Silencing of dopamine receptor D5 inhibits the browning of 3T3-L1 adipocytes and ATP-consuming futile cycles in C2C12 muscle cells.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-10-01 Epub Date: 2023-05-04 DOI:10.1080/13813455.2023.2206983

Kiros Haddish, Jong Won Yun

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Abstract

Background: As a part of the catecholamines, dopamine receptors (DRs) have not been extensively studied like β3-AR in the thermogenesis process. The present study investigates the effect of DRD5 in browning events and ATP-consuming futile cycles.

Methods: siRNA technology, qPCR, immunoblot analysis, immunofluorescence, and staining methods were used to investigate the effect of DRD5 on 3T3-L1 and C2C12 cells.

Results: siDdr5 increased lipogenesis-associated effectors, and adipogenesis markers while reducing the expression of beige fat effectors. ATP-consuming futile cycle markers were also reduced following the siDrd5. On the contrary, pharmacological activation of DRD5 stimulated these effectors. Our mechanistic studies elucidated that DRD5 mediates fat browning via the cAMP-PKA-p38 MAPK signalling pathway in 3T3-L1 cells as well as the cAMP-SERCA-RyR pathway for the ATP-consuming futile cycles in both cells.

Conclusions: siDrd5 positively regulates browning and ATP-consuming futile cycles, and understanding its functions will provide insights into novel strategies to treat obesity.

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沉默多巴胺受体D5可抑制3T3-L1脂肪细胞的褐变和C2C12肌肉细胞的ATP消耗性徒劳循环。

背景：作为儿茶酚胺的一部分，多巴胺受体（DRs）在产热过程中与β3-AR一样尚未被广泛研究。本研究探讨了 DRD5 在褐变事件和 ATP 消耗无效循环中的作用。方法：采用 siRNA 技术、qPCR、免疫印迹分析、免疫荧光和染色等方法研究 DRD5 对 3T3-L1 和 C2C12 细胞的影响。siDrd5 还降低了 ATP 消耗的无效循环标记物的表达。相反，DRD5的药理激活会刺激这些效应因子。我们的机理研究阐明，DRD5 在 3T3-L1 细胞中通过 cAMP-PKA-p38 MAPK 信号通路介导脂肪褐变，在这两种细胞中通过 cAMP-SERCA-RyR 通路介导 ATP 消耗的无效循环。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.