Scientists in the field have discovered some significant roles that the microbiome has in the body. It has been found to be essential for human development, immunity, nutritional needs and most recently scientists believe that having a dysfunctional microbiome may link to a variety of autoimmune diseases such as type I diabetes, rheumatoid arthritis, muscular dystrophy and multiple sclerosis. The cause of such diseases have been hypothesised that the dysfunctional microbiome has accumulated over time, changing gene expression and metabolic processes within the body triggering an abnormal immune response. Moreover, environmental susceptibility to infectious diseases can contribute to microbiome changes and create chronic illnesses of the GIT, for example Inflammatory Bowel Disease. Due to such importance of the uprising discovering of the microbiome, researchers have been and are continuing to map the human microbiome to provide possible treatment programs and to find causes for certain diseases. By mapping the microbiome map, it enables us to figure out which are the “good” and “bad” bacteria that can either protect or harm us.
Brown, R., & Rother, K. (2012). Non-Nutritive Sweeteners and their Role in the Gastrointestinal Tract. The Journal Of Clinical Endocrinology & Metabolism, 97(8), 2597-2605. http://dx.doi.org/10.1210/jc.2012-1475
In vitro studies with mice and rodents displayed an increase secretion of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) in the enteroendocrine cells when given artificial sweeteners. By adding these sweeteners these rats and rodents increased the rate of glucose reabsorption, but at the same time maintained normal gut hormone secretion. In the same study, human subjects were also tested, in which when the subject consumed cola with the artificial sweetener; the same trend was shown; as glucose reabsorption increased while the gut hormones are maintained. The mechanism of action of these artificial sweeteners is that they bind to taste receptors in the oral cavity, pancreatic cells and enteroendocrine cells. Studies suggest that, acting on multiple organs that are responsible for endocrine function; can alter enzyme and hormone activity.
Pepino, M., & Bourne, C. (2011). Non-nutritive sweeteners, energy balance, and glucose homeostasis. Current Opinion In Clinical Nutrition And Metabolic Care, 14(4), 391-395. http://dx.doi.org/10.1097/mco.0b013e3283468e7e
Research from Pepino and Bourne displays that the contradicting effects from the artificial sweeteners (AS) is due to the sweetness interfering with normal physiological functions in rat studies. AS has also been found to be associated to trigger inflammation that are associated with metabolic disorders. Further rat studies have shown that AS interacts with the incretin effect which then up-regulates glucose transporters.
Feehley, T., & Nagler, C. (2014). Health: The weighty costs of non-caloric sweeteners. Nature. http://dx.doi.org/10.1038/nature13752
AS might not actually contribute to overall calorie intake but it most definitely contributes to the plasma blood glucose concentration. It has been found that AS has not been so successful in weight loss but it does prevent weight gain. This paper suggests that it is due to the diet variation that lead to a constantly change gut microbiome. By treating animal subjects with antibiotics, it got rid of the glucose induced intolerance as well. Multiple papers referenced in this article mentioned that AS consumption is correlated with obesity and increasing fasting blood glucose concentration.
Links to Websites/Articles:
Learn.genetics.utah.edu,. (2015). Your Changing Microbiome. Retrieved 14 October 2015, from http://learn.genetics.utah.edu/content/microbiome/changing/
Mayoclinic.org,. (2015). Metabolic syndrome – Mayo Clinic. Retrieved 14 October 2015, from http://www.mayoclinic.org/diseases-conditions/metabolic-syndrome/basics/definition/con-20027243
Medscape,. (2015). Microbiota and Diabetes: An Evolving Relationship. Retrieved 14 October 2015, from http://www.medscape.com/viewarticle/829967