Abstract
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.
Highlights
Muscle satellite cells reside beneath the basal lamina and are responsible for postnatal muscle growth and regeneration [1]
There was no obvious difference between 4 and 7 days after SB216763 treatment. These results suggest that GSK3β inhibition decreases the lipid accumulation of skeletal muscle satellite cells
Previous studies have demonstrated that GSK3β plays a key regulatory role in the regulation of adipocyte differentiation
Summary
Muscle satellite cells reside beneath the basal lamina and are responsible for postnatal muscle growth and regeneration [1]. Muscle satellite cells are multipotential stem cells that can transdifferentiate into adipocytes, osteoblasts and myotubes [2]. PRDM16 (PR domain containing 16) interacts with C/EBP-β (CCAAT enhancer binding protein β) and controls the transdifferentiation from myoblast to brown adipocyte [3]. MiR-133 targets the PRDM16 gene and prevents satellite cells from differentiating into brown adipocytes [4]. Liver kinase B1 (Lkb1) deletion in myoblasts promotes the lipid accumulation and the expression of lipid metabolism related genes through activating the AMPK (AMP-activated protein kinase) pathway [5]. There is more lipid accumulation in skeletal muscle of Wnt10bknockout mice compared to WT mice and Wnt10b deletion promotes adipogenic differentiation in myoblasts [6]. The molecular mechanisms involved in lipid metabolism in muscle satellite cells are still elusive
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
