open access

https://hdl.handle.net/2115/87053

2-Arachidonoyl glycerol potently induces cholecystokinin secretion in murine enteroendocrine STC-1 cells via cannabinoid receptor CB1

英語

cholecystokinin

2021-11

John Wiley & Sons

Lipids

56(6)

603-611

Cholecystokinin (CCK) is a peptide hormone secreted from enteroendocrine cells and regulates the exocrine pancreas, gastric motility, and appetite. Dietary triacylglycerols are hydrolyzed to fatty acids (FA) and 2-monoacylglycerols (2-MAG) in the small intestine. Although it is well known that FA stimulate CCK secretion, whether 2-MAG have the CCK-releasing activity remains unclear. We examined the CCK-releasing activity of four commercially available 2-MAG in a murine CCK-producing cell line, STC-1, and the molecular mechanism underlying 2-MAG-induced CCK secretion. CCK released from the cells was measured using ELISA. Among four 2-MAG (2-palmitoyl, 2-oleoyl, 2-linoleoyl, and 2-arachidonoyl monoacylglycerols) examined, 2-arachidonoyl glycerol (2-AG) potently stimulated CCK secretion in a dose-dependent manner. Structurally related compounds, such as 2-arachidonoyl glycerol ether and 1-arachidonoyl glycerol, did not stimulate CCK secretion. Both arachidonic acid and 2-AG stimulated CCK secretion at 100 mu M, but only 2-AG did at 50 mu M. 2-AG-induced CCK secretion but not arachidonic acid-induced CCK secretion was attenuated by treatment with a cannabinoid receptor 1 (CB1) antagonist. These results indicate that a specific 2-MAG, 2-AG, directly stimulates CCK secretion via CB1.

学術雑誌論文

Accepted Manuscript

This is the peer reviewed version of the following article: Ochiai, K, Hirooka, R, Sakaino, M, Takeuchi, S, Hira, T. 2-Arachidonoyl glycerol potently induces cholecystokinin secretion in murine enteroendocrine STC-1 cells via cannabinoid receptor CB1. Lipids. 2021; 56: 603– 611, which has been published in final form at https://doi.org/10.1002/lipd.12323. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.

0024-4201