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Domestic animal endocrinology

Publication date: 2001-11-01
Volume: 21 Pages: 319 - 327
Publisher: Elsevier science inc

Author:

Taouis, M
Dridi, Sami ; Cassy, S ; Benomar, Y ; Raver, N ; Rideau, N ; Picard, M ; Williams, J ; Gertler, A

Keywords:

chicken leptin, lipogenic activity, liver, food-intake, plasma leptin, gene-expression, growth-hormone, adipose-tissue, messenger-rna, serum leptin, obese gene, insulin, Science & Technology, Life Sciences & Biomedicine, Agriculture, Dairy & Animal Science, Endocrinology & Metabolism, Agriculture, FOOD-INTAKE, PLASMA LEPTIN, GENE-EXPRESSION, GROWTH-HORMONE, ADIPOSE-TISSUE, MESSENGER-RNA, SERUM LEPTIN, OBESE GENE, INSULIN, LIVER, Adipose Tissue, Animals, Carrier Proteins, Chickens, Eating, Gene Expression Regulation, Leptin, Liver, Receptors, Cell Surface, Receptors, Leptin, 0702 Animal Production, 0707 Veterinary Sciences, Dairy & Animal Science, 3003 Animal production

Abstract:

Chicken leptin cDNA shows a high homology to mammalian homologous, with an expression localized in the liver and adipose tissue. It is noteworthy, that the hepatic expression is most likely associated with the primary role that this organ plays in lipogenic activity in avian species. As in mammals, chicken leptin expression is regulated by hormonal and nutritional status. This regulation is tissue-specific and with a high sensitivity in the liver compared to adipose tissue. The blood leptin levels are regulated by the nutritional state with high levels in the fed state compared to the fasted state. The recombinant chicken leptin markedly inhibits food intake as reported in mammals, suggesting the presence of an hypothalamic leptin receptor. The chicken leptin receptor has been identified and all functional motifs are highly conserved compared to mammalian homologous. Chicken leptin receptor is expressed in the hypothalamus but also in other tissues such as pancreas, where leptin inhibits insulin secretion and thus may have a key role in regulating nutrient utilization in this species. (C) 2002 Elsevier Science Inc. All rights reserved.