spartam orsakar inte insulinfrisättning.
Am J Clin Nutr. 2005 Nov;82(5):1011-6. Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories.
"Evidence exists that beverages do not trigger appropriate anticipatory physiologic responses, such as cephalic phase insulin release. Therefore, it is of interest to elucidate the food properties necessary for triggering adaptive responses. Previously, we found a prolonged dose-dependent decrease in the hypothalamic functional magnetic resonance imaging signal after ingestion of a glucose solution. OBJECTIVES: The aims of the present study were to measure the effects of sweet taste and energy content on the hypothalamic response to glucose ingestion and to measure the concomitant changes in blood glucose and insulin concentrations. DESIGN: Five healthy, normal-weight men participated in a randomized crossover design trial. The subjects were scanned 4 times for 37 min on separate days with functional magnetic resonance imaging. After 7 min, they ingested 1 of the following 4 stimuli (300 mL of each): water (control), a glucose solution, an aspartame (sweet taste) solution, or a maltodextrin (nonsweet carbohydrate) solution. RESULTS: Glucose ingestion resulted in a prolonged and significant signal decrease in the upper hypothalamus (P < 0.05). Water, aspartame, and maltodextrin had no such effect. Glucose and maltodextrin ingestions resulted in similar increases in blood glucose and insulin concentrations. However, only glucose triggered an early rise in insulin concentrations. Aspartame did not trigger any insulin response."
Aspartame--the sweet-tasting dipeptide--does not affect the pancreatic insulin-secreting function
Sadovnikova NV, Fedotov VP, Aleshina LV, Shvachkin IuP, Girin SK.
The action of a synthetic dipeptide aspartam (150 to 180 times as sweet as glucose) on pancreatic insulin-secretory function of rats was studied in vivo and in vitro. The drug was given orally while drinking (300 mg/kg body weight) or was added to the incubation medium of cultivated pancreatic cells (20 mM). It was shown that insulin content in the rat blood serum remained unchanged 10 and 35 minutes after aspartam administration. The drug did not exert any stimulating effect upon insulin secretion following the addition to the pancreatic cell culture medium. It is concluded that aspartam exhibits no direct or mediated action on pancreatic insulin-secretory function.
J Nutr Sci Vitaminol (Tokyo). 1985 Oct;31(5):533-40. Effects of aspartame on diabetic rats and diabetic patients.
The effects of aspartame (L-aspartyl-L-phenylalanine methyl ester) on plasma glucose and insulin levels were investigated in diabetic rats and patients with non-insulin-dependent diabetes mellitus. The oral administration of 0.45 mg aspartame per 100g body weight, which is equivalent to 150 mg of glucose in sweetness, to streptozotocin-induced diabetic rats had no effect on the plasma glucose or insulin levels. Also, 225 mg oral aspartame loading, which is equivalent to 75 g of glucose in sweetness, to patients with non-insulin-dependent diabetes mellitus did not increase plasma glucose or insulin levels, although 75 g of oral glucose loading increased plasma glucose and insulin levels in diabetic patients as expected. Aspartame ingestion for three days at a dose of 24-48 mg per day and the intake of snacks flavored with 240 mg of aspartame also did not increase fasting plasma glucose levels. These results suggest that acute administration of aspartame has no influence on plasma glucose or insulin levels in diabetic rats and patients with non-insulin-dependent diabetes mellitus.
Cell Signal. 1998 Nov;10(10):727-33. Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.
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.
Am J Clin Nutr. 1998 Sep;68(3):531-7. Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.
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.
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