Sucralose = sécrétion d'insuline à vide ?

[Wylde]

Salut,


Etant un gros consommateur de sucralose Nutrimuscle, j'aurais une question à l'admin (et aux autres aussi) à propos du sucralose

J'ai entendu parlé dernièrement du phénomène de production d'insuline à vide, comme quoi il suffirait au cerveau de détecter le gout sucré pour produire de l'insuline (donc même avec les édulcorants... et le sucralose) !

Qu'en pensez-vous ?


Merci d'avance

[Nutrimuscle-Conseils]

au début, c'est possible (bien que de mémoire, je crois que les études montrent que non), mais au bout de 2 à 3 fois, le cerveau sera faire la différence

[Wylde]

des études qui confirment vos dires svp ?

[Administrateur]

Bonjour Wylde.

Sucralose : pas d'impact hormonal : Ma J. Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. Am J Physiol Gastrointest Liver Physiol. 5009 Apr;296(4):G735-9.

Bien à vous.

[Wylde]

Bonsoir Admin,

We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans.

donc ça ne parle pas du problème dont je parle, qui est la sécrétion d'insuline suite à la détection du gout sucré

ensuite y a ça aussi :

In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells.

et ça:

Sucralose activates the sweet receptors in taste buds, and some in vitro studies have shown that sucralose can stimulate the release of incretin hormones, which increase the secretion of insulin, via the sweet taste receptors in enteroendocrine cells (located in the gut).

Read more: http://www.marksdailyapple.com/artifici ... z2IAHNajXb

Qu'en pensez-vous ?

[Nutrimuscle-Conseils]

Qu'en pensez-vous ?

comme expliqué plus haut, si cela arrive 1 à 2 fois, le corps va vite détecter la supercherie et s’adapte pour ne plus se faire berner

[Wylde]

Salut,

Comme demandé plus haut, des études qui confirment ces affirmations ?

[Nutrimuscle-Conseils]

Effects of different sweet preloads on incretin hormone secretion, gastric emptying, and postprandial glycemia in healthy humans
Tongzhi Wu Am J Clin Nutr January 2012 vol. 95 no. 1 78-83

Background: Macronutrient “preloads” can stimulate glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), slow gastric emptying, and reduce postprandial glycemic excursions. After sweet preloads, these effects may be signaled by sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors, or both.

Objective: We determined the effects of 4 sweet preloads on GIP and GLP-1 release, gastric emptying, and postprandial glycemia.

Design: Ten healthy subjects were studied on 4 separate occasions each. A preload drink containing 40 g glucose, 40 g tagatose/isomalt mixture (TIM), 40 g 3-O-methylglucose (3OMG; a nonmetabolized substrate of SGLT1), or 60 mg sucralose was consumed 15 min before a 13C-octanoic acid–labeled mashed potato meal. Blood glucose, plasma total GLP-1 and GIP, serum insulin, and gastric emptying were determined.

Results: Both glucose and 3OMG stimulated GLP-1 and GIP release in advance of the meal (each P < 0.05), whereas TIM and sucralose did not. The overall postprandial GLP-1 response was greater after glucose, 3OMG, and TIM than after sucralose (P < 0.05), albeit later after TIM than the other preloads. The blood glucose and insulin responses in the first 30 min after the meal were greatest after glucose (each P < 0.05). Gastric emptying was slower after both 3OMG and TIM than after sucralose (each P < 0.05).

Conclusions: In healthy humans, SGLT1 substrates stimulate GLP-1 and GIP and slow gastric emptying, regardless of whether they are metabolized, whereas the artificial sweetener sucralose does not. Poorly absorbed sweet tastants (TIM), which probably expose a greater length of gut to nutrients, result in delayed GLP-1 secretion but not in delayed GIP release. These observations have the potential to optimize the use of preloads for glycemic control. This trial was registered at www.actr.org.au as ACTRN12611000775910.

