A recent study shows the consumption of low-calorie sweeteners allows more glucose to enter the fat cells.
The sweeteners are associated with the upregulation of gene expression for glucose transporters in experiments using human mesenchymal stromal cells and adipose tissue. This effect was seen to be strongest in individuals with obesity.
Using human subcutaneous fat tissue from individuals who consumed low-calorie sweeteners, the researchers showed that these cells had at least double the over expression of glucose transporters. Also over expressed were sweet taste receptors and adipogenic genes (obesity genes).
The adipose tissue biopsies were examined for mRNA expression of adipogenic genes, as well as for glucose transporters and inflammatory markers. In individuals with low-calorie sweetener exposure, the glucose transporter GLUT1 was over expressed by 2- to 2.2-fold, while the glucose transporter GLUT4 was over expressed by a factor of 2.7-4.3.
In addition, low-calorie sweetener consumption was associated with up to 2.5-fold over expression of the sweet taste receptor TAS1R3. Sweet taste receptors are G protein–coupled receptors that are present in taste buds and in other tissues, serving as carbohydrate sensors. Adipogenic genes were also over expressed; a 1.5- to 2.4-fold increase was seen in PPARG, for example.
The study supports the theory that low-calorie sweeteners are promoting additional fat formation by allowing more glucose to enter the cells and promote inflammation which may be even more detrimental to obese individuals. This inflammation can affect cardiac function and cause neuroinflammation associated with dementia, Alzheimer's and other neurological disorders.
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