Literature DB >> 35052799

Saccharin Stimulates Insulin Secretion Dependent on Sweet Taste Receptor-Induced Activation of PLC Signaling Axis.

Joan Serrano1, Nishita N Meshram1, Mangala M Soundarapandian2, Kathleen R Smith2, Carter Mason1, Ian S Brown1, Björn Tyrberg3, George A Kyriazis1.   

Abstract

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.

Entities:  

Keywords:  Munc13-1; PLC; T1R2; T1R3; T1r2-Cre; TRPM5; Tdtomato; artificial sweeteners; beta cells; calcium; glucose tolerance; insulin secretion; saccharin; sweet taste receptors

Year:  2022        PMID: 35052799      PMCID: PMC8773316          DOI: 10.3390/biomedicines10010120

Source DB:  PubMed          Journal:  Biomedicines        ISSN: 2227-9059


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