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Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F.
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Beta-L-glucose pentaacetate, but not alpha-D-galactose pentaacetate, was recently reported to taste bitter and to stimulate insulin release. This finding led, in the present study, to the investigation of the effects of both bitter and non-bitter artificial sweeteners on insulin release and cationic fluxes in isolated rat pancreatic islets. Sodium saccharin (1.0-10.0 mM), sodium cyclamate (5.0-10.0 mM), stevioside (1.0 mM) and acesulfame-K (1.0-15.0 mM), all of which display a bitter taste, augmented insulin release from islets incubated in the presence of 7.0 mM D-glucose. In contrast, aspartame (1.0-10.0 mM), which is devoid of bitter taste, failed to affect insulin secretion. A positive secretory response to acesulfame-K was still observed when the extracellular K+ concentration was adjusted to the same value as that in control media. No major changes in 86Rb and 45Ca outflow from pre-labelled perifused islets could be attributed to the saccharin, cyclamic or acesulfame anions. It is proposed that the insulinotropic action of some artificial sweeteners and, possibly, that of selected hexose pentaacetate esters may require G-protein-coupled receptors similar to those operative in the recognition of bitter compounds by taste buds.
Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.Spiers PA, Sabounjian L, Reiner A, Myers DK, Wurtman J, Schomer DL.
Clinical Research Center, Massachusetts Institute of Technology, Cambridge 02139, USA.
BACKGROUND: Neurobehavioral symptoms have been reported anecdotally with aspartame. OBJECTIVE: This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals. DESIGN: Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each. Order was randomized and subjects were assigned to either a high- (45 mg x kg body wt(-1) x d(-1)) or low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects. RESULTS: Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure. CONCLUSION: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults
Sweet taste: effect on cephalic phase insulin release in men.Teff KL, Devine J, Engelman K.
Monell Chemical Senses Center, Philadelphia, PA 19104, USA.
To determine whether sweet-tasting solutions are effective elicitors of cephalic phase insulin release (CPIR) in humans, two studies were conducted using nutritive and nonnutritive sweeteners as stimuli. Normal weight men sipped and spit four different solutions: water, aspartame, saccharin, and sucrose. A fifth condition involved a modified sham-feed with apple pie. The five stimuli were administered in counterbalanced order, each on a separate day. In study 1, subjects tasted the stimuli for 1 min (n = 15) and in study 2 (n = 16), they tasted the stimuli for 3 min. Arterialized venous blood was drawn to establish a baseline and then at 1 min poststimulus, followed by every 2 min for 15 min and then every 5 min for 15 min. In both study 1 and study 2, no significant increases in plasma insulin were observed after subjects tasted the sweetened solutions. In contrast, significant increases in plasma insulin occurred after the modified sham-feed with both the 1 min and 3 min exposure. These results suggest that nutritive and nonnutritive sweeteners in solution are not adequate stimuli for the elicitation of CPIR.
wychodzi na to ze slodzik ma sie nijak do insy
Zmieniony przez - e-lite w dniu 2008-03-07 16:44:52
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Beta-L-glucose pentaacetate, but not alpha-D-galactose pentaacetate, was recently reported to taste bitter and to stimulate insulin release. This finding led, in the present study, to the investigation of the effects of both bitter and non-bitter artificial sweeteners on insulin release and cationic fluxes in isolated rat pancreatic islets. Sodium saccharin (1.0-10.0 mM), sodium cyclamate (5.0-10.0 mM), stevioside (1.0 mM) and acesulfame-K (1.0-15.0 mM), all of which display a bitter taste, augmented insulin release from islets incubated in the presence of 7.0 mM D-glucose. In contrast, aspartame (1.0-10.0 mM), which is devoid of bitter taste, failed to affect insulin secretion. A positive secretory response to acesulfame-K was still observed when the extracellular K+ concentration was adjusted to the same value as that in control media. No major changes in 86Rb and 45Ca outflow from pre-labelled perifused islets could be attributed to the saccharin, cyclamic or acesulfame anions. It is proposed that the insulinotropic action of some artificial sweeteners and, possibly, that of selected hexose pentaacetate esters may require G-protein-coupled receptors similar to those operative in the recognition of bitter compounds by taste buds.
Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.Spiers PA, Sabounjian L, Reiner A, Myers DK, Wurtman J, Schomer DL.
Clinical Research Center, Massachusetts Institute of Technology, Cambridge 02139, USA.
BACKGROUND: Neurobehavioral symptoms have been reported anecdotally with aspartame. OBJECTIVE: This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals. DESIGN: Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each. Order was randomized and subjects were assigned to either a high- (45 mg x kg body wt(-1) x d(-1)) or low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects. RESULTS: Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure. CONCLUSION: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults
Sweet taste: effect on cephalic phase insulin release in men.Teff KL, Devine J, Engelman K.
Monell Chemical Senses Center, Philadelphia, PA 19104, USA.
To determine whether sweet-tasting solutions are effective elicitors of cephalic phase insulin release (CPIR) in humans, two studies were conducted using nutritive and nonnutritive sweeteners as stimuli. Normal weight men sipped and spit four different solutions: water, aspartame, saccharin, and sucrose. A fifth condition involved a modified sham-feed with apple pie. The five stimuli were administered in counterbalanced order, each on a separate day. In study 1, subjects tasted the stimuli for 1 min (n = 15) and in study 2 (n = 16), they tasted the stimuli for 3 min. Arterialized venous blood was drawn to establish a baseline and then at 1 min poststimulus, followed by every 2 min for 15 min and then every 5 min for 15 min. In both study 1 and study 2, no significant increases in plasma insulin were observed after subjects tasted the sweetened solutions. In contrast, significant increases in plasma insulin occurred after the modified sham-feed with both the 1 min and 3 min exposure. These results suggest that nutritive and nonnutritive sweeteners in solution are not adequate stimuli for the elicitation of CPIR.
wychodzi na to ze slodzik ma sie nijak do insy
Zmieniony przez - e-lite w dniu 2008-03-07 16:44:52
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