Ja, insuline afgifte start ook door alleen maar en zoete smaak. Eiwit op zich geeft trouwens ook al een insuline response.
The effect of artificial sweetener on insulin secretion. 1. The effect of acesulfame K on insulin secretion in the rat (studies in vivo).Liang Y, Steinbach G, Maier V, Pfeiffer EF.
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 microU/ml to 58.6 +/- 4.2 microU/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 microU/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
Entrez PubMed
The effect of artificial sweetener on insulin secretion. II. Stimulation of insulin release from isolated rat islets by Acesulfame K (in vitro experiments).Liang Y, Maier V, Steinbach G, Lalic L, Pfeiffer EF.
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 microU/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 microU/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 propranolol 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.
Entrez PubMed
Volgens dit zou aspartaam geen insuline opwekken en gaat het enkel om `bittere``zoetstof
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.
Entrez PubMed
---------- Toegevoegd om 18:53 ---------- De post hierboven werd geplaatst om 18:51 ----------
Ook nog dit:
De smaakzin is een gespecialiseerd sensorisch systeem dat zo'n 500 miljoenjaar terug is ontstaan, met als primaire functie instandhouding van het individudoor aanzet tot en sturing van voedselopname. Zodra voedsel in aanrakingkomt met de smaakreceptoren in de mond- en keelholte, zorgt de smaakzinvoor informatie betreffende de kwaliteit en intensiteit van het voedsel. Deze'smaak-analyse' leidt tot een voorlopige beoordeling betreffende degeschiktheid van het voedsel, uit het oogpunt van het fysiologisch welzijn vanhet organisme. Naast smaakperceptie is de smaakzin sterk geassocieerd metmetabole factoren die een rol spelen bij voedselopname. Aan de ene kantwordt de smaakzin benvloed door de metabole consequenties vanvoedselopname en aan de andere kant benvloedt smaak de autonome uitvoernaar de viscera. De metabole gevolgen van voedselopname kunnensmaakresponsies (de neurale code) en eetgedrag veranderen, zoalsbijvoorbeeld in een geconditioneerde smaakaversie gebeurt. De fysiologischeconditie van een organisme kan leiden tot veranderingen in smaakgevoeligheidmet als gevolg stimulatie of remming van voedselopname. De invloed van desmaakzin op metabolisme zorgt voor het behoud van homeostase en wordtweerspiegeld in de smaakafhankelijke autonome regulatie van abdominaleorganen. De invloed van smaak op de viscera wordt tot stand gebracht doormiddel van de zogenaamde cefale fase responsies (CFRs). Dit zijnparasympatische reflexen die genduceerd worden door sensorisch (meestalsmaak- en geur-) contact met voedsel en niet door de metabole consequentiesvan voedselopname. Door middel van CFRs is de smaakzin in staat hetspijsverteringsstelsel te informeren over de komst van het op te nemenvoedsel. Voorbeelden van CFRs zijn de afscheiding van speeksel en de afgiftevan maagsappen, pancreas-enzymen en insuline.
http://dissertations.ub.rug.nl/FILES/faculties/science/1998/c.streefland/samenvat.pdf
