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

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 120
Author(s):  
Joan Serrano ◽  
Nishita N. Meshram ◽  
Mangala M. Soundarapandian ◽  
Kathleen R. Smith ◽  
Carter Mason ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Signaling Cascade ◽  
Artificial Sweetener ◽  
Potential Health ◽  
Peripheral Tissues ◽  
Imaging Results

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.

scholarly journals 82 Ice Melts Phantogeusia: Cold Inhibition of Gustatory Hallucinations

CNS Spectrums ◽  
2019 ◽  
Vol 24 (1) ◽  
pp. 216-217
Author(s):  
Suhanna Mutti ◽  
Alan R. Hirsch
Keyword(s):  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Receptor Potential ◽  
Sweet Taste ◽  
Temperature Dependent ◽  
Left Handed ◽  
Ice Cube ◽  
Metallic Taste ◽  
Old Left ◽  
Transient Receptor

AbstractIntroductionRelief of phantogeusia through ice cube stimulation has not heretofore been noted.MethodsThis 70-year-old left handed (familial) female noted the onset, three and a half years ago, of reduced taste 80 percent of normal, distorted taste, hallucinated metallic taste, and BMS. Upon application of an ice cube to the tongue, both the metallic taste and the BMS resolved for a few seconds, without impairing her true taste ability. With repeat application, the alleviation effect persists.ResultsAbnormalities in Neurologic Examination: Sensory Examination: Decreased pinprick and temperature bilateral lower extremities. Reflexes: 3+ throughout. Bilateral positive Hoffman’s reflexes. Chemosensory testing: Olfaction: Brief Smell Identification Test: 9 (normosmia). Retronasal Smell Index: 10 (normosmia). Gustation: Propylthiouracil Disc Taste Test: 5 (normogeusia).DiscussionTransient Receptor Potential 5, is expressed in tongue taste buds, facilitating sweet perception, and is temperature dependent (Fujiyama, 2010). Ice may act to reduce such sweet taste receptor discharge, causing an imbalance in taste fiber discharge thus inhibiting the perceived metallic taste. In those who suffer from intractable phantogeusia, a trial of ice cubes or mechanisms to reduce temperature of the tongue is warranted.

scholarly journals Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells

2008 ◽  
Vol 100 (4) ◽  
pp. 2177-2191 ◽  
Author(s):  
Kyle Hacker ◽  
Kathryn F. Medler
Keyword(s):  
Signaling Pathways ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Mitochondrial Calcium ◽  
Calcium Buffering ◽  
Taste Cells

Taste stimuli are detected by taste receptor cells present in the oral cavity using diverse signaling pathways. Some taste stimuli are detected by G protein–coupled receptors (GPCRs) that cause calcium release from intracellular stores, whereas other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). Although taste cells use two distinct mechanisms to transmit taste signals, increases in cytosolic calcium are critical for normal responses in both pathways. This creates a need to tightly control intracellular calcium levels in all transducing taste cells. To date, however, the mechanisms used by taste cells to regulate cytosolic calcium levels have not been identified. Studies in other cell types have shown that mitochondria can be important calcium buffers, even during small changes in calcium loads. In this study, we used calcium imaging to characterize the role of mitochondria in buffering calcium levels in taste cells. We discovered that mitochondria make important contributions to the maintenance of resting calcium levels in taste cells by routinely buffering a constitutive calcium influx across the plasma membrane. This is unusual because in other cell types, mitochondrial calcium buffering primarily affects large evoked calcium responses. We also found that the amount of calcium that is buffered by mitochondria varies with the signaling pathways used by the taste cells. A transient receptor potential (TRP) channel, likely TRPV1 or a taste variant of TRPV1, contributes to the constitutive calcium influx.

scholarly journals Sweet Taste Receptor Expressed in Pancreatic β-Cells Activates the Calcium and Cyclic AMP Signaling Systems and Stimulates Insulin Secretion

PLoS ONE ◽  
2009 ◽  
Vol 4 (4) ◽  
pp. e5106 ◽  
Author(s):  
Yuko Nakagawa ◽  
Masahiro Nagasawa ◽  
Satoko Yamada ◽  
Akemi Hara ◽  
Hideo Mogami ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cyclic Amp ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Signaling Systems ◽  
Sweet Taste Receptor ◽  
Cyclic Amp Signaling

scholarly journals 3-Deoxyglucosone Induces Glucagon-Like Peptide-1 Secretion from STC-1 Cells via Upregulating Sweet Taste Receptor Expression under Basal Conditions

