Dietary Sugar and Anthropometrics among Young Children in the Guelph Family Health Study: Longitudinal Associations.

Purpose: Our understanding of the influence of sugar intake on anthropometrics among young children is limited. Most existing research is cross-sectional and has focused on sugar-sweetened beverages. The study objective was to investigate longitudinal associations between young children's total, free, and added sugar intake from all food sources at baseline with anthropometric measures at baseline and 18 months.Methods: The Guelph Family Health Study (GFHS) is an ongoing randomized controlled trial and a family-based health promotion study. Food records and anthropometric data were collected at baseline (n = 109, 55 males; 3.7 ± 1.1 y, mean ± SD) and 18 months (n = 109, 55 males; 5.1 ± 1.1 y) of the GFHS pilots. Associations between sugar intakes and anthropometrics were estimated using linear regression models with generalized estimating equations adjusted for age, sex, household income, and intervention status.Results: Total sugar intake was inversely associated with body weight at 18 months (P = 0.01). There was no effect of time on any other associations between total, free, and added sugar intakes and anthropometrics.Conclusions: Early life dietary sugar intakes may not relate to anthropometric measures in the short term. Further investigation into potential associations between dietary sugar intakes and anthropometric variables over longer time periods is warranted.

Intake of Sugar and Food Sources of Sugar and Colorectal Cancer Risk in the Multiethnic Cohort Study.

BACKGROUND: The influence of sugar intake on the risk of colorectal cancer (CRC) remains controversial, and there is a need to investigate the heterogeneity of effects among racial and ethnic groups. OBJECTIVES: To examine the association of intake of simple sugars and their food sources with CRC risk according to race/ethnicity in a multiethnic cohort study. METHODS: We analyzed data from 192,651 participants who participated in the Multiethnic Cohort Study comprising African American, Japanese American, Latino, Native Hawaiian, and White older adults living in Hawaii and California with an average follow-up of 19 y. Intakes of total and specific types of sugars and sugary foods were estimated from a quantitative food frequency questionnaire completed by the participants in 1993-1996. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CRC risk according to quintiles (Q) of sugar and food intakes using Cox models adjusted for potential confounders. RESULTS: As of December 2017, 4403 incident CRC cases were identified. Among all participants, multivariable-adjusted CRC HRs for Q2, Q3, Q4, and Q5 compared with Q1 for total sugars were 1.03 (95% CI: 0.94, 1.13), 1.05 (95% CI: 0.96, 1.16), 1.12 (95% CI: 1.01, 1.24), and 1.13 (95% CI: 1.01, 1.27), respectively. A similar positive association was observed for total fructose, glucose, fructose, and maltose but not for added sugars and sugary foods. The increased risk appeared to be limited to colon cancer and to be strongest among younger participants (i.e., 45-54 y at baseline); an association with CRC was observed for sugar-sweetened beverages in the latter group. Among racial and ethnic groups, increased risk of CRC was most apparent in Latinos. CONCLUSIONS: In this diverse cohort, intakes of total sugar, total fructose, glucose, fructose, and maltose were associated with an increased risk of CRC, and the association was strongest for colon cancer, younger participants, and Latinos.

Association between dietary sugar intake and depression in US adults: a cross-sectional study using data from the National Health and Nutrition Examination Survey 2011-2018.

BACKGROUND: Studies examining whether diet sugar intake increases the risk of depression have produced inconsistent results. Therefore, we investigated this relationship, using the US' National Health and Nutrition Examination Survey (NHANES) database. METHODS: This cross-sectional study included 18,439 adults (aged ≥ 20 years) from NHANES (2011-2018). Depressive symptoms were assessed using the nine-item version of the Patient Health Questionnaire (PHQ-9). Covariates, including age, sex, race/ethnicity, poverty-income ratio, education, marital status, hypertension, diabetes mellitus, cardiovascular disease, alcohol intake, smoking status, physical activity, and dietary energy intake, were adjusted in multivariate logistic regression models. Subgroup and threshold saturation effect analyses were performed. RESULTS: After adjusting for potential confounders, we found that a 100 g/day increase in dietary sugar intake correlated with a 28% higher prevalence of depression (odds ratio = 1.28, 95% confidence interval = 1.17-1.40, P < 0.001). CONCLUSION: Dietary sugar intake is positively associated with depression in US adults.

