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 (T₃) 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 T₃ and MMI feed formulations on the AMPK pathways. Feed intake and body weight were reduced in both hypothyroid and hyperthyroid conditions. In hyperthyroid conditions (T₃ 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.

为了研究在肉鸡中甲状腺激素和通过 AMP 活化蛋白激酶 (AMPK) 对能量稳态的中枢调节之间是否存在重要的相互作用，我们在肉鸡中诱导了功能性甲状腺功能亢进和甲状腺功能减退状态，并量化了与全身和下丘脑 AMPK 相关的基因表达及相关蛋白。通过膳食补充三碘甲状腺原氨酸 (T ₃ ) 或甲巯咪唑 (MMI) 7 天来控制甲状腺状态。下丘脑 AMPK 抑制剂 0.1% α-硫辛酸 (α-LA) 用于评估 T ₃和 MMI 饲料配方对 AMPK 途径的影响。在甲状腺功能减退和甲状腺功能亢进的情况下，采食量和体重均有所降低。在甲状腺功能亢进的情况下（T ₃补充）AMPKα1 亚基的表达增加，而在甲状腺功能减退条件下（MMI 补充）下丘脑中活性磷酸化 AMPK 水平下降，但 AMPKα1 和 α2 亚基的基因表达增加。对于FAS和ACC（参与脂肪酸代谢），以及CRH、TRH和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调节可能通过 AMPK 途径进行调节。我们的研究结果表明，下丘脑 AMPK 的表达以及来自 AMPK 通路的其他几个基因的表达都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不同。