Decreased skeletal muscle intramyocellular lipid droplet-mitochondrial contact contributes to myosteatosis in cancer cachexia

Author:

Cardaci Thomas D.1ORCID,VanderVeen Brandon N.1ORCID,Huss Alexander R.1,Bullard Brooke M.1ORCID,Velázquez Kandy T.12ORCID,Frizzell Norma3ORCID,Carson James A.4ORCID,Price Robert L.5,Murphy E. Angela1ORCID

Affiliation:

1. Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, South Carolina, United States

2. Columbia Department of Veterans Affairs Health Care System, Columbia, South Carolina, United States

3. Department of Pharmacology, Physiology, and Neuroscience, University of South Carolina School of Medicine, Columbia, South Carolina, United States

4. Department of Kinesiology and Sports Management, JL Huffines Institute for Sports Medicine & Human Performance, Texas A&M University, College Station, Texas, United States

5. Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, United States

Abstract

We sought to advance our understanding of skeletal muscle lipid metabolism and dynamics in cancer cachexia. Cachexia increased the number and size of intramyocellular lipid droplets (LDs). Furthermore, decreases in LD-mitochondrial touch, contact length, and relative contact along with increased LD shape complexity with decreases in circularity and roundness. Dysregulation in lipid metabolism and LD-associated proteins was also documented. Collectively, we show that myosteatosis, altered LD morphology, and decreased LD-mitochondrial interactions occur in cancer cachexia.

Funder

HHS | NIH | National Cancer Institute

Publisher

American Physiological Society

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