FTO genotypes (rs9939609 T>A) are Associated with Increased Added Sugar Intake in Healthy Young Adults.

INTRODUCTION: Single-nucleotide polymorphism (SNP) rs9939609 in the FTO gene has been associated with dietary intake and appetite traits, mainly in participants with obesity; however, it remains widely unexplored in normal weight participants. Thus, the aims of this study were (1) to compare the changes in subjective appetite sensations, ghrelin, and insulin concentrations according to the SNP rs9939609 T>A in FTO and (2) to compare dietary intake between rs9939609 genotype groups in normal weight young participants. METHODS: We conducted a quasi-experimental study involving 88 normal weight participants to analyze subjective perception of appetite, hormonal response for hunger and satiety, and dietary intake according to the rs9939609 SNP. Participants received a standardized single breakfast. Visual analogue scales (VAS) were utilized for assessing the subjective perception of appetite at fasting and immediately after breakfast and at 30, 60, 90, and 120 min postprandially. Glucose, lipid profile, ghrelin, and insulin were measured at fasting and at 120 min after breakfast. Dietary intake was assessed with a 3-day food record. The SNP was determined by allelic discrimination with TaqMan probes. To compare dietetic, biochemical, and the subjective appetite sensations, Student t test, ANCOVA test, and the repeated measures ANOVA were used. The linear regression model and the linear mixed model were used for the association analysis. Pearson correlation was used to test the correlation between two quantitative variables. RESULTS: A total of 88 people participated, 81.8% were female, with a mean body mass index of 21.8 ± 2.0 kg/m2 and a mean age of 20.6 ± 2.0. Genotype frequencies of the rs9939609 SNP were 52% for the TT allele and 48% for the TA/AA. The subjective perception of appetite named hunger, fullness, satiety, desire to eat, and prospective food consumption were similar between genotypes of the rs9939609. Participants with the TA/AA genotype showed a higher intake of added sugar (p = 0.039) than TT participants. No differences were found in ghrelin, insulin, glucose, or lipid parameters between genotypes. CONCLUSION: Carriers of the A allele from FTO gene SNP rs9939609 may have an increased preference for foods, specifically for added sugars.

Longitudinal Associations of Dietary Sugars and Glycaemic Index with Indices of Glucose Metabolism and Body Fatness during 3-Year Weight Loss Maintenance: A PREVIEW Sub-Study.

BACKGROUND: Dietary sugars are often linked to the development of overweight and type 2 diabetes (T2D) but inconsistencies remain. OBJECTIVE: We investigated associations of added, free, and total sugars, and glycaemic index (GI) with indices of glucose metabolism (IGM) and indices of body fatness (IBF) during a 3-year weight loss maintenance intervention. DESIGN: The PREVIEW (PREVention of diabetes through lifestyle Intervention and population studies in Europe and around the World) study was a randomised controlled trial designed to test the effects of four diet and physical activity interventions, after an 8-week weight-loss period, on the incidence of T2D. This secondary observational analysis included pooled data assessed at baseline (8), 26, 52, 104 and 156 weeks from 514 participants with overweight/obesity (age 25-70 year; BMI ≥ 25 kg⋅m-2) and with/without prediabetes in centres that provided data on added sugars (Sydney and Helsinki) or free sugars (Nottingham). Linear mixed models with repeated measures were applied for IBF (total body fat, BMI, waist circumference) and for IGM (fasting insulin, HbA1c, fasting glucose, C-peptide). Model A was adjusted for age and intervention centre and Model B additionally adjusted for energy, protein, fibre, and saturated fat. RESULTS: Total sugars were inversely associated with fasting insulin and C-peptide in all centres, and free sugars were inversely associated with fasting glucose and HbA1c (Model B: all p < 0.05). Positive associations were observed between GI and IGM (Model B: fasting insulin, HbA1c, and C-peptide: (all p < 0.01), but not for added sugars. Added sugar was positively associated with body fat percentage and BMI, and GI was associated with waist circumference (Model B: all p < 0.01), while free sugars showed no associations (Model B: p > 0.05). CONCLUSIONS: Our findings suggest that added sugars and GI were independently associated with 3-y weight regain, but only GI was associated with 3-y changes in glucose metabolism in individuals at high risk of T2D.

