Summary
The effect of the artificial sweetener Acesulfame K on insulin release in vitro was investigated. Pancreatic islets were obtained from Male Wistar rats. Acesulfame
K produced a significant increase in insulin release from incubated islets. This effect
was dose- and glucose-dependent. When islets were incubated with different amounts
of Acesulfame K (2.5, 7.5 and 15 mM) and 15 mM glucose in the media for one hour,
insulin concentrations were 140.2 ± 21.1, 246.7 ± 32.4 and 313.9 ± 37.7 μU/ml, respectively.
When 15 mM Acesulfame K was added to a media containing 0, 2.5, 5, 10 and 15 mM glucose,
insulin release from incubated islets after 60 min were 25.6 ± 6.4, 65.4 ± 12.1, 109.0
± 10.0, 229.6 ± 28.0 and 313.9 ± 37.7 μU/ml. Incubating islets in the media containing
arginine or acetylcholine increased insulin release significantly. However, when Acesulfame
K was added to the media containing either arginine or acetylcholine, no further potentiating
effect could be detected. The effect of Acesulfame K on insulin secretion was decreased
by noradrenaline. However, the addition of naloxone, atropine and propranol had no
significant effect. Somatostatin inhibited insulin release from isolated pancreatic
islets, but did not antagonize the action of Acesulfame K. When 2.5 mM Acesulfame
K was added to a medium containing somatostatin, the inhibitory effect of somatostatin
was totally neutralized. In a perifusion system, Acesulfame K stimulated both phases
of insulin secretion. In conclusion, Acesulfame K acts directly on the pancreatic
islets and potentiates glucose-induced insulin release.
Key-Words
Artificial Sweetener
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Acesulfame K
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Insulin Secretion
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Isolated Pancreatic Islets
