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GPR55:新陈代谢的一个新的有前景的靶点?

GPR55: a new promising target for metabolism?

作者信息

Tudurí Eva, Imbernon Monica, Hernández-Bautista Rene Javier, Tojo Marta, Fernø Johan, Diéguez Carlos, Nogueiras Rubén

机构信息

Instituto de Investigaciones Sanitarias (IDIS)CIMUS, University of Santiago de Compostela, Santiago de Compostela, Spain.

CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn)Santiago de Compostela, Spain.

出版信息

J Mol Endocrinol. 2017 Apr;58(3):R191-R202. doi: 10.1530/JME-16-0253. Epub 2017 Feb 14.

DOI:10.1530/JME-16-0253
PMID:28196832
Abstract

GPR55 is a G-protein-coupled receptor (GPCR) that has been identified as a new cannabinoid receptor. Given the wide localization of GPR55 in brain and peripheral tissues, this receptor has emerged as a regulator of multiple biological actions. Lysophosphatidylinositol (LPI) is generally accepted as the endogenous ligand of GPR55. In this review, we will focus on the role of GPR55 in energy balance and glucose metabolism. We will summarize its actions on feeding, nutrient partitioning, gastrointestinal motility and insulin secretion in preclinical models and the scarce data available in humans. The potential of GPR55 to become a new pharmaceutical target to treat obesity and type 2 diabetes, as well as the foreseeing difficulties are also discussed.

摘要

GPR55是一种已被鉴定为新型大麻素受体的G蛋白偶联受体(GPCR)。鉴于GPR55在脑和外周组织中的广泛定位,该受体已成为多种生物学作用的调节因子。溶血磷脂酰肌醇(LPI)被普遍认为是GPR55的内源性配体。在本综述中,我们将聚焦于GPR55在能量平衡和葡萄糖代谢中的作用。我们将总结其在临床前模型中对进食、营养分配、胃肠蠕动和胰岛素分泌的作用以及人类中可用的稀少数据。还讨论了GPR55成为治疗肥胖症和2型糖尿病新药物靶点的潜力以及可预见的困难。

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GPR55: a new promising target for metabolism?GPR55:新陈代谢的一个新的有前景的靶点?
J Mol Endocrinol. 2017 Apr;58(3):R191-R202. doi: 10.1530/JME-16-0253. Epub 2017 Feb 14.
2
GPR55, a lysophosphatidylinositol receptor with cannabinoid sensitivity?GPR55,一种具有大麻素敏感性的溶血磷脂酰肌醇受体?
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GPR55: from orphan to metabolic regulator?GPR55:从孤儿受体到代谢调节剂?
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Atypical responsiveness of the orphan receptor GPR55 to cannabinoid ligands.孤儿受体GPR55对大麻素配体的非典型反应性。
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What is the natural ligand of GPR55?GPR55 的天然配体是什么?
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The G protein-coupled receptor 55 ligand l-α-lysophosphatidylinositol exerts microglia-dependent neuroprotection after excitotoxic lesion.G 蛋白偶联受体 55 的配体 l-α-溶血磷脂酰肌醇在兴奋性损伤后发挥小胶质细胞依赖性神经保护作用。
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Modulation of L-α-lysophosphatidylinositol/GPR55 mitogen-activated protein kinase (MAPK) signaling by cannabinoids.大麻素对 L-α-溶血磷脂酰肌醇/GPR55 有丝分裂原激活蛋白激酶(MAPK)信号的调节。
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