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Volume 57, issue 1
Arch. Anim. Breed., 57, 29, 2014
https://doi.org/10.7482/0003-9438-57-029
© Author(s) 2014. This work is distributed under
the Creative Commons Attribution 3.0 License.
Arch. Anim. Breed., 57, 29, 2014
https://doi.org/10.7482/0003-9438-57-029
© Author(s) 2014. This work is distributed under
the Creative Commons Attribution 3.0 License.

  29 Oct 2014

29 Oct 2014

A second look at leptin and adiponectin actions on the growth of primary porcine myoblasts under serum-free conditions

Katja Will1, Judith Kuzinski1, Marie-France Palin2, Jan-Peter Hildebrandt3, and Charlotte Rehfeldt1 Katja Will et al.
  • 1Institute for Muscle Biology and Growth, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany
  • 2Dairy & Swine R & D Centre, Agriculture and Agri-Food Canada, Sherbrooke, QC, Canada
  • 3Animal Physiology and Biochemistry, Zoological Institute, Ernst Moritz Arndt-University, Greifswald, Germany

Abstract. Cross-talk between adipose tissue and skeletal muscle may be mediated in part by adipokines. This study was conducted to elucidate further aspects of a possible role of recombinant adiponectin and leptin in the in vitro growth of primary porcine skeletal muscle cells cultured in energetically balanced, growth factor-supplemented, serum-free medium (GF-SFM). Therefore, the effects of these adipokines on cell number (DNA content), DNA synthesis rate, cell death and on key intracellular signalling molecules were investigated. Short-term adiponectin and leptin treatment decreased DNA synthesis, measured as [3H]-thymidine incorporation, as early as after 4-h exposure (P<0.01), without alterations in DNA content. Both adipokines attenuated the rate of cell death in terms of lactate dehydrogenase (LDH) activity in the culture medium after 48-h treatment (P<0.05). The specific activation of p44/42 MAP kinase (MAPK) was reduced (P<0.05) after 15-min incubation with either adipokine. In conclusion, the early decreases in DNA synthesis of primary porcine myoblasts cultured in GF-SFM in response to adiponectin or leptin are related to p44/42 MAPK signalling and adipokine treatment does not impair cell viability.

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