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Adiponectin reduces lipid content in chicken myoblasts by activating AMPK signaling pathway

Studies in mammals have shown that adiponectin is secreted mainly by adipocytes, and it plays a crucial role in glucose and lipid metabolism in muscles. Clarifying the cross-talk role of adiponectin between adipose tissue and skeletal muscle tissue is very important for internal homeostasis. The glu...

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Detalles Bibliográficos
Autores principales: Hu, Qingmei, Wang, Dan, Lin, Hai, Li, Haifang, Zhao, Jingpeng, Jiao, Hongchao, Wang, Xiaojuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9171728/
https://www.ncbi.nlm.nih.gov/pubmed/35603780
http://dx.doi.org/10.1042/BSR20212549
Descripción
Sumario:Studies in mammals have shown that adiponectin is secreted mainly by adipocytes, and it plays a crucial role in glucose and lipid metabolism in muscles. Clarifying the cross-talk role of adiponectin between adipose tissue and skeletal muscle tissue is very important for internal homeostasis. The glucose and lipid metabolism of chicken is different from that of mammals, and the role of adiponectin in chickens is unclear. Therefore, it is of great significance to study the effect and mechanism of adiponectin on lipid metabolism in chickens. In the present study, the regulating effect of adiponectin on lipid metabolism in chicken myoblasts was explored by adding a certain concentration of exogenous recombinant adiponectin. Results showed that adiponectin reduced intracellular lipid content, increasing the mRNA expression of adiponectin receptor and cellular uptake of glucose and fatty acids. In addition, adiponectin activated the 5′ adenosine monophosphate activated protein kinase (AMPK) signaling pathway. The above results suggested that adiponectin reduced intracellular lipid content, mainly by binding to adiponectin receptor, activating AMPK pathway, increasing cellular uptake of glucose and fatty acids and promoting lipid oxidation.