Contribution of skeletal muscle-specific microRNA-133b to insulin resistance in heart failure

Author:

Velasquez Fernanda Carrizo1ORCID,Roman Barbara2,Hernández-Ochoa Erick O.3ORCID,Leppo Michelle K.4,Truong Sharon K.1,Steenbergen Charles2,Schneider Martin F.3,Weiss Robert G.4,Das Samarjit12ORCID

Affiliation:

1. Department of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States

2. Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland, United States

3. Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, United States

4. Division of Cardiology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States

Abstract

Heart failure is associated with systemic insulin resistance and abnormalities in glucose metabolism but the underlying mechanisms are poorly understood. In the skeletal muscle, the major peripheral site of glucose utilization, we observe an increase in miR-133b in heart failure mice, which reduces the insulin-sensitive glucose transporter (GLUT4), glucose uptake, and metabolism in C2C12 and in myocytes. The antagomir for miR-133b restores GLUT4 protein and markers of metabolism in skeletal myocytes from heart failure mice demonstrating that miR-133b is an exciting target for systemic insulin resistance in heart failure and an important player in the cross talk between the heart and the periphery in the heart failure syndrome.

Funder

HHS | NIH | National Institute on Aging

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases

American Heart Association

HHS | NIH | National Center for Advancing Translational Sciences

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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