39
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Dexamethasone alters the expression of genes related to the growth of skeletal muscle in chickens (Gallus gallus domesticus).

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Glucocorticoids (GCs) are involved in the muscle wasting caused by trauma, inactivity, and stress. In the present study, three experiments were conducted to investigate the effect of GCs on the expression of genes related to muscle development in chickens. Broilers at 7 or 35 days of age were subjected to dexamethasone (DEX) treatment (2 mg/kg body mass (BM)) for 3 or 7 days. The expression levels of genes such as IGF1, IGF1 receptor, MSTN, WW domain containing E3 ubiquitin (UB) protein ligase 1, myogenic determining factor, and myogenic factor 5 were measured. The results showed that BM gain was significantly suppressed by DEX treatment. The plasma level of insulin was increased (P<0.05) by DEX treatment at feeding, whereas IGF1 was decreased (P<0.05). The expression of genes in the IGF1, myostatin, and UB-proteasome (UBP) pathways were altered by DEX treatment in age- and exposure time-related ways. These results suggest that GCs suppress IGF1 and upregulate myostatin and/or activated myostatin and the UBP pathway, which might be the source of the effect of GCs on muscle development.

          Related collections

          Author and article information

          Journal
          J. Mol. Endocrinol.
          Journal of molecular endocrinology
          1479-6813
          0952-5041
          Jun 2011
          : 46
          : 3
          Affiliations
          [1 ] Departments of Animal Science Food Science, Shandong Agricultural University, Taian, People's Republic of China.
          Article
          JME-10-0162
          10.1530/JME-10-0162
          21325373
          e7fb05d2-4305-496b-8460-a7c0218f048a
          History

          Comments

          Comment on this article