i Study on the Activation of Bitter Taste Receptors and Glucose Consumption of Intestinal Epithelial Cells by the Exopolysaccharides of Bacillus amyloliquefaciens

Putri, Diwyacitta Antya (2018) i Study on the Activation of Bitter Taste Receptors and Glucose Consumption of Intestinal Epithelial Cells by the Exopolysaccharides of Bacillus amyloliquefaciens. Magister thesis, Universitas Brawijaya.

Abstract

Exopolysaccharides (EPS) dari Bacillus amyloliquefaciens telah terbukti memiliki efek hipoglikemik. Sementara itu, solusi EPS rasanya pahit, sedangkan aktivasi reseptor rasa pahit telah disarankan untuk berhubungan dengan pengaturan glukosa darah. Oleh karena itu, tujuan dari penelitian ini adalah untuk mengkarakterisasi apakah efek hipoglikemik EPS terkait dengan aktivasi reseptor rasa pahit (TAS2R). NCI-H716, dan sel IEC-18 digunakan sebagai model sel enteroendokrin usus, dan sel epitel usus, masing-masing. Ketika sel NCI-H716 diobati dengan EPS, peningkatan konsentrasi Ca2+ intraseluler iv diamati. Sekresi GLP-1 dari sel NCI-H716 juga dipromosikan setelah pengobatan EPS. Sementara itu, ketika sel IEC-18 diobati dengan EPS, konsumsi glukosa sel jelas ditingkatkan, dan AKT, a faktor pensinyalan dalam jalur pensinyalan insulin, diaktifkan di dalam sel. Hasil ini mendukung bahwa EPS mungkin mengaktifkan TAS2R di usus sel enteroendokrin, yang menyebabkan sekresi GLP-1, suatu hormon mempromosikan sekresi insulin. Sementara itu, EPS mengaktifkan efektor di jalur pensinyalan insulin dan meningkatkan konsumsi glukosa usus sel epitel. Efek EPS pada sel usus ini kemungkinan berperan dalam fungsi hipoglikemik EPS.

English Abstract

Exopolysaccharides (EPS) from Bacillus amyloliquefaciens have been demonstarted to have a hypoglycemic effect. Meanwhile, the EPS solution tastes bitter, while the activation of bitter taste receptors has been suggested to be associated with the regulation of blood glucose. Therefore, the purpose of this study is to characterize whether the hypoglycemic effect of EPS is associated with the activation of bitter taste receptors (TAS2R). NCI-H716, and IEC-18 cells were used as a model of the intestinal enteroendocrine cells, and that of intestinal epithelial cells, respectively. When NCI-H716 cells were treated with EPS, an increase in the intracellular Ca2+ concentration was iv observed. The secretion of GLP-1 from NCI-H716 cells was also promoted after EPS treatment. Meanwhile, when IEC-18 cells were treated with EPS, glucose consumption of the cells was obviously enhanced, and AKT, a signaling factor in the insulin-signaling pathway, was activated in the cells. These results supported that EPS might activate TAS2R in intestinal enteroendocrine cells, leading to the secretion of GLP-1, a hormone promoting the secretion of insulin. Meanwhile, EPS activated effectors in the insulin-signaling pathway and increased the glucose consumption of intestinal epithelial cells. These effects of EPS on the intestinal cells likely play roles in the hypoglycemic function of EPS.

Other obstract

已經證明來自液化芽孢桿菌的胞外多醣 (Exopolysaccharides; EPS) 具有降血糖作用。同時,EPS 溶液味道苦,而苦味接受器的活化已被認 為與血糖的調節有關。因此,本研究的目的是分析 EPS 的降血糖作用是 否與苦味接受器(TAS2R)的活化有關。 NCI-H716 和 IEC-18 細胞分別 作為腸上皮內分泌細胞和腸上皮細胞的模型。以 EPS 處理 NCI-H716 細 胞時,觀察到細胞內 Ca2+濃度的增加;同時 EPS 也促進 NCI-H716 細胞 分泌 GLP-1。以 EPS 處理 IEC-18 細胞時,細胞的葡萄糖消耗明顯增加, 且胰島素訊息傳遞路徑中的因子,AKT,被活化。這些結果支持 EPS 可 能活化腸內分泌細胞上的 TAS2R,導致 GLP-1 的分泌,GLP-1 是一種 促進胰島素分泌的激素。同時,EPS 活化胰島素訊息傳遞路徑中的因子 並增加腸上皮細胞的葡萄糖消耗。EPS 的降血糖功能可能與 EPS 對腸道 細胞的這些作用有關。

Item Type: Thesis (Magister)
Identification Number: TES/660.63/PUT/s/2018/041811527
Uncontrolled Keywords: Exopolysaccharides, Bacillus amyloliquefaciens, hypoglycemic effect, bitter taste receptor, intestinal cells,-胞外多醣,液化澱粉芽孢桿菌,降血糖作用,苦味接收器,腸 道細胞
Subjects: 600 Technology (Applied sciences) > 660 Chemical engineering and related technologies > 660.6 Biotechnology
Divisions: S2/S3 > Magister Teknologi Hasil Pertanian, Fakultas Teknologi Pertanian
Depositing User: Endang Susworini
Date Deposited: 28 Jul 2022 05:31
Last Modified: 28 Jul 2022 05:31
URI: http://repository.ub.ac.id/id/eprint/192852
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