期刊
BIOMEDICINES
卷 10, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines10010120
关键词
saccharin; artificial sweeteners; sweet taste receptors; PLC; TRPM5; calcium; Munc13-1; insulin secretion; beta cells; glucose tolerance; Tdtomato; T1r2-Cre
资金
- National Institutes of Health [R01DK127444, P30NS104177, S10OD026842]
- National Institute of Food and Agriculture [NIFA-2018-67001-28246]
The study found that the ingestion of saccharin can stimulate insulin secretion by activating the STR signaling pathway. These findings are important for understanding the potential health impact of saccharin use and the role of STR in peripheral tissues.
Background: Saccharin is a common artificial sweetener and a bona fide ligand for sweet taste receptors (STR). STR can regulate insulin secretion in beta cells, so we investigated whether saccharin can stimulate insulin secretion dependent on STR and the activation of phospholipase C (PLC) signaling. Methods: We performed in vivo and in vitro approaches in mice and cells with loss-of-function of STR signaling and specifically assessed the involvement of a PLC signaling cascade using real-time biosensors and calcium imaging. Results: We found that the ingestion of a physiological amount of saccharin can potentiate insulin secretion dependent on STR. Similar to natural sweeteners, saccharin triggers the activation of the PLC signaling cascade, leading to calcium influx and the vesicular exocytosis of insulin. The effects of saccharin also partially require transient receptor potential cation channel M5 (TRPM5) activity. Conclusions: Saccharin ingestion may transiently potentiate insulin secretion through the activation of the canonical STR signaling pathway. These physiological effects provide a framework for understanding the potential health impact of saccharin use and the contribution of STR in peripheral tissues.
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