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在禁食海豹中,脂肪组织和肌肉中的细胞内负反馈机制调节急性应激反应。

Intracellular negative feedback mechanisms in blubber and muscle moderate acute stress responses in fasting seals.

机构信息

Department of Biological Sciences, University of the Pacific, Stockton, CA 95211, USA.

Department of Biology, Sonoma State University, Rohnert Park, CA 94928, USA.

出版信息

J Exp Biol. 2023 Dec 15;226(24). doi: 10.1242/jeb.246694. Epub 2023 Dec 18.

DOI:10.1242/jeb.246694
PMID:38009222
Abstract

Animals may limit the cost of stress responses during key life history stages such as breeding and molting by reducing tissue sensitivity to energy-mobilizing stress hormones (e.g. cortisol). We measured expression of genes encoding glucocorticoid receptor (GR, NR3C1), GR inhibitor (FKBP5) and cortisol-inactivating enzyme (HSD11B2) in blubber and muscle of northern elephant seals before and after stress axis stimulation by adrenocorticotropic hormone (ACTH) early and late in a fasting period associated with molting. ACTH elevated cortisol levels for >24 h and increased FKBP5 and HSD11B2 expression while downregulating NR3C1 expression in blubber and muscle, suggesting robust intracellular negative feedback in peripheral tissues. This feedback was maintained over prolonged fasting, despite differences in baseline cortisol and gene expression levels between early and late molt, suggesting that fasting-adapted animals use multiple tissue-specific, intracellular negative feedback mechanisms to modulate downstream impacts of acute stress responses during key life history stages.

摘要

动物可能会通过降低组织对能量动员应激激素(如皮质醇)的敏感性来限制关键生命史阶段(如繁殖和换羽)的应激反应成本。我们在北象海豹禁食期的早期和晚期测量了应激轴刺激(ACTH)前后,其脂肪和肌肉中编码糖皮质激素受体(GR,NR3C1)、GR 抑制剂(FKBP5)和皮质醇失活酶(HSD11B2)的基因表达。ACTH 使皮质醇水平升高超过 24 小时,并增加了 FKBP5 和 HSD11B2 的表达,同时下调了脂肪和肌肉中的 NR3C1 表达,这表明外周组织中存在强大的细胞内负反馈。尽管早期和晚期换羽之间的基础皮质醇和基因表达水平存在差异,但这种反馈在长时间禁食中得以维持,这表明适应禁食的动物利用多种组织特异性的细胞内负反馈机制来调节关键生命史阶段急性应激反应的下游影响。

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