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姜黄素通过刺激胰高血糖素样肽-1分泌来改善葡萄糖耐量。

Curcumin improves glucose tolerance via stimulation of glucagon-like peptide-1 secretion.

作者信息

Kato Masaki, Nishikawa Sho, Ikehata Akiho, Dochi Kojiro, Tani Tsubasa, Takahashi Tsukasa, Imaizumi Atsushi, Tsuda Takanori

机构信息

College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.

Theravalues Corporation, Tokyo, Japan.

出版信息

Mol Nutr Food Res. 2017 Mar;61(3). doi: 10.1002/mnfr.201600471. Epub 2016 Dec 19.

Abstract

SCOPE

Glucagon-like peptide-1 (GLP-1) is a type of incretin secreted from enteroendocrine L-cells. Our previous studies demonstrated that curcumin (a yellow pigment of turmeric) significantly increases the secretion of GLP-1 in enteroendocrine L cell line (GLUTag cells). However, it is not clear whether its action in vivo directly enhances GLP-1 secretion, which then leads to a reduction in blood glucose levels via the stimulation of insulin secretion. In addition, the molecular target of curcumin-induced GLP-1 secretion has not been clarified.

METHODS AND RESULTS

Glucose tolerance was significantly improved in rats after pre-administered curcumin (1.5 mg/kg) followed by intraperitoneal glucose injections via the stimulation of GLP-1 secretion and the induction of insulin secretion. In GLUTag cells, curcumin-induced GLP-1 secretion was associated with G protein-coupled receptor (GPR) 40/120. Furthermore, the glucose-lowering effect induced by curcumin was significantly reduced after the administration of a GPR40/120 antagonist in rats.

CONCLUSION

These findings demonstrate the biological function of curcumin as a GLP-1 secretagogue and the possible molecular target that mediates GLP-1 secretion. Increases in the secretion of endogenous GLP-1 induced by curcumin may allow the dosages of other diabetic medicines to be reduced and aid in the prevention of diabetes.

摘要

范围

胰高血糖素样肽-1(GLP-1)是一种由肠内分泌L细胞分泌的肠促胰岛素。我们之前的研究表明,姜黄素(姜黄中的一种黄色色素)可显著增加肠内分泌L细胞系(GLUTag细胞)中GLP-1的分泌。然而,尚不清楚其在体内的作用是否直接增强GLP-1分泌,进而通过刺激胰岛素分泌导致血糖水平降低。此外,姜黄素诱导GLP-1分泌的分子靶点尚未明确。

方法与结果

预先给予姜黄素(1.5毫克/千克),随后腹腔注射葡萄糖,通过刺激GLP-1分泌和诱导胰岛素分泌,大鼠的糖耐量显著改善。在GLUTag细胞中,姜黄素诱导的GLP-1分泌与G蛋白偶联受体(GPR)40/120有关。此外,在大鼠中给予GPR40/120拮抗剂后,姜黄素诱导的降糖作用显著降低。

结论

这些发现证明了姜黄素作为GLP-1促分泌剂的生物学功能以及介导GLP-1分泌的可能分子靶点。姜黄素诱导的内源性GLP-1分泌增加可能会减少其他糖尿病药物的用量,并有助于预防糖尿病。

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