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Lifestyle and Its Relationship to Pain
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Sucralose is derived from sucrose by substituting three atoms of chlorine for three hydrogen-oxygen groups of the sucrose molecule. A study in male rats demonstrated altered gut microflora and other effects after a 12-week exposure.31 In 2006 there was a case report of sucralose causing migraine.32
Nonnutritive Dietary Supplements in Pediatrics
Published in Fima Lifshitz, Childhood Nutrition, 2020
Michael B. Zimmermann, Norman Kretchmer
Sucralose—Sucralose (1,4,6-trideoxy-trichlorogalactosucrose) (Figure 7) is a derivative of sucrose in which three chlorine groups have been substituted for three hydroxyl groups.43 It is approximately 600× sweeter than sucrose. Sucralose is soluble in water and stable within a large range of temperature and pH43,34 It is poorly absorbed and passes through the gut mostly undigested. In man, less than 5% of an oral dose is biotransformed into a glucoronide conjugate and is excreted in the urine.43 A food additive petition was filed with the FDA in 1987 and is pending.19
Carbohydrates
Published in Geoffrey P. Webb, Nutrition, 2019
Although these intense sweeteners mimic the sweetness of sugar, they do not have the preservative or textural effects of sugar; this means that even with sucralose recipes need to be modified if the sugar is serving other functions besides just adding sweetness. Sometimes they are mixed with the less intense bulk sweeteners discussed briefly in the next section.
The development of metabolic endotoxemia is dependent on the type of sweetener and the presence of saturated fat in the diet
Published in Gut Microbes, 2020
Mónica Sánchez-Tapia, Aaron W. Miller, Omar Granados-Portillo, Armando R. Tovar, Nimbe Torres
Our results clearly established that the effects of caloric and NCS differentially modify weight gain and body composition despite the consumption of a high-fat diet. The groups that consumed sucrose and sucrose+HFD had the highest body weight gain, % body fat and the lowest lean mass, whereas sucralose intake resulted in an increase in % body fat, although it is an NCS, probably due to the highest total intake of all of groups (Figure S9); of note, however, this group showed the highest ketone body formation. It has been demonstrated that drinking several artificial sweeteners increases hunger ratings,18 and in fact in our study, the group fed sucralose showed the highest total energy intake and the highest levels of ketone bodies. This result may be because sucralose was the sweetener that most stimulated the expression of the transcription factor PPARα, which is involved in fatty acid oxidation, ketone body formation, and gluconeogenesis.19 This may explain why the consumption of sucralose considerably increased the formation of ketone bodies and gluconeogenesis, increasing glucose and insulin levels and producing glucose intolerance of the same magnitude as that seen with sucrose.
Maternal sucralose intake alters gut microbiota of offspring and exacerbates hepatic steatosis in adulthood
Published in Gut Microbes, 2020
Xin Dai, Zixuan Guo, Danfeng Chen, Lu Li, Xueli Song, Tianyu Liu, Ge Jin, Yun Li, Yi Liu, Aihemaiti Ajiguli, Cheng Yang, Bangmao Wang, Hailong Cao
In summary, this study first demonstrates that MS intake can change the composition and diversity of gut microbiome, reduce butyrate-producing bacteria and butyrate, interfere intestinal development, induce low-grade inflammation as well as disrupt gut barrier function in 3-week-old offspring. Additionally, the microbial analysis in adulthood reveals that the impact of dysbiosis induced by MS is long-lasting, which may contribute to the exacerbation of the susceptibility of hepatic steatosis in adulthood. And finally, MS exacerbated HFD-induced hepatic steatosis in adulthood. These data strongly support the conception of “gut-liver axis,” and that MS intake may be a potential threat for NAFLD in adulthood. As sucralose is widely used around the world, our findings may remind the pregnant women that more caution should be given to excessive sucralose consumption.
Significance of DopEcR, a G-protein coupled dopamine/ecdysteroid receptor, in physiological and behavioral response to stressors
Published in Journal of Neurogenetics, 2020
Emily Petruccelli, Arianna Lark, James A. Mrkvicka, Toshihiro Kitamoto
DopEcR’s first documented function in behavior was for the dopaminergic modulation of enhanced proboscis extension response (PER) following starvation (Inagaki et al., 2012). The PER assay has been used to evaluate taste sensitivity as well as the overall motivation to consume food in flies (Dethier, 1976). Inagaki and colleagues show that starvation increases dopaminergic release onto Gr5a sugar-sensing neurons, and that DopEcR is required in these sensory neurons to mediate evoked calcium in response to extra dopamine release and ultimately increase PER (Inagaki et al., 2012). Thus, DopEcR is required for starvation-dependent enhancement in sugar sensitivity and PER behavioral response. Building upon this finding, a follow up study by Inagaki and colleagues showed that DopEcR is not required for the reciprocal starvation-induced reductions in bitter compound sensitivity, which is instead mediated by sNPF (short neuropeptide F) via sNPFR (Inagaki, Panse, & Anderson, 2014). DopEcR is also required for increasing appetite in flies chronically fed sucralose. Sucralose is a non-nutritive synthetic sweetener, which is known to trigger a neuronal fasting response in control flies and increases the motivation to eat (Wang et al., 2016). Thus, DopEcR appears to be necessary in specific pathways in the nervous system for higher-order detection and/or response to starvation.