Non-Nutritive Sweeteners and Their Implications on the Development of Metabolic Syndrome.

Iryna Liauchonak, Bessi Qorri, Fady Dawoud, Yatin Riat, Myron R Szewczuk

Journal: Nutrients 2019;11(3):644

PMID: 30884834

Plain Language Summary

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Artificial sweeteners, such as aspartame, neotame, saccharin, sucralose, and stevia are widely promoted as low-calorie alternatives to sugar and are known as non-nutritive sweeteners (NNS). Generally, they have been considered as a healthy option to replace sugars, but data is emerging that they may influence obesity and metabolic syndrome (METs) and contribute to the development of type II diabetes. These non-nutritive sweeteners can be thousands of times sweeter than sugar and have been widely adopted by the food industry to help reduce calories, and promote weight loss and diabetic products. It is believed that 25% of children and 41% of adults consume low-calorie sweeteners regularly, with the beverage industry relying heavily on them. However, it is now been shown that these sweeteners can cause imbalances to gut bacteria and interact with taste receptors and insulin signalling. These findings mean that artificial sweeteners may trigger the same hormonal response as sugar by releasing insulin and overtime lead to insulin resistance, obesity, and overall metabolic syndrome. Finally, there is evidence that our body develops a learned response to sweeteners which paradoxically leads to weight gain.

Abstract

Individuals widely use non-nutritive sweeteners (NNS) in attempts to lower their overall daily caloric intake, lose weight, and sustain a healthy diet. There are insufficient scientific data that support the safety of consuming NNS. However, recent studies have suggested that NNS consumption can induce gut microbiota dysbiosis and promote glucose intolerance in healthy individuals that may result in the development of type 2 diabetes mellitus (T2DM). This sequence of events may result in changes in the gut microbiota composition through microRNA (miRNA)-mediated changes. The mechanism(s) by which miRNAs alter gene expression of different bacterial species provides a link between the consumption of NNS and the development of metabolic changes. Another potential mechanism that connects NNS to metabolic changes is the molecular crosstalk between the insulin receptor (IR) and G protein-coupled receptors (GPCRs). Here, we aim to highlight the role of NNS in obesity and discuss IR-GPCR crosstalk and miRNA-mediated changes, in the manipulation of the gut microbiota composition and T2DM pathogenesis.

Address: Graduate Diploma and Professional Master in Medical Sciences, Postgraduate Medical Education, School of Medicine, Queen's University, Kingston, ON K7L 3N6, Canada. [email protected].; Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON K7L 3N6, Canada. [email protected].; Graduate Diploma and Professional Master in Medical Sciences, Postgraduate Medical Education, School of Medicine, Queen's University, Kingston, ON K7L 3N6, Canada. [email protected].; Graduate Diploma and Professional Master in Medical Sciences, Postgraduate Medical Education, School of Medicine, Queen's University, Kingston, ON K7L 3N6, Canada. [email protected].; Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON K7L 3N6, Canada. [email protected].
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