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Nutrients Apr 2022Artificial sweeteners are additives widely used in our diet. Although there is no consensus, current evidence indicates that sucralose and saccharin could influence the... (Review)
Review
Artificial sweeteners are additives widely used in our diet. Although there is no consensus, current evidence indicates that sucralose and saccharin could influence the gut microbiota. The aim of this study was to analyze the existing scientific evidence on the effects of saccharin and sucralose consumption on gut microbiota in humans. Different databases were used with the following search terms: sweeteners, non-caloric-sweeteners, sucralose, splenda, saccharin, sugartwin, sweet'n low, microbiota, gut microbiota, humans, animal model, mice, rats, and/or in vitro studies. In vitro and animal model studies indicate a dose-dependent relationship between the intake of both sweeteners and gut microbiota affecting both diversity and composition. In humans, long-term study suggests the existence of a positive correlation between sweetener consumption and some bacterial groups; however, most short-term interventions with saccharin and sucralose, in amounts below the ADI, found no significant effect on those groups, but there seems to be a different basal microbiota-dependent response of metabolic markers. Although studies in vitro and in animal models seem to relate saccharin and sucralose consumption to changes in the gut microbiota, more long-term studies are needed in humans considering the basal microbiota of participants and their dietary and lifestyle habits in all population groups. Toxicological and basal gut microbiota effects must be included as relevant factors to evaluate food safety and nutritional consequences of non-calorie sweeteners. In humans, doses, duration of interventions, and number of subjects included in the studies are key factors to interpret the results.
Topics: Animals; Gastrointestinal Microbiome; Humans; Mice; Rats; Saccharin; Sucrose; Sweetening Agents
PubMed: 35458244
DOI: 10.3390/nu14081682 -
Food and Chemical Toxicology : An... Aug 2017Sucralose is a non-caloric high intensity sweetener that is approved globally for use in foods and beverages. This review provides an updated summary of the literature... (Review)
Review
Sucralose is a non-caloric high intensity sweetener that is approved globally for use in foods and beverages. This review provides an updated summary of the literature addressing the safety of use of sucralose. Studies reviewed include chemical characterization and stability, toxicokinetics in animals and humans, assessment of genotoxicity, and animal and human feeding studies. Endpoints evaluated include effects on growth, development, reproduction, neurotoxicity, immunotoxicity, carcinogenicity and overall health status. Human clinical studies investigated potential effects of repeated consumption in individuals with diabetes. Recent studies on the safety of sucralose focused on carcinogenic potential and the effect of sucralose on the gut microflora are reviewed. Following the discovery of sweet taste receptors in the gut and studies investigating the activation of these receptors by sucralose lead to numerous human clinical studies assessing the effect of sucralose on overall glycemic control. Estimated daily intakes of sucralose in different population subgroups, including recent studies on children with special dietary needs, consistently find that the intakes of sucralose in all members of the population remain well below the acceptable daily intake. Collectively, critical review of the extensive database of research demonstrates that sucralose is safe for its intended use as a non-caloric sugar alternative.
Topics: Animals; Consumer Product Safety; Food Safety; Humans; Sucrose; Sweetening Agents
PubMed: 28558975
DOI: 10.1016/j.fct.2017.05.047 -
Journal of Hepatology Jul 2021Excessive fructose intake is associated with increased de novo lipogenesis, blood triglycerides, and hepatic insulin resistance. We aimed to determine whether fructose... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND & AIMS
Excessive fructose intake is associated with increased de novo lipogenesis, blood triglycerides, and hepatic insulin resistance. We aimed to determine whether fructose elicits specific effects on lipid metabolism independently of excessive caloric intake.
METHODS
A total of 94 healthy men were studied in this double-blind, randomized trial. They were assigned to daily consumption of sugar-sweetened beverages (SSBs) containing moderate amounts of fructose, sucrose (fructose-glucose disaccharide) or glucose (80 g/day) in addition to their usual diet or SSB abstinence (control group) for 7 weeks. De novo fatty acid (FA) and triglyceride synthesis, lipolysis and plasma free FA (FFA) oxidation were assessed by tracer methodology.
RESULTS
Daily intake of beverages sweetened with free fructose and fructose combined with glucose (sucrose) led to a 2-fold increase in basal hepatic fractional secretion rates (FSR) compared to control (median FSR %/day: sucrose 20.8 (p = 0.0015); fructose 19.7 (p = 0.013); control 9.1). Conversely, the same amounts of glucose did not change FSR (median of FSR %/day 11.0 (n.s.)). Fructose intake did not change basal secretion of newly synthesized VLDL-triglyceride, nor did it alter rates of peripheral lipolysis, nor total FA and plasma FFA oxidation. Total energy intake was similar across groups.
