huntsville, Alabama 35899, USA
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Corresponding Author

Ahmed Lawan, al0122@uah.edu

Received Date: September 15, 2020

Accepted Date: October 01, 2020

Abstract

Obesity has reached a global epidemic and it predisposes to the development of insulin resistance, type 2 diabetes and related metabolic diseases. Current interventions against obesity and/or type 2 diabetes such as calorie restriction, exercise, genetic manipulations or established pharmacological treatments have not been successful for many patients with obesity and/or type 2 diabetes. There is an urgent need for new strategies to treat insulin resistance, T2D and obesity. Increased activity of stress-responsive pathways has been linked to the pathogenesis of insulin resistance in obesity. In this commentary, we argue that chronic upregulation of MKP-1 in skeletal muscle is part of a stress response that contributes to the development of insulin resistance, T2D and obesity. Therefore, inhibition of MKP-1 in skeletal muscle is a potential strategy for the treatment of T2D and obesity. We highlight therapeutic strategies for potential targeting of MKP-1 in skeletal muscle for the treatment of metabolic diseases as well as other diseases of skeletal muscle.

Keywords

MAP kinase, MAP kinase phosphatase, Obesity, Insulin resistance

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