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Title: EFFECTS OF GROWTH HORMONE AND PAIR-FEEDING ON LEPTIN MRNA EXPRESSION IN LIVER AND ADIPOSE TISSUE

Author
item Ashwell, Christopher
item McMurtry, John
item WANG, X.-H - PENN STATE UNIV
item ZHOU, Y. - PENN STATE UNIV
item VASILATOS-YOUNKEN, R. - PENN STATE UNIVERSITY

Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/26/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Previous research has reported that elevations in circulating growth hormone (GH) levels in meat-type chickens depresses feed intake (FI) more than 30%. It is known that the product of the obese gene, leptin, functions to regulate FI and energy expenditure. To investigate the effect of GH on leptin gene expression, broiler chickens were treated with synthetic chicken GH. To separate any secondary effects of a GH-induced reduction in FI on leptin expression, groups of birds were pair-fed to an average level of voluntary intake similar to GH-treated birds, but received no GH-treatment. GH treatment induced a dose-dependent increase in liver leptin gene expression, whereas leptin expression in adipose tissue was unchanged. Conversely, in chickens pair-fed (feed-restricted) there was a decrease in leptin gene expression in both tissues. These results provide evidence of a direct effect of GH on leptin gene expression, which is independent of any effects on feed intake due to GH-treatment, and suggest differential regulation of leptin expression between adipose tissue and liver. The results of these experiments provide the first evidence of a relationship between GH and leptin in domestic birds.

Technical Abstract: Previous research has reported that elevations in circulating growth hormone (GH) levels in meat-type chickens depresses feed intake (FI) more than 30%. It is known that the product of the obese gene, leptin, functions to regulate FI and energy expenditure. To investigate the effect of GH on leptin gene expression, broiler chickens were infused with recombinant cGH. To separate any secondary effects of a GH-induced reduction in FI on leptin expression, groups of birds were pair-fed to an average level of voluntary intake similar to GH-treated birds, but received no GH-treatment. GH treatment induced a dose-dependent increase in liver leptin gene expression, as measured by RT-PCR, whereas leptin expression in adipose tissue was unchanged. Conversely, in chickens pair-fed (feed-restricted) there was a decrease in leptin gene expression in both tissues. These results provide evidence of a direct effect of GH on leptin gene expression, which is independent of any effects on intake due to GH-treatment, and suggest differential regulation of leptin expression between adipose tissue and liver. The results of these experiments provide the first evidence of a relationship between GH and leptin in domestic birds.