合肥工业大学食品与生物工程学院的Song-Zi Xie、Guang Yang和Jian-Ping Luo*等人旨在调查黄精多糖（Polygonatum cyrtonema polysaccharide，PCP）在结构鉴定后对GLP-1分泌的影响以及黄精多糖刺激GLP-1分泌的可能机制。
发现在大鼠口服给药5 周（（13.9±0.3）–（35.8±0.3）pmol/L)、2 小时内回肠给药（（13.6±0.4）–（34.1±1.1）pmol/L) ，或是24 小时内直接刺激肠内分泌NCI-H716细胞（（2.05 ± 0.3）–（20.7 ± 0.2）pmol/L)，黄精多糖都能有效地促进GLP-1的分泌（p<0.01）。已确定甜味受体T1R2/T1R3对于NCI-H716细胞直接识别黄精多糖是必不可少的。干预实验表明，抗体、siRNA和T1R2/T1R3抑制剂以及腺苷酸环化酶抑制剂均能显着抑制黄精多糖刺激的GLP-1分泌（p<0.01）。这些结果表明，黄精多糖通过激活T1R2/T1R3介导的cAMP信号通路来刺激肠内分泌细胞分泌GLP-1。
Abstract
Polygonatum cyrtonema Hua Polysaccharide Promotes GLP-1 Secretion from Enteroendocrine L-Cells through Sweet Taste Receptor-Mediated cAMP Signaling
Song-Zi Xie, Guang Yang, Xian-Min Jiang, Dan-Yang Qin, Qiang-Ming Li, Xue-Qiang Zha, Li-Hua Pan, Chuan-Shan Jin, and Jian-Ping Luo*
School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China
Glucagon-like peptide-1 (GLP-1) secreted from enteroendocrine L-cells is a pleiotropic hormone with beneficial potential related to islet function, diet control, glucose homeostasis, inflammation relief, and cardiovascular protection. The present study aimed at investigating the effect of Polygonatum cyrtonema polysaccharide (PCP) after structural identification on GLP-1 secretion and the possible mechanism involved in the PCP-stimulated secretion of GLP-1. It was found that GLP-1 secretion was effectively promoted (p < 0.01) by PCP both in rats with oral administration for 5 weeks (13.9 ± 0.3–35.8 ± 0.3 pmol/L) and ileal administration within 2 h (13.6 ± 0.4–34.1 ± 1.1 pmol/L) and in enteroendocrine NCI-H716 cells with direct stimulation within 24 h (2.05 ± 0.3–20.7 ± 0.2 pmol/L). The sweet taste receptor T1R2/T1R3 was identified to be essential for NCI-H716 cells to directly recognize PCP. The intervention experiments showed that PCP-stimulated GLP-1 secretion was significantly depressed (p < 0.01) not only by antibodies, siRNA, and the inhibitor of T1R2/T1R3 but also by an adenylate cyclase inhibitor. These results suggest that PCP stimulates GLP-1 secretion from enteroendocrine cells possibly through activation of the T1R2/T1R3-mediated cAMP signaling pathway.
