Lamberigts C, Wang Y, Dierckx T, Buys N, Everaert N, Buyse J
Laboratory of Livestock Physiology, Department of Biosystems, KU Leuven, Kasteelpark Arenberg 30, 3001 Leuven, Belgium.
Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, Herestraat 49 box 1030, 3000 Leuven, Belgium.
Gen Comp Endocrinol. 2021 Sep 15;311:113838. doi: 10.1016/j.ygcen.2021.113838. Epub 2021 Jun 26.
To investigate whether there are important interactions in play in broilers between thyroid hormones and the central regulation of energy homeostasis through AMP-activated protein kinase (AMPK), we induced a functional hyperthyroid and hypothyroid state in broiler chicks, and quantified systemic and hypothalamic AMPK related gene expression and related protein. Thyroid state was manipulated through dietary supplementation of triiodothyronine (T) or methimazole (MMI) for 7 days. A hypothalamic AMPK suppressor, 0.1% α-lipoic acid (α-LA) was used to assess the effects of the T and MMI feed formulations on the AMPK pathways. Feed intake and body weight were reduced in both hypothyroid and hyperthyroid conditions. In hyperthyroid conditions (T supplementation) expression of the AMPKα1 subunit increased, while in hypothyroid conditions (MMI supplementation) active phosphorylated AMPK levels in the hypothalamus dropped, but gene expression of the AMPKα1 and α2 subunit increased. For FAS and ACC (involved in fatty acid metabolism), and CRH, TRH and CNR1 (anorexigenic neuropeptides stimulating energy expenditure) there were indications that their regulation in response to thyroid state might be modulated through AMPK pathways. Our results indicate that the expression of hypothalamic AMPK as well as that of several other genes from AMPK pathways are involved in thyroid-hormone-induced changes in appetite, albeit differently according to thyroid state.
为了研究甲状腺激素与通过AMP激活蛋白激酶（AMPK）对能量稳态进行中枢调节之间在肉鸡中是否存在重要相互作用，我们诱导肉鸡雏鸡出现功能性甲状腺功能亢进和甲状腺功能减退状态，并对全身和下丘脑与AMPK相关的基因表达及相关蛋白进行定量分析。通过在饲料中添加三碘甲状腺原氨酸（T）或甲巯咪唑（MMI）7天来调控甲状腺状态。使用一种下丘脑AMPK抑制剂，即0.1%的α-硫辛酸（α-LA）来评估T和MMI饲料配方对AMPK途径的影响。甲状腺功能减退和甲状腺功能亢进状态下，采食量和体重均降低。在甲状腺功能亢进状态（添加T）下AMPKα1亚基的表达增加，而在甲状腺功能减退状态（添加MMI）下，下丘脑活性磷酸化AMPK水平下降，但AMPKα1和α2亚基的基因表达增加。对于脂肪酸合成酶（FAS）和乙酰辅酶A羧化酶（ACC）（参与脂肪酸代谢），以及促肾上腺皮质激素释放激素（CRH）、促甲状腺激素释放激素（TRH）和促食欲素受体1（CNR1）（刺激能量消耗的厌食性神经肽），有迹象表明它们对甲状腺状态的反应调节可能通过AMPK途径进行。我们的结果表明，下丘脑AMPK以及AMPK途径中其他几个基因的表达参与了甲状腺激素诱导的食欲变化，尽管根据甲状腺状态的不同而有所差异。
