Horm Metab Res 1987; 19(6): 233-238
DOI: 10.1055/s-2007-1011788
© Georg Thieme Verlag, Stuttgart · New York

The Effect of Artificial Sweetener on Insulin Secretion 1. The Effect of Acesulfame K on Insulin Secretion in the Rat (Studies In Vivo)

Yin Liang, G. Steinbach, V. Maier, E. F. Pfeiffer
  • Zentnum für Inhere Medizin der Universität Ulm, Abteilung Innere Medizin I, Ulm, Germany
Dedicated to Prof. Dr. Dr. h.c. mult. E.F. Pfeiffer on behalf of his 65th birthday.
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Publication Date:
14 March 2008 (online)


Acesulfame K is an artificial sweetener which has been used in the food industry for some years. As yet no metabolic effects have been reported. It was reported that the sweetener can induce a cephalic phase of insulin secretion. To analyse the mechanism of this phenomenon, we studied the effect of Acesulfame K on insulin secretion in vivo. Male Wistar rats, weighing 250-300 g were fasted overnight and anaesthetized with phenobarbital. A silicon catheter was inserted into the right cervical vein for injection of test substances and for obtaining blood samples. In some experiments, another catheter was inserted into the left cervical vein for continuous infusion. Blood samples were drawn at 0, 5, 10, 15, 30 and 60 min after injection, and at - 10, 0, 10, 20, 30, 40, 60, 80, 100 and 120 min after the infusion started. Injection of Acesulfame K (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3±3.0 μU/ml to 58.6±4.2 μU/ml without any significant change in the blood glucose. Infusion of Acesulfame K (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 μU/ml) during this period, and at the same time blood glucose was gradually reduced from 103.0±7.3 to 72.0±7.2 mg/dl. When using different amounts of Acesulfame K, the insulin secretion was stimulated in a dose-dependent fashion. The effect of Acesulfame K on insulin secretion was similar to that observed by injecting or infusing the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K. Infusion of somatostatin markedly inhibited the increase in insulin secretion produced by glucose. However, when somatostatin was infused together with Acesulfame K, its inhibitory effect was not seen. In conclusion, Acesulfame K not only acts as a sweetener, but in higher doses, can also induce insulin secretion in vivo. Hence, the hypothesis of a cephalic phase of insulin secretion stimulated by sweetener should be reexamined.