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肽 YY 对于酰基乙醇胺受体 Gpr119 诱导的胃肠道黏膜反应的激活至关重要。

Peptide YY is critical for acylethanolamine receptor Gpr119-induced activation of gastrointestinal mucosal responses.

机构信息

King's College London, Wolfson Centre for Age-Related Diseases, Guy's Campus, London SE1 1UL, UK.

出版信息

Cell Metab. 2010 Jun 9;11(6):532-42. doi: 10.1016/j.cmet.2010.04.014.

DOI:10.1016/j.cmet.2010.04.014
PMID:20519124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2890049/
Abstract

Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear. Enteroendocrine L cells contain PYY and express the acylethanolamine receptor, Gpr119. Here, we show that Gpr119 activation inhibited epithelial electrolyte secretion in human and mouse colon in a glucose-sensitive manner. Endogenous PYY selectively mediated these effects, since PYY(-/-) mice showed no Gpr119 response, but responses were observed in NPY(-/-) mice. Importantly, Gpr119 responses in wild-type (WT) mouse tissue and human colon were abolished by Y(1) receptor antagonism, but were not enhanced by dipeptidylpeptidase IV blockade, indicating that PYY processing to PYY(3-36) was not important. In addition, Gpr119 agonism reduced glycemic excursions after oral glucose delivery to WT mice but not PYY(-/-) mice. Taken together, these data demonstrate a previously unrecognized role of PYY in mediating intestinal Gpr119 activity and an associated function in controlling glucose tolerance.

摘要

肽 YY（PYY）在进食后释放，调节肠道功能和葡萄糖稳态，但这些过程的机制尚不清楚。肠内分泌 L 细胞含有 PYY 并表达酰基乙醇胺受体 Gpr119。在这里，我们表明 Gpr119 的激活以葡萄糖敏感的方式抑制人源和鼠源结肠的上皮电解质分泌。内源性 PYY 选择性地介导这些作用，因为 PYY（-/-）小鼠没有 Gpr119 反应，但在 NPY（-/-）小鼠中观察到反应。重要的是，野生型（WT）小鼠组织和人结肠中的 Gpr119 反应被 Y1 受体拮抗剂阻断，但不受二肽基肽酶 IV 阻断的增强，表明 PYY 向 PYY（3-36）的加工不重要。此外，Gpr119 激动剂可减少 WT 小鼠口服葡萄糖后血糖波动，但对 PYY（-/-）小鼠则无此作用。综上所述，这些数据表明 PYY 在介导肠道 Gpr119 活性和相关控制葡萄糖耐量的功能中具有以前未被认识的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/f23ebcda12c7/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/c94757e617f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/381865ff8c65/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/374bee0b77c0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/ecbd3ea98a6c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/52d27e3a9009/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/f23ebcda12c7/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/c94757e617f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/381865ff8c65/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/374bee0b77c0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/ecbd3ea98a6c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/52d27e3a9009/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88e4/2890049/f23ebcda12c7/gr6.jpg

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