Ascorbic acid attenuates obesity induced myogenic impairment in C2C12 cells.
Pinto JR., Bhat K D., Bose B., Shenoy P S.
Laboratory Study on Chronic Inflammation, published in Life Sci (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Life Sci (2026)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42547010
- DOI
- 10.1016/j.lfs.2026.124612
Abstract (original English)
Obesity is commonly associated with skeletal muscle atrophy and is attributed to chronic inflammation, oxidative stress, and impaired adipose-muscle cross talk. Ascorbic acid, a potent antioxidant and its role in obesity induced muscle atrophy is not clearly understood. Hence, the aim of the study was to rescue obesity induced skeletal muscle atrophy with ascorbic acid in vitro. C3H10T1/2 mesenchymal stem cells were developed into obesogenic adipocytes by palmitic acid treatment to generate obesogenic adipocyte-conditioned media (ObCM). C2C12 myoblasts and differentiated myotubes were treated with ObCM in the presence or absence of ascorbic acid (AsA). Cell viability and reactive oxygen species generation were evaluated by MTT assay and DCFDA staining. Gene and protein expression analyses were performed using quantitative real-time PCR and western blotting. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test. In the present study, we have established a palmitic acid induced hypertrophic adipocyte model using C3H10T1/2 mesenchymal stem cells and generated obese conditioned medium to replicate obese microenvironment. Differentiated C2C12 myotubes when exposed to obese conditioned media resulted in reduced myotube diameter, increased expression in ROS, inflammatory cytokines, activation of ubiquitin proteasome system and upregulated muscle atroph
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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