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HCA 在调节肠道稳态和抑制结肠癌发生中的作用。

Role of HCA in Regulating Intestinal Homeostasis and Suppressing Colon Carcinogenesis.

机构信息

Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL, United States.

出版信息

Front Immunol. 2021 Feb 23;12:606384. doi: 10.3389/fimmu.2021.606384. eCollection 2021.

DOI:10.3389/fimmu.2021.606384
PMID:33708203
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7940178/
Abstract

Hydroxycarboxylic acid receptor 2 (HCA) is vital for sensing intermediates of metabolism, including β-hydroxybutyrate and butyrate. It also regulates profound anti-inflammatory effects in various tissues, indicating that HCA may serve as an essential therapeutic target for mediating inflammation-associated diseases. Butyrate and niacin, endogenous and exogenous ligands of HCA, have been reported to play an essential role in maintaining intestinal homeostasis. HCA, predominantly expressed in diverse immune cells, is also present in intestinal epithelial cells (IECs), where it regulates the intricate communication network between diet, microbiota, and immune cells. This review summarizes the physiological role of HCA in intestinal homeostasis and its pathological role in intestinal inflammation and cancer.

摘要

羟基羧酸受体 2(HCA)对于感应代谢中间产物,包括β-羟丁酸和丁酸至关重要。它还在各种组织中调节着深远的抗炎作用,表明 HCA 可能作为一种重要的治疗靶点,用于调节与炎症相关的疾病。HCA 的内源性和外源性配体,如丁酸和烟酰胺,已被报道在维持肠道内稳态中发挥重要作用。HCA 主要在各种免疫细胞中表达,也存在于肠道上皮细胞(IEC)中,在那里它调节着饮食、微生物群和免疫细胞之间复杂的通讯网络。本综述总结了 HCA 在肠道内稳态中的生理作用及其在肠道炎症和癌症中的病理作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/1fffb669f8bd/fimmu-12-606384-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/2d15eb1c1322/fimmu-12-606384-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/a0037f8249ff/fimmu-12-606384-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/1fffb669f8bd/fimmu-12-606384-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/2d15eb1c1322/fimmu-12-606384-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/a0037f8249ff/fimmu-12-606384-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e73/7940178/1fffb669f8bd/fimmu-12-606384-g0003.jpg

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Niacin Ameliorates Hepatic Steatosis by Inhibiting De Novo Lipogenesis Via a GPR109A-Mediated PKC-ERK1/2-AMPK Signaling Pathway in C57BL/6 Mice Fed a High-Fat Diet.
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Clostridium butyricum upregulates GPR109A/AMPK/PGC-1α and ameliorates acute pancreatitis-associated intestinal barrier injury in mice.丁酸梭菌上调 GPR109A/AMPK/PGC-1α,改善急性胰腺炎相关的肠道屏障损伤。
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