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Role of Hypothalamic Transforming Growth Factor-β (TGF-β)/Smad Signaling in Feeding Regulation in Chickens

Saneyasu, Takaoki Ueda, Miku Nagata, Kanami Chai, Jiawei Honda, Kazuhisa Kamisoyama, Hiroshi 神戸大学

2022

概要

Previous studies in mammalian obesity models have suggested that central transforming growth factor-β (TGF-β) controls the gene expression of appetite-regulating neuropeptides and peripheral energy metabolism. In the present study, we investigated the possible involvement of central TGF-β/Smad signaling in feeding regulation in chickens. Central administration of TGF-β1 resulted in phosphorylation of Smad2 in the hypothalamus of chicks and suppressed feed intake without changing the gene expression of hypothalamic appetite-regulating neuropeptides (neuropeptide Y, agouti-related protein, proopiomelanocortin, and corticotropin-releasing factor). However, neither fasting nor refeeding induced the phosphorylation of hypothalamic Smad2. These findings suggest that the activation of hypothalamic TGF-β/Smad signaling suppresses feed intake in chicks but it might not occur in response to feeding status.

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参考文献

Fig. 5. Effects of the feeding conditions on phosphory-

lation of Smad2/3 in chicken hypothalamus. Representative images of Western blot analysis are shown. Ad, ad

libitum feeding conditions; F, fasting conditions; R, refeeding conditions.

between the release of NEFA into the blood stream by basal

lipolysis in the adipose tissue and the uptake of plasma NEFA

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et al. reported that the central injection of neuropeptides

modifies lipid metabolism in chicks (Tachibana et al., 2006,

2007). Further studies are warranted to clarify whether the

central TGF-β/Smad signaling pathway regulates peripheral

lipid metabolism.

Finally, we examined whether feeding conditions affected

Smad2/3 phosphorylation in the hypothalamus of chicks.

Surprisingly, phosphorylated Smad2/3 was not detected under

any conditions in the hypothalamus of broiler and layer chicks

(Fig. 5). In mice, a high-fat diet increased the weight of white

adipose tissue and phosphorylated Smad2/3 protein in the

hypothalamus (Mendes et al., 2018). Therefore, we further

analyzed the phosphorylated Smad2/3 in the hypothalamus of

4- and 7-week-old broiler chickens, which store more abdominal fat compared to 1-week old chicken, but no signal

was observed (unpublished data). These findings suggest that

the hypothalamic Smad signaling pathway is not involved in

the regulation of appetite, in response to feeding status in

chickens.

In the present study, we only administered 1 µg/chick of

TGF-β, and collected tissue samples 30 or 60 min after administration. Therefore in further studies, administering several doses and collection at several points in time would

provide a better understanding of the roles of the hypothalamic

TGF-β/Smad signaling pathway in feeding regulation in

chickens.

Acknowledgments

This work was supported by JSPS KAKENHI (grant number: 19K06353).

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