Cell Biology International · 2011 · 47 citations · 26 references
Life SciencesCell BiologyMolecular BiologyCell SignalingGene ExpressionSignal TransductionAdipocyte DifferentiationAdipose TissueFatty Acid MetabolismLipid MetabolismMetabolic SignalingPathway RegulationAdipocyte BiologyAdipocyte MetabolismExtracellular Signal-regulated Kinase PathwayExtracellular Signal-regulated Kinase SignalingHormone-sensitive LipaseLipid Metabolism During Adipocyte DifferentiationMyostatin SignalingPreadipocyte Differentiation
Myostatin is known as an inhibitor of muscle development, but its role in adipogenesis and lipid metabolism is still unclear, especially the underlying mechanisms. Here, we demonstrated that myostatin inhibited 3T3-L1 preadipocyte differentiation into adipocyte by suppressing C/EBPα (CCAAT/enhancer-binding protein α) and PPARγ (peroxisome-proliferator-activated receptor γ), also activated ERK1/2 (extracellular-signal-regulated kinase 1/2). Furthermore, myostatin enhanced the phosphorylation of HSL (hormone-sensitive lipase) and ACC (acetyl-CoA carboxylase) in fully differentiated adipocytes, as well as ERK1/2. Besides, we noted that myostatin markedly raised the levels of leptin and adiponectin release and mRNA expression during preadipocyte differentiation, but the levels were inhibited by myostatin treatments in fully differentiated adipocytes. These results suggested that myostatin suppressed 3T3-L1 preadipocyte differentiation and regulated lipid metabolism of mature adipocyte, in part, via activation of ERK1/2 signalling pathway.
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Inhibition of Adipogenesis Through MAP Kinase-Mediated Phosphorylation of PPARγ
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