CONCLUSIONS
Regular consumption of both fructose- and sucrose-sweetened beverages in moderate doses - associated with stable caloric intake - increases hepatic FA synthesis even in a basal state; this effect is not observed after glucose consumption. These findings provide evidence of an adaptative response to regular fructose exposure in the liver.
LAY SUMMARY
This study investigated the metabolic effects of daily sugar-sweetened beverage consumption for several weeks in healthy lean men. It revealed that beverages sweetened with the sugars fructose and sucrose (glucose and fructose combined), but not glucose, increase the ability of the liver to produce lipids. This change may pave the way for further unfavorable effects on metabolic health.
CLINICAL TRIAL REGISTRATION NUMBER
NCT01733563.
Topics: Adult; Double-Blind Method; Energy Intake; Fatty Acids; Fructose; Glucose; Healthy Volunteers; Humans; Lipid Metabolism; Lipogenesis; Lipoproteins, VLDL; Liver; Male; Sucrose; Sugar-Sweetened Beverages; Sweetening Agents; Triglycerides
PubMed: 33684506
DOI: 10.1016/j.jhep.2021.02.027 -
Nutrients Apr 2020Sweeteners that are a hundred thousand times sweeter than sucrose are being consumed as sugar substitutes. The effects of sweeteners on gut microbiota composition have... (Review)
Review
Sweeteners that are a hundred thousand times sweeter than sucrose are being consumed as sugar substitutes. The effects of sweeteners on gut microbiota composition have not been completely elucidated yet, and numerous gaps related to the effects of nonnutritive sweeteners (NNS) on health still remain. The NNS aspartame and acesulfame-K do not interact with the colonic microbiota, and, as a result, potentially expected shifts in the gut microbiota are relatively limited, although acesulfame-K intake increases Firmicutes and depletes populations. On the other hand, saccharin and sucralose provoke changes in the gut microbiota populations, while no health effects, either positive or negative, have been described; hence, further studies are needed to clarify these observations. Steviol glycosides might directly interact with the intestinal microbiota and need bacteria for their metabolization, thus they could potentially alter the bacterial population. Finally, the effects of polyols, which are sugar alcohols that can reach the colonic microbiota, are not completely understood; polyols have some prebiotics properties, with laxative effects, especially in patients with inflammatory bowel syndrome. In this review, we aimed to update the current evidence about sweeteners' effects on and their plausible biological interactions with the gut microbiota.
Topics: Aspartame; Diterpenes, Kaurane; Gastrointestinal Microbiome; Glucosides; Humans; Non-Nutritive Sweeteners; Polymers; Saccharin; Sucrose; Thiazines
PubMed: 32326137
DOI: 10.3390/nu12041153 -
JAMA Internal Medicine Nov 2016Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents,...
Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review's objective, contributed articles for inclusion, and received drafts. The SRF's funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry-funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.
Topics: Biomedical Research; Coronary Disease; Evidence-Based Medicine; Food Industry; History, 20th Century; History, 21st Century; Humans; Sucrose; Sweetening Agents; United States
PubMed: 27617709
DOI: 10.1001/jamainternmed.2016.5394 -
Biochemistry Oct 2011Nearly 100 years ago Michaelis and Menten published their now classic paper [Michaelis, L., and Menten, M. L. (1913) Die Kinetik der Invertinwirkung. Biochem. Z. 49,...
Nearly 100 years ago Michaelis and Menten published their now classic paper [Michaelis, L., and Menten, M. L. (1913) Die Kinetik der Invertinwirkung. Biochem. Z. 49, 333-369] in which they showed that the rate of an enzyme-catalyzed reaction is proportional to the concentration of the enzyme-substrate complex predicted by the Michaelis-Menten equation. Because the original text was written in German yet is often quoted by English-speaking authors, we undertook a complete translation of the 1913 publication, which we provide as Supporting Information . Here we introduce the translation, describe the historical context of the work, and show a new analysis of the original data. In doing so, we uncovered several surprises that reveal an interesting glimpse into the early history of enzymology. In particular, our reanalysis of Michaelis and Menten's data using modern computational methods revealed an unanticipated rigor and precision in the original publication and uncovered a sophisticated, comprehensive analysis that has been overlooked in the century since their work was published. Michaelis and Menten not only analyzed initial velocity measurements but also fit their full time course data to the integrated form of the rate equations, including product inhibition, and derived a single global constant to represent all of their data. That constant was not the Michaelis constant, but rather V(max)/K(m), the specificity constant times the enzyme concentration (k(cat)/K(m) × E(0)).
