Free fatty acids are converted to acyl-CoA by long-chain acyl-CoA synthetases (ACSLs) before entering into metabolic pathways for lipid biosynthesis or degradation. ACSL family members have highly conserved amino acid sequences except for their N-terminal regions. Several reports have shown that ACSL1, among the ACSLs, is located in mitochondria and mainly leads fatty acids to the β-oxidation pathway in various cell types. In this study, we investigated how ACSL1 was localized in mitochondria and whether ACSL1 overexpression affected fatty acid oxidation (FAO) rates in C2C12 myotubes. We generated an ACSL1 mutant in which the N-terminal 100 amino acids were deleted and compared its localization and function with those of the ACSL1 wild type. We found that ACSL1 adjoined the outer membrane of mitochondria through interaction of its N-terminal region with carnitine palmitoyltransferase-1b (CPT1b) in C2C12 myotubes. In addition, overexpressed ACSL1, but not the ACSL1 mutant, increased FAO, and ameliorated palmitate-induced insulin resistance in C2C12 myotubes. These results suggested that targeting of ACSL1 to mitochondria is essential in increasing FAO in myotubes, which can reduce insulin resistance in obesity and related metabolic disorders.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8490201 | PMC |
| http://dx.doi.org/10.14348/molcells.2021.0077 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Enhancing diabetic muscle repair through W-GA nanodots: a nanomedicinal approach to ameliorate myopathy in type 2 diabetes.
Burns Trauma
January 2025
Department of Arthroscopic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Xuhui District, Shanghai 200233, China.
Objective: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that significantly impairs muscle regeneration following injuries, contributing to numerous complications and reduced quality of life. There is an urgent need for therapeutic strategies that can enhance muscle regeneration and alleviate these pathological mechanisms. In this study, we evaluate the therapeutic efficacy of W-GA nanodots, which are composed of gallic acid (GA) and tungstate (W6+), on muscle regeneration in type 2 diabetes mellitus (T2D)-induced muscle injury, with a focus on their anti-inflammatory and antioxidative effects.
View Article and Find Full Text PDFBrussels Chicory Enhances Exhaustive Aerobic Exercise Performance and Post-Exercise Recovery, Possibly Through Promotion of Lactate Oxidation: A Pilot Randomized, Single-Blind, Placebo-Controlled, Two-Way Crossover Study.
Nutrients
January 2025
Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), 74 Zhongshan Road II, Guangzhou 510080, China.
Background: Brussels chicory affluent in phenolic acids could inhibit atherosclerosis; however, its effects on exercise performance and post-exercise recovery are unknown. We hypothesized that Brussels chicory could enhance exhaustive aerobic exercise performance and post-exercise recovery by promoting lactate oxidation.
Methods: This is a single-blind, randomized, placebo-controlled two-way cross-over trial involving 32 untrained college students (men 18) who consumed either Brussels chicory juice (100 g of Brussels chicory containing ~130 mg phenolic acids and 180 mL fresh milk) or placebo (180 mL fresh milk) for 7 days with a 2-week washout period.
Leaf Extract Protects C2C12 Mouse Myoblasts Against the Suppressive Effects of Bisphenol-A on Myogenic Differentiation.
Int J Mol Sci
January 2025
Research Center for Non-Infectious Diseases and Environmental Health Sciences, Research Institute for Health Sciences, Chiang Mai University, Chiang Mai 50200, Thailand.
Recently, toxicological and epidemiological research has provided strong support for the unfavorable effects of bisphenol-A (BPA, 2,2'-bis(4-hydroxyphenyl) propane) on myogenesis and its underlying mechanisms. Researchers have therefore been looking for new strategies to prevent or mitigate these injurious effects of BPA on the human body. It has been found that plant extracts may act as potential therapeutic agents or functional foods, preventing human diseases caused by BPA.
View Article and Find Full Text PDFCCL5 Induces a Sarcopenic-like Phenotype via the CCR5 Receptor.
Antioxidants (Basel)
January 2025
Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile.
Sarcopenia corresponds to a decrease in muscle mass and strength. CCL5 is a new myokine whose expression, along with the CCR5 receptor, is increased in sarcopenic muscle. Therefore, we evaluated whether CCL5 and CCR5 induce a sarcopenic-like effect on skeletal muscle tissue and cultured muscle cells.
View Article and Find Full Text PDFCalponin 3 Regulates Myoblast Proliferation and Differentiation Through Actin Cytoskeleton Remodeling and YAP1-Mediated Signaling in Myoblasts.
Cells
January 2025
Department of Biochemistry, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Republic of Korea.
An actin-binding protein, known as Calponin 3 (CNN3), modulates the remodeling of the actin cytoskeleton, a fundamental process for the maintenance of skeletal muscle homeostasis. Although the roles of CNN3 in actin remodeling have been established, its biological significance in myoblast differentiation remains largely unknown. This study investigated the functional significance of CNN3 in myogenic differentiation, along with its effects on actin remodeling and mechanosensitive signaling in C2C12 myoblasts.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!