Skeletal muscle carnitine-acylcarnitine translocase deletion reveals vulnerability of oxidative muscle to fatty acid oxidation deficiency

American Journal of Physiology-Endocrinology and Metabolism 2026 Open access

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Authors: Filip Jevtovic, Nicholas C. Williamson, Andrea S. Pereyra, Molly Alexander, Espen E. Spangenburg, Jessica M. Ellis
DOI: 10.1152/ajpendo.00117.2026
Cited by: 1
References: 26

Abstract

Novel model of CACT loss in muscle to demonstrate that CACT is required for long, medium, and short-chain fatty acid oxidation in skeletal muscle. Deletion of CACT drives oxidative and glycolytic muscle lipid remodeling and impairs oxidative, but not glycolytic, muscle contractile capacity. Oxidative soleus muscle mitochondria compensate for CACT loss by increasing mitochondrial content and muscle capacity for oxidation of nonfatty acid substrates.

Fields of Study & Subjects

Metabolism and Genetic Disorders Mitochondrial Function and Pathology Adipose Tissue and Metabolism

Publication details

Journal / source
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Volume
331
Issue
1
Pages
E68–E75
Publication date
1 June 2026
Language
EN