[Nutrimuscle-Conseils]

[Nutrimuscle-Conseils]

Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects.
Eur J Clin Nutr. 2011 Apr;65(4):508-13 Ford HE

The sweet-taste receptor (T1r2+T1r3) is expressed by enteroendocrine L-cells throughout the gastrointestinal tract. Application of sucralose (a non-calorific, non-metabolisable sweetener) to L-cells in vitro stimulates glucagon-like peptide (GLP)-1 secretion, an effect that is inhibited with co-administration of a T1r2+T1r3 inhibitor. We conducted a randomised, single-blinded, crossover study in eight healthy subjects to investigate whether oral ingestion of sucralose could stimulate L-cell-derived GLP-1 and peptide YY (PYY) release in vivo.
METHODS:
Fasted subjects were studied on 4 study days in random order. Subjects consumed 50 ml of either water, sucralose (0.083% w/v), a non-sweet, glucose-polymer matched for sweetness with sucralose addition (50% w/v maltodextrin+0.083% sucralose) or a modified sham-feeding protocol (MSF=oral stimulation) of sucralose (0.083% w/v). Appetite ratings and plasma GLP-1, PYY, insulin and glucose were measured at regular time points for 120 min. At 120 min, energy intake at a buffet meal was measured.
RESULTS:
Sucralose ingestion did not increase plasma GLP-1 or PYY. MSF of sucralose did not elicit a cephalic phase response for insulin or GLP-1. Maltodextrin ingestion significantly increased insulin and glucose compared with water (P<0.001). Appetite ratings and energy intake were similar for all groups.
CONCLUSIONS:
At this dose, oral ingestion of sucralose does not increase plasma GLP-1 or PYY concentrations and hence, does not reduce appetite in healthy subjects. Oral stimulation with sucralose had no effect on GLP-1, insulin or appetite.

[Nutrimuscle-Conseils]

Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects.
Am J Physiol Gastrointest Liver Physiol. 2009 Apr;296(4):G735-9 Ma J

The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells. We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. Blood glucose increased only in response to sucrose (P<0.05). GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. Gastric emptying of sucrose was slower than that of saline (t50: 87.4+/-4.1 min vs. 74.7+/-3.2 min, P<0.005), whereas there were no differences in t50 between sucralose 0.4 mM (73.7+/-3.1 min) or 4 mM (76.7+/-3.1 min) and saline. We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans.

[Wylde]

Salut Nutrimuscle-Conseils,


Merci pour ces études, ça a l'air très convaincant (surtout l'avant dernière)

Je vais pouvoir continuer à consommer mon sucralose tranquille


A plus

[Gilles]

Artificial Sweeteners Have No Effect on Gastric Emptying, Glucagon-Like Peptide-1, or Glycemia After Oral Glucose in Healthy Humans
Diabetes Care Volume 36 December 2013

Extrait : Ten healthy males (mean age 33.6 ± 5.9 years; BMI: 25.5 ± 1.0 kg/m2) were studied on four occasions each, separated by ≥3 days, in single-blinded randomized fashion. Informed consent and ethics approval were obtained. After an overnight fast, each subject consumed either 240 mL water alone or equivalently sweetened with 1) 52 mg sucralose, 2) 200 mg AceK, or 3) 46 mg sucralose plus 26 mg AceK (3). Ten minutes later, each drank 75 g of glucose, made up to 300 mL with water, and containing 150 mg 13C-acetate. Blood glucose (glucometer), plasma insulin (ELISA), total GLP-1 (radioimmunoassay), and gastric emptying (breath test) were evaluated over 240 min.

Blood glucose, plasma insulin, and total GLP-1 concentrations did not change after either water or sweetened drinks, prior to glucose ingestion, but all increased after oral glucose (P < 0.001 for each), without any difference between the 4 days (Fig. 1 A–C). Neither the 13CO2:12CO2 ratio nor the half-emptying time (T50) differed between the 4 days (Fig. 1 D and E).


Conclusion : In conclusion, sucralose and AceK, either alone or in combination, have no acute effect on gastric emptying, GLP-1, or glycemic responses after oral glucose in healthy humans.

Etude complète