Interpretive Summary: Myostatin suppresses adipogenic differentiation and lipid accumulation by activating crosstalk between ERK1/2 and PKA signaling pathways in porcine subcutaneous preadipocytes
By Anne Zinn
A study recently published in the Journal of Animal Science aimed to determine the effect of myostatin on lipid accumulation in porcine subcutaneous preadipocytes and to further explore the potential molecular mechanisms. Porcine subcutaneous preadipocytes isolated from Meishan weaned piglets were added with various concentrations of myostatin recombinant protein during the entire period of adipogenic differentiation process. Results demonstrated that myostatin treatment significantly reduced the lipid accumulation, intracellular triglyceride content, glucose consumption, and glycerol phosphate dehydrogenase activity, while increased glycerol and free fatty acid release. Additionally, results demonstrated that the extracellular signal-regulated kinase 1/2 pathway was activated and therefore key adipogenic transcription factors were all inhibited. Overall, this study presented the first experimental evidence for the functional roles of myostatin action as a negative regulator of porcine subcutaneous adipose tissue deposition by the crosstalk between the protein kinase A and extracellular signal-regulated kinases 1/2 pathways, which decreased adipogenesis and increased lipolysis by inhibiting peroxisome proliferator-activated receptor-γ, and stimulating perilipin and hormone-sensitive lipase phosphorylation. These results provide a comprehensive basis for the inhibitory effect of hyperexpression of myostatin on adipogenic differentiation and subcutaneous fat deposition, which leads to a better understanding of the mechanism of the molecular regulation of subcutaneous adipose tissue in pigs.
The full paper can be found on the Journal of Animal Science webpage.