Inhibition of GSK3β Reduces Ectopic Lipid Accumulation and Induces Autophagy by the AMPK Pathway in Goat Muscle Satellite Cells
Wang L., Liu X., Zhan S., Guo J., Yang S., Zhong T.
Animal Study, published in Cells (2019) — 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
- Animal Study
- Journal
- Cells (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31683987
- PMCID
- PMC6912237
- DOI
- 10.3390/cells8111378
- Citations
- 9
Abstract (original English)
Ectopic lipid accumulation in muscle is important not only for obesity and myopathy treatment, but also for meat quality improvement in farm animals. However, the molecular mechanisms involved in lipid metabolism in muscle satellite cells are still elusive. In this study, SB216763 reduced GSK3β activation by increasing the level of pGSK3β (Ser9) and decreasing the level of total GSK3β protein. GSK3β inhibition decreased lipid accumulation and downregulated the expression level of lipogenesis-related genes in the adipogenic differentiation of goat muscle satellite cells. Furthermore, SB216763 treatment increased the levels of pAMPKα (T172) and pACC (Ser79). Further, we found that GSK3β inhibition promoted levels of LC3B-II and reduced the protein levels of p62 to induce the autophagy in muscle satellite cells. Taken together, our results provide new insight into a critical function for GSK3β: modulating lipid accumulation in goat muscle satellite cells through activating the AMPK pathway.
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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