Do Pancreatic β Cells “Taste” Nutrients to Secrete Insulin?

@article{Henquin2012DoP,
  title={Do Pancreatic $\beta$ Cells “Taste” Nutrients to Secrete Insulin?},
  author={Jean-Claude Henquin},
  journal={Science Signaling},
  year={2012},
  volume={5},
  pages={pe36 - pe36}
}
  • J. Henquin
  • Published 28 August 2012
  • Biology, Medicine
  • Science Signaling
The role of β cell taste receptors in the control of insulin secretion is unclear. Insulin secretion from pancreatic β cells is controlled by nutrients, hormones, and neurotransmitters. Unlike the latter, which work through classic receptors, glucose and most other nutrients do not interact with membrane receptors but must be metabolized by β cells to induce insulin secretion. Studies have revealed the presence of umami and sweet taste receptors and their downstream effectors in β cells. That… 
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30 Citations

Electrophysiology of the pancreatic islet β-cell sweet taste receptor TIR3
TLDR
Data indicate that sucralose, acting as an agonist of the TIR3 receptor, exerts an excitatory effect upon pancreatic β-cell bioelectrical activity.
Insulin secretion in health and disease: nutrients dictate the pace
TLDR
The physiological and pathological effects of nutrients on insulin secretion are highlighted, and the mechanisms mediating nutrient-induced β-cell dysfunction are discussed, to improve treatment and find a cure for diabetes.
Chronic fructose renders pancreatic β-cells hyper-responsive to glucose-stimulated insulin secretion through extracellular ATP signaling.
TLDR
Results reveal an important function of ATP signaling in pancreatic β-cells mediating fructose-induced hyper-responsiveness in insulinoma cells and isolated mouse and human pancreatic islets.
Regulation of Pancreatic α and β Cell Function by the Bile Acid Receptor TGR5
TLDR
The studies identified the expression of TGR5 receptors in β cells and demonstrated that activation of these receptors by both pharmacological ligands and physiological ligands induced insulin secretion, which stimulated insulin secretion under hyperglycemia.
Olfactory receptors are expressed in pancreatic β-cells and promote glucose-stimulated insulin secretion
TLDR
The findings suggest that the OR system in pancreatic β-cells has a chemo-sensor function allowing recognition of environmental substances obtained from food, and potentiates insulin secretion in a cell-autonomous manner, thereby modulating systemic glucose metabolism.
Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum
TLDR
It is concluded that luminal glucose induced GLP-1 secretion from perfused rat ileum in a concentration-dependent manner, and this secretion was mediated by sweet taste receptor transducing signal for GLp-1 release on the gut of rat.
Functional roles of the sweet taste receptor in oral and extraoral tissues
TLDR
The newly recognized role of the sweet taste receptor makes this receptor a potential novel therapeutic target for the treatment of obesity and related metabolic dysfunctions, such as diabetes and hyperlipidemia.
Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum [Rapid Communication].
TLDR
It is concluded that luminal glucose induced GLP-1 secretion from perfused rat ileum in a concentration-dependent manner, and this secretion was mediated by sweet taste receptor transducing signal for GLp-1 release on the gut of rat.
Pharmacological significance of extra-oral taste receptors.
Expression of the glucose-sensing receptor T1R3 in pancreatic islet: changes in the expression levels in various nutritional and metabolic states.
TLDR
The results indicate that T1R3 is expressed mainly in β-cells and the expression levels are different depending upon the nutritional and metabolic conditions.
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