Topics: Biochemistry; History, 20th Century; Kinetics; Sucrose; Translations; beta-Fructofuranosidase
PubMed: 21888353
DOI: 10.1021/bi201284u -
Cell Metabolism Mar 2020There is a general consensus that overconsumption of sugar-sweetened beverages contributes to the prevalence of obesity and related comorbidities such as type 2 diabetes... (Clinical Trial)
Clinical Trial
There is a general consensus that overconsumption of sugar-sweetened beverages contributes to the prevalence of obesity and related comorbidities such as type 2 diabetes (T2D). Whether a similar relationship exists for no- or low-calorie "diet" drinks is a subject of intensive debate and controversy. Here, we demonstrate that consuming seven sucralose-sweetened beverages with, but not without, a carbohydrate over 10 days decreases insulin sensitivity in healthy human participants, an effect that correlates with reductions in midbrain, insular, and cingulate responses to sweet, but not sour, salty, or savory, taste as assessed with fMRI. Taste perception was unaltered and consuming the carbohydrate alone had no effect. These findings indicate that consumption of sucralose in the presence of a carbohydrate rapidly impairs glucose metabolism and results in longer-term decreases in brain, but not perceptual sensitivity to sweet taste, suggesting dysregulation of gut-brain control of glucose metabolism.
Topics: Adult; Area Under Curve; Brain; Feeding Behavior; Humans; Insulin Resistance; Middle Aged; Polysaccharides; Sucrose; Sugars; Taste; Time Factors; Young Adult
PubMed: 32130881
DOI: 10.1016/j.cmet.2020.01.014 -
The New Phytologist Apr 2022Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of...
Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3, the orthologue of the Arabidopsis F-box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3, D14 overexpression enhances D53 protein levels and sucrose-induced tillering, even in the presence of SL. Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients.
Topics: Arabidopsis; Gene Expression Regulation, Plant; Lactones; Oryza; Plant Proteins; Sucrose
PubMed: 34716593
DOI: 10.1111/nph.17834 -
International Journal of Molecular... Mar 2023Sucrose and its derivative hexoses are key metabolites of the plant metabolism, structural units of cell walls and stored reserves (e [...].
Sucrose and its derivative hexoses are key metabolites of the plant metabolism, structural units of cell walls and stored reserves (e [...].
Topics: Plants; Biological Transport; Sucrose; Hexoses; Cell Wall; Carbohydrate Metabolism
PubMed: 36982729
DOI: 10.3390/ijms24065655 -
Medicine Feb 2017Both oral sucrose (OS) and nonnutritive sucking (NNS) are effective nonpharmacological methods to alleviate procedures pain in neonatal intensive care unit (NICU)... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Both oral sucrose (OS) and nonnutritive sucking (NNS) are effective nonpharmacological methods to alleviate procedures pain in neonatal intensive care unit (NICU) newborns when they were used alone, but the combined effect of OS+NNS remains controversial. So, we conducted this study to evaluate the efficiency of NNS combined with oral sucrose on pain relief in NICU newborns undergoing painful procedures.
METHODS
We searched PubMed, Ovid (Medline), Embase (Medline), Cochrane Central Library, and other resources such as Google Scholar, bibliographies of included literatures for all available articles. Two reviewers screened literatures and extracted data independently. The fixed effects model was used to pool the results using Reviewer Manager (RevMan) 5.3. As each study included in our meta-analysis had been approved by Ethics Committee or institutional review board, thus our study did not need ethical approval.
RESULTS
Seven randomized controlled trials, including 599 participants, were contained in our meta-analysis. The combination of oral sucrose and NNS is associated with reduced pain scores (mean difference [MD], -0.52; 95% confidence interval [CI], -0.68 to -0.36); shortened crying time (MD,-0.92; 95% CI, -1.39 to -0.44); but the 2 groups did not differ significantly in reducing bradycardia (MD, 0.73; 95% CI, 0.32-1.68), tachycardia (MD, 0.65; 95% CI, 0.38-1.10), or desaturations (MD, 0.73; 95% CI, 0.32-1.68).
CONCLUSION
The pooled evidence indicates that the combination measures may serve as an evidence-based guideline for pain relief among patients having minor pain. Besides, it also indicates that OS combined with NNS can be an alternative for better prevention and management of procedure pain in NICU newborns. Nevertheless, the results may be limited due to incomplete data, and thus, more randomized controlled trials or well-designed studies are required to determine the effects of OS+NNS in the future.
Topics: Crying; Humans; Intensive Care Units, Neonatal; Pain Management; Sucking Behavior; Sucrose
PubMed: 28178172
DOI: 10.1097/MD.0000000000006108