激肽 B1 受体缺乏会促进脂肪组织对β3-肾上腺素能刺激的生热反应。

IF 4.8 3区 医学 Q2 CELL BIOLOGY
Inflammation Research Pub Date : 2024-09-01 Epub Date: 2024-07-17 DOI:10.1007/s00011-024-01917-1
Jéssica Branquinho, Raquel L Neves, Renan P Martin, Júlia G Arata, Clarissa A Bittencourt, Ronaldo C Araújo, Marcelo Y Icimoto, João B Pesquero
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引用次数: 0

摘要

目的和设计:激肽B1受体(B1R)在脂肪细胞中具有保护肥胖和血糖代谢的关键作用,因此成为调节能量代谢和脂肪组织产热的潜在靶点:对 Kinin B1 基因剔除小鼠(B1KO)进行 CL 316,243 的急性诱导和慢性冷暴露:方法:对小鼠肩胛间棕色脂肪组织(iBAT)和腹股沟白色脂肪组织(iWAT)进行代谢和组织学分析、基因和蛋白质表达以及RNA-seq:结果:在 CL 316,243 的急性作用下,B1KO 小鼠的能量消耗增加,iWAT 中的致热基因上调。它们还受到慢性寒冷的保护,表现出更强的非颤抖性产热,iBAT 质量增加(约 90%),iWAT 中米色脂肪细胞的募集增加(约 50%)。生热基因和电子传递链基因受到积极调节,iWAT 中的 Ucp1 增加了 14.5 倍。RNA-seq显示,iBAT的胰岛素信号通路被激活,而iWAT的氧化磷酸化、三羧酸循环和褐变通路被激活:结论:B1R 缺乏会诱导脂肪组织的代谢和基因表达发生改变,激活生热途径并增加能量代谢。B1R 拮抗剂有望成为调节肥胖及相关代谢紊乱(如炎症和糖尿病)的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Kinin B1 receptor deficiency promotes enhanced adipose tissue thermogenic response to β3-adrenergic stimulation.

Kinin B1 receptor deficiency promotes enhanced adipose tissue thermogenic response to β3-adrenergic stimulation.

Objective and design: Kinin B1 receptor (B1R) has a key role in adipocytes to protect against obesity and glycemic metabolism, thus becoming a potential target for regulation of energy metabolism and adipose tissue thermogenesis.

Material or subjects: Kinin B1 knockout mice (B1KO) were subjected to acute induction with CL 316,243 and chronic cold exposure.

Methods: Metabolic and histological analyses, gene and protein expression and RNA-seq were performed on interscapular brown adipose tissue (iBAT) and inguinal white adipose tissue (iWAT) of mice.

Results: B1KO mice, under acute effect of CL 316,243, exhibited increased energy expenditure and upregulated thermogenic genes in iWAT. They were also protected from chronic cold, showing enhanced non-shivering thermogenesis with increased iBAT mass (~ 90%) and recruitment of beige adipocytes in iWAT (~ 50%). Positive modulation of thermogenic and electron transport chain genes, reaching a 14.5-fold increase for Ucp1 in iWAT. RNA-seq revealed activation of the insulin signaling pathways for iBAT and oxidative phosphorylation, tricarboxylic acid cycle, and browning pathways for iWAT.

Conclusion: B1R deficiency induced metabolic and gene expression alterations in adipose tissue, activating thermogenic pathways and increasing energy metabolism. B1R antagonists emerge as promising therapeutic targets for regulating obesity and associated metabolic disorders, such as inflammation and diabetes.

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来源期刊
Inflammation Research
Inflammation Research 医学-免疫学
CiteScore
9.90
自引率
1.50%
发文量
134
审稿时长
3-8 weeks
期刊介绍: Inflammation Research (IR) publishes peer-reviewed papers on all aspects of inflammation and related fields including histopathology, immunological mechanisms, gene expression, mediators, experimental models, clinical investigations and the effect of drugs. Related fields are broadly defined and include for instance, allergy and asthma, shock, pain, joint damage, skin disease as well as clinical trials of relevant drugs.
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