4. Conclusions

NCS [92]. This group also performed a smaller trial of seven healthy volunteers (five males, two females, and ages 28–36) who did not normally consume NCS and who received saccharin for 1 week at a dose of 5 mg/kg, IDA for these sweeteners. Most of these (4/7), known as "NCSs responders" developed lower glucose tolerance and altered IM compared to "non-responders of NCS" [92]. Microbiome of "NCS responders" showed changes in composition by 16S rRNA analysis. Due this control group was not included in the design, it is unclear whether some healthy individuals exposed to seven consecutive tests of oral glucose tolerance (daily intake of 75 g of glucose) would have developed changes in glucose metabolism in the absence of saccharin. Palmnas et al. [107], demonstrated that 8 weeks of exposure to aspartame (at an equal dose to subjects consuming approximately 2–3 sodas/day) disrupted the intestinal microbiota; aspartame + high fat diet vs. water + high fat diet increased total bacteria; Enterobacteraceae, Clostridium leptum, and Roseburia spp. reduced Bifidobacterium sp. On the contrary, when the diet was low fat + aspartame or low-fat + water, Clostridium leptum increased, resulting in elevated levels of fasting glucose and insufficiency tolerance to insulin in rats [51]. However, the mechanism by which aspartame disrupted the IM is unclear, as aspartame is metabolized before it reaches the colon by intestinal esterases and peptidases in amino acids

Figure 1. NCSs: sucralose, saccharin and acesulfame-K have been found to modify the balance of the HIM, either by

D-tagatose (D-tag) is an isomer of fructose approximately 90% sweeter than sucrose. Only 20% of the oral intake of tagatose is completely metabolized, mainly in the liver [49]. The mayor part of this molecule is not digested or absorbed and passes through colon where water is absorbed and D-tag is fermented by colonic bacteria. This natural sweetener can be artificially

and methanol (Figure 1) [49].

3.2. Tagatose and prebiotic potential activity

decreasing or increasing the number of Bacteroidetes.

192 Diabetes Food Plan

The use of prebiotics obtained from functional fiber sources such as fructo-oligosaccharides and beta-glucans, as well as lignin and prebiotics such as keffir, can contribute to the development of a healthy HIM by promoting the growth of bacterial species that have been associated with obesity and diabetes prevention. On the other hand, it has been described that some low GI monosaccharides can positively modify the composition of the HIM in animal models, by regulating the mechanism of insulin sensitivity. More investigations are needed to evaluate the effect of saccharides, such as fructose, lactose and isomaltose in the human microbiome. Although, some NCS such as sucralose, saccharin, and acesulfame-K can modify the balance of HIM, mainly through the alteration in the number of Bacteroidetes species. Nevertheless, more studies in humans are required. In this sense, a new caloric sugar called D-tag has proposed as possible hypoglycemic and probiotic effects. Finally, the new information presented in this chapter allows us to map out the near future where the integration of nutrigenomics and nutritional treatment focused on the microbiota modification will be plausible. Futhermore, the use of bioactive compounds that alter gene expression and/or affects immunity of pancreatic beta cells represent a projection toward the treatment and/or prevention of DM2.

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