The effect of aspartam and diet changes on blood sugar in prediabetics

It is presented in Type 2 DM that the anomalies in incretin axe have a significant role in terms of progressive beta cell insufficiency. Recent researchs has shown that T1R1 and T1R3 receptors which provide the sense of taste exist in enteroendocrin cells which exist in intestines and have hormone secreting attributes. It is shown that besides glucose also artificial sweeteners are comprehended by intestines as glucose and enable GLP-1 and GIP hormones secretion. It is proposed in experimental researches on artificial sweeteners that when they are given to healthy individuals in company with glucose they increase the secretion and this probably happen via gustation receptors existing in L cells. Based on short term studies run with sweeteners; Our point is to show whether aspartam which is one of the sweeteners that do not have any calorie effect and taken regularly during nutrition has metabolic effect on prediabetic patient group. Total 54 patients applied to the Polyclinics of Endocrine and Metabolic Diseases were taken to the study. In this 3-month crossover study, patients were separated into two groups particularly as aspartam and diet randomly. First group was started with diet and in the 3rd month aspartam was adjoined, concluded in the 6th month. Second group was started with aspartam and diet and in the 3rd month aspartam was cut off, concluded in the 6th month. At the beginning of the study, they were consulted with dietitians expert in nutrition and diabetes with regards to medical nutrition treatment. The dose of aspartame were given as 6tb/day (1tb is 18mg, 2 given by dissolving on tongue before every main meal). Two groups were observed on the months 0-3-6. The parameters of weight-height, BMI, waist circumference, preprandial and postprandial glucose, Hemoglobin A1c (HbA1c), Fructosemin, Alanine Aminotranferase (ALT), Gamma Glutamyl Transferase (GGT), Blood Urea Nitrogen (BUN), Creatinine, Direct LDL Cholesterol, HDL Cholesterol and Triglyceride and insulin were evaluated. In the group that started with diet weight loss was achieved at the end of the 3rd month and after the 3rd month when aspartam adjoined weight loss continued also at the end of the 6th month. In the group that started with aspartam and diet weight loss was achieved, however when aspartam was cut off at the end of the 3rd month, weight gain was observed at the end of the 6th month. When the weight changes were compared in two groups, the weight loss in the 6th month was bigger in the group that had solely diet initially (p>0,027). There was also a similar change in BMI. Between the groups, there were no statistically meaningful difference in terms of the parameters studied. In our study, the situation that aspartame does not have an effect on blood glucose and HbA1c did not support the idea that artificial sweeteners increases the secretion of GLP-1 via gustatory receptors when given in company with glucose. However, that does not mean that sweeteners do not stimulate the secretion of GLP-1. Through these data, the possibility of the secretion of incretin via receptors apart from gustatory can be proposed. In addition, the weight loss provided with aspartam may show antidiabetic effect in long term. Because weight loss is one of the most important parameters in avoiding diabetes. As a conclusion, concerning sweeteners, there is a need of long term studies that both incretin hormones and other metabolic parameters are evaluated. Additionally, the results obtained from these studies need to be synthesized with clinic and interpreted well