New insights reveal how stevia controls blood sugar levels

The two major glycosides found in the leaves are stevioside and rebaudioside A. Both taste approximately 200–300 times sweeter than sucrose.©iStock/Heike Rau

How stevia controls blood sugar levels has remained a mystery until now as researchers think they have unravelled the natural, no-calorie sweetener's action that results in its observed health benefits.

Writing in the Nature Communications journal, the research team have identified a protein called TRPM5 that is activated by stevia.

This protein plays a role in taste perception as well as in the release of the hormone insulin after eating.

“TRPM5 is first and foremost essential for the taste perception of sweet, bitter, and umami on the tongue,” explained Dr Koenraad Philippaert from the University of Leuven in Belgium.

“The taste sensation is made even stronger by the stevia component steviol, which stimulates TRPM5.”

Steviol’s effectiveness in controlling blood sugar levels has raised the possibility of the sugar alternative itself forming a new treatment to control or possibly prevent diabetes.

Stevia extracts have been shown to possess insulin stimulating properties as well as anti-hyperglycaemic effects in type 2 diabetic animal models.

However, insights into the mechanisms of action of the stevia extract and its glycosides are currently lacking.

Industry use of stevia

Nevertheless, its 2011 approval in the European Union as a sweetening food additive has made it a first-choice candidate in the plans of food makers looking to reformulate their products in order to reduce sugar content.

Its adoption in drinks such as Coca-Cola Life and Pepsi True has propelled stevia further into the limelight although Coca-Cola recently announced its product was to be withdrawn from UK markets from June.

Stevia has had a mixed reaction from consumers, who’ve found its taste to be an acquired one.

Chemical substances found in the plant mingle with sweet and bitter taste receptors, leading to its familiar bitter aftertaste.

Companies working with stevia have seen fit to blend it with natural dietary fibres as the carrier to mimic the bulking properties of sugar whilst masking stevia’s taste.

In a collaboration that involved a team from the University of Oxford, cell cultures were used to first confirm that stevia homed in on the TRPM5 protein - a calcium-activated channel that are also found in pancreatic β-cells.

Next, the team used wild-type mice and mice that lack the TRPM5 (Trpm5–/– mice) protein.

Here, the animals were fed a high fat diet and given free access to drinking water containing a stevioside solution (25 mg stevioside per kg in a 0.1% solution in water).

The team found that the mice did not develop type 2 diabetes. This was in contrast to mice that lacked the TRPM5 protein.

“If mice consume a high-fat diet for a long period of time they eventually develop diabetes,” said fellow study author Dr Rudi Vennekens, also from the University of Leuven.

 “But this is less the case for mice that also receive a daily dose of stevioside: they are protected against diabetes.

“Stevia did not have this protective effect on mice without TRPM5. This indicates that the protection against abnormally high blood sugar levels and diabetes is due to the stimulation of TRPM5 with stevia components.”

Stevia: diabetes treatment?

When asked about its potential as a diabetic treatment, Dr Philippaert said that there was still much work to be done.

“We must not get ahead of ourselves. This is fundamental research,” he said. “For one thing, the dosages that the mice received are much higher than the amount of stevioside found in beverages and other products for human consumption.”

“Further research is necessary in order to show if our findings readily apply to humans. All this means that new treatments for diabetes will not be for the very near future.”

Source: Nature Communications

Published online ahead of print: doi:10.1038/ncomms14733

“Steviol glycosides enhance pancreatic beta-cell function and taste sensation by potentiation of TRPM5 channel activity.”

Authors: Rudi Vennekens, Koenraad Philippaert et al

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