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Xiudao Song ◽  
Fei Wang ◽  
Heng Xu ◽  
Guoqiang Liang ◽  
Liang Zhou ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Oral Glucose ◽  
Intragastric Administration ◽  
Sweet Taste Receptor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

3-Deoxyglucosone (3DG) is derived from D-glucose during food processing and storage and under physiological conditions. We reported that glucagon-like peptide-1 (GLP-1) secretion in response to an oral glucose load in vivo and high-glucose stimulation in vitro was decreased by acute 3DG administration. In this study, we determined the acute effect of 3DG on GLP-1 secretion under basal conditions and investigated the possible mechanisms. Normal fasting rats were given a single acute intragastric administration of 50 mg/kg 3DG. Plasma basal GLP-1 levels and duodenum 3DG content and sweet taste receptor expression were measured. STC-1 cells were acutely exposed to 3DG (80, 300, and 1000 ng/ml) for 1 h under basal conditions (5.6 mM glucose), and GLP-1 secretion, intracellular concentrations of cyclic adenosine monophosphate (cAMP) and Ca2+, and molecular expression of STR signaling pathway were measured. Under the fasted state, plasma GLP-1 levels, duodenum 3DG content, and duodenum STR expression were elevated in 3DG-treated rats. GLP-1 secretion was increased in 3DG-treated cells under either 5.6 mM glucose or glucose-free conditions. 3DG-induced acute GLP-1 secretion from STC-1 cells under 5.6 mM glucose was inhibited in the presence of the STR inhibitor lactisole, which was consistent with the observation under glucose-free conditions. Moreover, acute exposure to 3DG increased the protein expression of TAS1R2 and TAS1R3 under either 5.6 mM glucose or glucose-free conditions, with affecting other components of STR signaling pathway, including the upregulation of transient receptor potential channel type M5 TRPM5 and the increment of intracellular Ca2+ concentration. In summary, the glucose-free condition was used to first demonstrate the involvement of STR in 3DG-induced acute GLP-1 secretion. These results first showed that acute 3DG administration induces basal GLP-1 secretion in part through upregulation of STR expression.

Energetic requirement of insulin secretion distal to calcium influx

Diabetes ◽  
1997 ◽  
Vol 46 (8) ◽  
pp. 1305-1311 ◽  
Author(s):  
I. Rustenbeck ◽  
C. Herrmann ◽  
T. Grimmsmann
Keyword(s):  
Insulin Secretion ◽  
Calcium Influx

Effect of taste receptor protein T1R3 on the development of islet tissue of the murine pancreas

2019 ◽  
Vol 484 (1) ◽  
pp. 117-120
Author(s):  
V. O. Murovets ◽  
E. A. Sozontov ◽  
T. G. Zachepilo
Keyword(s):  
Parent Strain ◽  
Gene Knockout ◽  
Taste Receptor ◽  
Morphological Characteristics ◽  
Sweet Taste ◽  
Pancreatic Tissue ◽  
Receptor Protein ◽  
Gene Encoding ◽  
Islet Tissue ◽  
Knockout Animals

Protein T1R3, the main subunit of sweet, as well as amino acid, taste receptor, is expressed in the epithelium of the tongue and gastro intestinal tract, in β–cells of the pancreas, hypothalamus, and numerous other organs. Recently, convincing witnesses of T1R3 involvement in control of carbohydrate and lipid metabolism, and control of production of incretines and insulin, have been determined. In the study on Tas1r3-gene knockout mouse strain and parent strain C57Bl/6J as control, priority data concerning the effect of T1R3 on the morphological characteristics of Langerhans islets in the pancreas, are obtained. In Tas1r3 knockout animals, it is found that the size of the islets and their density in pancreatic tissue are reduced, as compared to the parent strain. Additionally, a decrease of expression of active caspase-3 in islets of gene-knockouts is demonstrated. The obtained data show that the lack of a functional, gene encoding sweet-taste receptor protein causes a dystrophy of the islet tissue and associates to the development of pathological changes in the pancreas specific to type-2 diabetes and obesity in humans.

Sign in / Sign up

Export Citation Format

Share Document