Could sweeteners presented as healthy alternatives to sugar ultimately pose problems similar to those they are meant to avoid?
A recent study sheds new light on sorbitol, a common substitute in products labeled 'sugar-free' or 'low-calorie'. This compound, found naturally in some fruits and added to many candies and gums, could, once in the body, behave like fructose, a sugar often singled out for its effects on the liver.
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Published in the journal Science Signaling, this work is part of a series of studies conducted by Gary Patti's team at Washington University in St. Louis. This group has long been interested in the metabolic effects of fructose, particularly its link to certain liver diseases. The novelty lies in demonstrating that sorbitol can follow metabolic pathways leading to fructose derivatives, which could contribute to liver overload.
Sorbitol can come directly from the diet, but it is also produced naturally in our gut from glucose, especially after a sugar-rich meal. To examine this process, the team used zebrafish as a model. A key observation was that when glucose levels are high in the intestine, an enzyme converts it to sorbitol, which can then be transported to the liver for further conversion.
The role of the gut microbiota then appears crucial. Certain bacterial strains, like those of the genus Aeromonas, are capable of degrading sorbitol into a harmless product. In their presence, the compound is effectively eliminated before reaching the liver. Conversely, in the absence of these appropriate bacteria or if the amount of sorbitol is too large, this natural barrier is bypassed.
Under these conditions, the undegraded sorbitol reaches the liver, where it is transformed. This conversion is similar to that undergone by fructose. For people regularly consuming products containing sorbitol, or whose diet generates a lot of glucose, this flow can become significant. This raises questions, particularly for individuals seeking sugar alternatives for health reasons.
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The system's ability to manage sorbitol therefore depends on a delicate balance. While moderate intake of glucose or dietary sorbitol can generally be handled by gut bacteria, high amounts can overwhelm these microorganisms, even in a person who has them. This observation nuances the idea that polyols, which include sorbitol, are always eliminated without consequence.
These findings lead us to reconsider the intricacy of the interactions between our diet, our gut flora, and our metabolism. They indicate that a sweetener can have very different fates depending on each individual. Research is ongoing to clarify the mechanisms of bacterial degradation of sorbitol and to better assess the long-term implications for liver health.
The journey of sorbitol in the body
Sorbitol's journey in the body begins mainly in the small intestine. After ingestion, it is either absorbed as is or produced locally from glucose through the action of an enzyme called aldose reductase. This internal production is favored by high glucose concentrations, such as those observed after a carbohydrate-rich meal.
Present in the intestine, sorbitol can follow two paths. The first, beneficial, involves its degradation by certain bacteria in the microbiota. These microorganisms ferment it into short-chain fatty acids, generally beneficial for gut health and which do not create a burden for the liver.
The second pathway occurs when the bacterial degradation capacity is insufficient. The unmetabolized sorbitol is then absorbed by the intestinal wall and enters the portal bloodstream, which transports it directly to the liver, the central organ for nutrient processing.
In liver cells, another enzyme, sorbitol dehydrogenase, converts sorbitol into fructose. This fructose can then be integrated into hepatic metabolic pathways, particularly that of lipogenesis, which can contribute to the accumulation of fat in the liver if the intake is chronically high.