Acesulfame Potassium

Acesulfame potassium activates two members of the human TAS2R family (hTAS2R43 and hTAS2R44) to stimulate bitter taste. Acesulfame potassium elicited robust elevation of cytosolic Ca²⁺ in hTAS2R44-expressing cells, with a threshold value of activation of 0.25 mM and an EC50 value of 2.5 mM. Acesulfame potassium elicited response of hTAS2R43-expressing cells with a threshold value of 3.1 mM and an estimated EC50 value ﹥10 mM [1] Acesulfame potassium acts directly on the pancreatic islets and potentiates glucose-induced insulin release. Acesulfame potassium (1.0-15.0 mM) augmented insulin release from islets incubated in the presence of 7.0 mM d-glucose. [2] Acesulfame Potassium enhanced glucose absorption via activating sweet taste receptors in the enterocyte to translocate GLUT2 to the apical membrane through the PLC βII. In Caco-2 and RIE-1 cells, Acesulfame potassium (10 mM) increased glucose uptake by 20-30 % when incubated for 10 min with glucose >25 mM. [3] Acesulfame potassium increased the contractile response of isolated rat detrusor muscle strips via increased extracellular Ca²⁺ influx. Acesulfame potassium (10^-7 M to 10^-2 M) enhanced the contractile response to 10 Hz EFS compared to control. The atropine-resistant response to EFS is marginally increased by Acesulfame potassium (10^-6 M). Acesulfame potassium (10^-6 M) increased the maximum contractile response to α, β methylene ATP by 35% and to KCl by 12%. Acesulfame potassium (10^-6 M) increased the log EC50 from -2.7 to -3.03. [4]

Acesulfame potassium acts on two members of the TAS1R family of G-protein-coupled receptors (TAS1R2 and TAS1R3) to stimulate sweet taste. Selective elimination of T1R-subunits differentially abolishes de tection and perception of these two taste modalities. [5] Acesulfame potassium can also induce insulin secretion in rats. Injection of Acesulfame potassium (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3 mU/mL to 58.6 mU/mL. Infusion of Acesulfame potassium (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 mU/mL). When using different amounts of Acesulfame potassium, the insulin secretion is stimulated in a dose-dependent fashion. [6] Oral administration of Acesulfame potassium (60, 450, 1500 and 2250 mg/kg body weight) induced a significant increase in the frequency of cellular damage and chromosome aberrations in the Bone marrow cells isolated from mice femora. [7] Oral administration of Acesulfame potassium at the concentration of 150, 300, and 600 mg/kg body weight is found to induce DNA damage in bone marrow cells of mice with a minimum effective concentration (MEC) value of 150 mg/kg in the comet assay. [8]