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Oleic acid in the absence of a PPARγ agonist increases adipogenic gene expression in bovine muscle satellite cells1.

  • Li, Xiang Z1
  • Yan, Yan1
  • Zhang, Jun F1
  • Sun, Jian F1
  • Sun, Bin1
  • Yan, Chang G1
  • Choi, Seong H2
  • Johnson, Bradley J3
  • Kim, Jong K3
  • Smith, Stephen B4
  • 1 Co-Innovation Center of Beef Cattle Science and Industry Technology, Yanbian University, Yanji, Jilin, P. R. China. , (China)
  • 2 Department of Animal Science, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea. , (North Korea)
  • 3 Department of Animal and Food Sciences, Texas Tech University, Lubbock, TX.
  • 4 Department of Animal Science, Texas A&M University, College Station, TX.
Published Article
Journal of animal science
Publication Date
Oct 03, 2019
DOI: 10.1093/jas/skz269
PMID: 31424542


We hypothesized that oleic acid (OA) in the absence of a thiazolidinedione (i.e., a synthetic peroxisome proliferator-activated receptorγ [PPARγ] agonist) would increase adipogenic gene expression in bovine muscle satellite cells (BSC). The BSC were cultured in differentiation medium containing 10 µM ciglitazone (CI), 100 µM OA, or 100 µM OA plus 10 µM CI (CI-OA). Control (CON) BSC were cultured only in differentiation media (containing 2% horse serum). The presence of myogenin, desmin, and paired box 7 proteins was confirmed in the BSC by immunofluorescence staining, demonstrating that we had isolated myogenic cells. The OA BSC had lesser paired box 3 (Pax3) and myogenic differentiation 1 expression but greater Pax7 and mygogenin (MYOG) expression (P < 0.05), than the CON BSC. The CI BSC had greater Pax3, Pax7, and MYOG expression than CON BSC (P < 0.05), suggesting that CI would promote BSC myogenesis under pro-myogenic conditions (i.e., when cultured with horse serum). However, both the OA and CI treatments upregulated the expression of PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and C/EBPß, sterol regulatory element-binding protein 1, lipoprotein lipase, and glycerol-3-phosphate acyltransferase 3 gene expression, as well as media adiponectin concentration (P < 0.05). The CI, OA, and CI-OA treatments also increased triacylglycerol and lipid droplet accumulation, in spite of upregulation (relative to CON BSC) of adenosine monophosphate-activated protein kinase alpha-1, perilipin 2 (PLIN2), and PLIN3 in BSC and downregulation of G protein-coupled protein receptor 43, acyl-CoA synthetase long chain family member 3, and stearoyl-CoA desaturase (P < 0.05). These results indicate that OA in the absence of a synthetic PPARγ agonist can effectively increase adipogenic gene expression in BSC. © The Author(s) 2019. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: [email protected]

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