T Nation

Sugar Substitutes and Insulin

Ok, once and for all, does anyone know for sure if sugar subs like aspartame, sucralose, etc. cause any insulin response? Does your body think you’re taking in sugar because of the sweet taste and then release insulin? What’s the scoop?

No, sugar substitutes will not trigger an insulin response. Insulin is released when receptor sights are activated by glucose in your blood, not by a sweet taste. If there is high blood glucose, then insulin will be released, if not the pathway by which insulin is created will have proteins that are stericaly inhibited, not allowing them to produce insulin.

Im sure you understand this already but there is always some circulating plasma insulin (even during fasting conditions). And when any caloric substance is put in the body, there is some insulin response (a release of more insulin from the pancreas). This response is usually dependent on the glycemic index, but not always. Take milk for example. A new study shows that although milk has a low glycemic index, it promotes insulin release similar to that of white bread! So GI and insulin release aren’t always dependent on one another (but they usually are).

Now as far as your question, some research shows small insulin responses to some sweeteners. Typically these studies are done in vitro. This means they take some pancreatic beta cells and and incubate with the sweetener (or whatever substance they want to test), then with no glucose, a small amount of glucose, a moderate amount of glucose and a high amount. Then they can see the effects of sweetener alone and sweetener plus diff levels of glucose. Typically some sweeteners alone promote a very small and (although statistically significant) unimportant response. In the presence of moderate to high glucose, however, there is more of an insulin response. And this response is not due to the “sweetness” but to potential membrane and intracellular interactions of the sweetener with the beta cells. And not all sweeteners promote this.

The bottom line is that although this is good evidence, we arent sure if the data can be dupicated in a living human (in vivo) or if these releases have any physiological repercussions. More research is needed to determine the answers to your questions. Remember, these types of investigations are costly and difficult to do. To study every sweetener in beta cells and in humans in different glucose concentrations would be a nightmare. And no one wants to fund these studies anyway so they probably won’t be done. So there is no “once and for all” statement that can be made just yet. (I’m not sure we can ever make “once and for all” statements in science).

I knew that some sugars, such as ribose, can lead to insulin response due to secondary receptors on the promoters. I was kind of surprised that they also had those responses to sugar substitutes because they are supossed to be undigestable (that is why they are made the way they are). If there has only been in vivo research then there is no way to know if they can reach the pancreatic cells in the first place. That is really where the research needs to begin to answer that question. My point was a sweet taste will not trigger a glycemic response. I am really interested in this though because I use suger substitutes all the time. What Journal did you get your info from, just because I would like to try to look into it further

One thing to consider here: most sweeteners use dextrose as a “bulking agent” due to their lack of volume (most sweetners are many times sweeter by weight than sugar). Packets, for example, usually contain about 1/2 of 1 gm of destrose. The “measures like sugar” forms are much worse and should be avoided entirely in my experience. I drink a lot of tea and coffee throughout the day and have found that I do better with tablets or best with liquid sweetners. Sucralose AKA Splenda (my fav sweetner)is now available in tab and liquid form from several online sources.

There are several in vitro (in a “dish”) studies looking at insulin response to sweeteners. Looking them over it is clear that in tissue preparations, some do increase insulin release. Many sweeteners are absorbed in the GI and can therfore stimulate small amounts of insulin secretion in vivo (in a living organism). Sucralose, saccharin and aspartame do not appear to do so in the in vivo human and rat studies when administered alone. Very few studies in vivo have examined them combined with carbs, though. And this is where I think we might see some effects (increased insulin secretion with carbs+sweetener vs. carbs alone). If there are effects, Im not sure. How large, I dont know that either.

Here is a interesting study evaluating the effects of several sweeteners on insulin release in isolated beta cells…from this study it appears that bitter taste and not sweet taste regulates insulin response in relation to sweeteners…In the presence of glucose, sodium saccharin, sodium cyclamate, stevioside, and acesulfame-K all released insulin when combined with carbs. Aspartame did not.

Cell Signal 1998 Nov;10(10):727-33…Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.

Mallaisse WJ, et al…Beta-L-glucose pentaacetate, but not alpha-D-galactose pentaacetate, was recently reported to taste bitter and to stimulate insulinrelease. 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.