低温通过激活尼罗罗非鱼(Oreochromis niloticus)的 TRPA1 通道抑制食物摄入。

IF 3.8 3区 医学 Q2 CELL BIOLOGY Molecular and Cellular Endocrinology Pub Date : 2024-07-22 DOI:10.1016/j.mce.2024.112333
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引用次数: 0

摘要

低温极大地影响了外温脊椎动物的摄食行为,但其潜在机制仍然难以捉摸。本研究调查了瞬态受体电位炔核素 1(TRPA1)通道在尼罗罗非鱼低温抑制食欲效应中的作用。研究发现,TRPA1在下丘脑中高度表达,并与神经肽Y(NPY)神经元共定位。暴露于低温会降低摄食频率并增加 TRPA1 的表达。体外实验表明,低温和TRPA1激动剂可诱导钙离子流入,而TRPA1抑制剂可阻断钙离子流入。TRPA1的表达在餐后增加,并在禁食后下调。TRPA1的激活剂量依赖性地抑制食物摄入,而抑制TRPA1则可恢复低温抑制的摄食。TRPA1的激活通过Ca2+/钙调蛋白依赖途径下调促厌食因子,上调促厌食因子。这些研究结果表明,TRPA1 在罗非鱼感知低温和调节摄食行为方面发挥着重要作用。
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Low temperature inhibits food intake via TRPA1 channel activation in Nile tilapia (Oreochromis niloticus)

Low temperatures significantly influence feeding behavior in ectothermic vertebrates, but the underlying mechanisms remain elusive. This study investigated the role of transient receptor potential ankyrin 1 (TRPA1) channels in mediating the appetite-suppressing effects of low temperature in Nile tilapia. TRPA1 was found to be highly expressed in the hypothalamus and co-localized with neuropeptide Y (NPY) neurons. Exposure to low temperatures reduced feeding frequency and increased TRPA1 expression. In vitro experiments demonstrated that low temperature and TRPA1 agonists induced calcium influx, which was blocked by a TRPA1 inhibitor. TRPA1 expression exhibited post-prandial increases and was downregulated by fasting. TRPA1 activation dose-dependently inhibited food intake, while its inhibition restored feeding suppressed by low temperature. TRPA1 activation downregulated orexigenic factors and upregulated anorexigenic factors through Ca2+/calmodulin-dependent pathways. These findings suggest that TRPA1 plays a crucial role in sensing low temperatures and regulating feeding behavior in tilapia.

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来源期刊
Molecular and Cellular Endocrinology
Molecular and Cellular Endocrinology 医学-内分泌学与代谢
CiteScore
9.00
自引率
2.40%
发文量
174
审稿时长
42 days
期刊介绍: Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the genetic and biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
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