Leptin reduces Atlantic salmon growth through the central pro-opiomelanocortin pathway

Leptin (Lep) is a key factor for the energy homeostasis in mammals, but the available data of its role in teleosts are not conclusive. There are large sequence differences among mammalian and teleost Lep, both at the gene and protein level. Therefore, in order to characterize Lep function in fish, t...

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Veröffentlicht in:Comparative biochemistry and physiology. Part A, Molecular & integrative physiology Molecular & integrative physiology, 2011, Vol.158 (1), p.79-86
Hauptverfasser: Murashita, Koji, Jordal, Ann-Elise Olderbakk, Nilsen, Tom Ole, Stefansson, Sigurd Olav, Kurokawa, Tadahide, Björnsson, Björn Thrandur, Moen, Anne-Grethe Gamst, Rønnestad, Ivar
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Sprache:eng
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Zusammenfassung:Leptin (Lep) is a key factor for the energy homeostasis in mammals, but the available data of its role in teleosts are not conclusive. There are large sequence differences among mammalian and teleost Lep, both at the gene and protein level. Therefore, in order to characterize Lep function in fish, the use of species-specific Lep is crucial. In this study, the cDNA sequence of salmon leptin a1 ( lepa1) was used to establish a production protocol for recombinant salmon LepA1 (rsLepA1) in Escherichia coli, that enabled a final yield of 1.7 mg pure protein L −1 culture. The effects of 20-day administration of rsLepA1 on growth and brain neuroendocrine peptide gene expression [ npy, cart, agrp ( -1 and -2), pomc ( -a1, -a2, -a2s, and -b)] were studied in juvenile, immature Atlantic salmon (96.5 ± 2.1 g) fed a commercial diet to satiation. Intraperitoneal osmotic pumps were used to deliver rsLepA1 at four different concentrations (calculated pumping rates were 0, 0.1, 1.0 and 10 ng g −1 h −1). In the highest dosage group (10 ng g −1 h −1), the growth rate was significantly reduced, and pomc-a1 gene expression was higher than in controls. The results support the lipostatic hypothesis and suggest that sLepA1 reduces growth in Atlantic salmon by affecting food intake through the central pro-opiomelanocortin pathway.
ISSN:1095-6433
1531-4332
DOI:10.1016/j.cbpa.2010.09.001