Submitted to: American Journal of Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/12/1998
Publication Date: N/A
Citation: N/A Interpretive Summary: In recent years a better understanding of the factors regulating food intake and appetite in mammals has been gained. This information was boosted by the discovery of a hormone secreted by fat cells, termed leptin, which was subsequently shown to be an important component to food intake regulation and energy expenditure. This study was conducted to clone the leptin gene in chickens and to determine the effect of various hormones on leptin gene expression in the chicken to gain a better understanding of factors influencing leptin gene expression in birds. The results of this study showed that the chicken leptin gene is 90 % identical to rat leptin and more than 80 % similar to other mammalian leptins, and that the leptin gene is expressed in both liver and fat tissue. We also demonstrated for the first time that the leptin gene is expressed by the chick embryo and yolk sac membrane, indicating that leptin has a role in embryonic development. It was also found that leptin gene expression is up-regulated by insulin and an adrenal hormone, and down-regulated by glucagon and estrogen. Liver and fat tissue leptin gene expression were differentially affected by the hormones. In conclusion, the results of this study suggests that the site and degree of leptin expression observed in chickens may be due to differences between birds and mammals in lipid metabolism.
Technical Abstract: Leptin, the polypeptide hormone encoded by the obese gene, is secreted by adipose tissue and has been shown to induce satiety and increase energy expenditure in mammals. In this study we have confirmed the presence of a leptin homolog in liver and adipose tissues of broiler chickens. Leptin expression was also detected in chicken embryonic liver and yolk sac. The effects of hormone treatment on leptin expression in chickens were also investigated. Leptin expression in the liver is increased by insulin and dexamethasone and decreased by glucagon and estrogen. There was no induction of leptin expression in adipose by any treatment, whereas only estrogen decreases adipose expression. The differential effect on liver and adipose tissue suggests that adipocytes in chickens may be expressing leptin at a maximal rate or its mechanism of expression regulation differs from liver. The localization of leptin expression and tissue specific effects of hormone treatments on leptin expression observed in chickens may be due to the differing physiology of mammalian and avian lipid metabolism.