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The Role of the Glucose-Sensing Receptor in Glucose-Induced Insulin Secretion in Pancreatic β-Cells

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Glucose-sensing Receptor in Pancreatic Beta-cells
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Abstract

Glucose activates the glucose-sensing receptor and induces rapid intracellular signals in pancreatic β-cells. When the glucose-sensing receptor is blocked by an inhibitor of T1R3 or deletion of the T1R3 gene, glucose-induced insulin secretion (GIIS) is significantly reduced. In perifusion system, both first and second phases of GIIS are attenuated by the inhibition of the glucose-sensing receptor. Collectively, the glucose-sensing receptor is involved in both rapid and sustained action of glucose. Indeed, activation of the receptor by either artificial sweeteners or nonmetabolizable glucose analog increases ATP levels in β-cells. Furthermore, inhibition of the glucose-sensing receptor attenuates glucose-induced increase in ATP. These results indicate that activation of the glucose-sensing receptor promotes glucose metabolism and thereby augments ATP production in β-cells. Thus, glucose first acts on the cell-surface glucose-sensing receptor and primes the metabolic pathway of glucose. Glucose then enters β-cells and is metabolized through already activated metabolic pathway. The receptor pathway and the metabolic pathway act coordinately to stimulate insulin secretion.

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Correspondence to Yuko Nakagawa .

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Nakagawa, Y., Medina, J. (2018). The Role of the Glucose-Sensing Receptor in Glucose-Induced Insulin Secretion in Pancreatic β-Cells. In: Kojima, I. (eds) Glucose-sensing Receptor in Pancreatic Beta-cells. Springer, Singapore. https://doi.org/10.1007/978-981-13-0002-8_5

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