Dietary sugars silence the master regulator of carbohydrate utilization in human gut Bacteroides species.

The mammalian gut microbiota is a critical human health determinant with therapeutic potential for remediation of many diseases. The host diet is a key factor governing the gut microbiota composition by altering nutrient availability and supporting the expansion of distinct microbial populations. Diets rich in simple sugars modify the abundance of microbial subsets, enriching for microbiotas that elicit pathogenic outcomes. We previously demonstrated that diets rich in fructose and glucose can reduce the fitness and abundance of a human gut symbiont, Bacteroides thetaiotaomicron, by silencing the production of a critical intestinal colonization protein, called Roc, via its mRNA leader through an unknown mechanism. We have now determined that dietary sugars silence Roc by reducing the activity of BT4338, a master regulator of carbohydrate utilization. Here, we demonstrate that BT4338 is required for Roc synthesis, and that BT4338 activity is silenced by glucose or fructose. We show that the consequences of glucose and fructose on orthologous transcription factors are conserved across human intestinal Bacteroides species. This work identifies a molecular pathway by which a common dietary additive alters microbial gene expression in the gut that could be harnessed to modulate targeted microbial populations for future therapeutic interventions.

Sugar intake and colorectal cancer risk: A prospective Japanese cohort study.

The influence of sugar consumption on the risk of colorectal cancer (CRC) remains controversial. Prospective cohort studies focusing on total and specific types of sugar intake among the Asian population who have different patterns of sugar intake sources than American and European populations are scarce. We intended to examine the association of sugar intake with CRC risk among middle-aged adults in a Japanese large-scale population-based cohort study. The participants (42,405 men and 48,600 women) who were 45-74 years old and answered the questionnaire in 1995-1999 in the Japan Public Health Center-based Prospective Study were followed up until December 2013. Total sugars, total fructose, and specific types of sugar intake were estimated using a validated 147-item food frequency questionnaire and divided into quintiles (Q1-Q5). We used Cox proportional hazard regression models adjusted for potential confounders to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During the follow-up, 2118 CRC cases (1226 men and 892 women) were identified. We did not observe any clear association between all types of sugar intake and an increased risk of CRC. Analyses by tumor sites yielded a positive association of total sugar consumption with rectal cancer in women (1.75 [1.07-2.87] for Q1 vs. Q5; p linear trend  = 0.03), but no statistically significant trend was detected among men. Sugar intake was not associated with CRC risk in middle-aged Japanese adults. However, for rectal cancer, the probability of an increased risk among women with a higher total sugar intake cannot be excluded.

Fat and not sugar as the determining factor for gut microbiota changes, obesity, and related metabolic disorders in mice.

Diet-induced obesity contributes to the development of type 2 diabetes, insulin resistance, metabolic inflammation, oxidative and endoplasmic reticulum (ER) stress. Overall, obesity is associated with deviations in the composition and functionality of the gut microbiota. There are many divergent findings regarding the link between the excessive intake of certain dietary components (i.e., fat and sugar) and obesity development. We therefore investigated the effect of specific diets, with a different content of sugar and fat, in promoting obesity and related comorbidities as well as their impact on microbial load and gut microbiota composition/diversity. C57BL/6J mice were fed either a low-sugar, low-fat control diet (CT), a high-sugar diet (HS), a high-fat, high-sugar diet (HF/HS), or a high-fat diet (HF) for 8 wk. The impact of the different diets on obesity, glucose metabolism, inflammation, and oxidative and ER stress was determined. Diet-induced changes in the gut microbiota composition and density were also analyzed. HF diet-fed mice showed the highest body weight and fat mass gains and displayed the most impaired glucose and insulin profiles. HS, HF/HS, and HF diets differently affected hepatic cholesterol content and mRNA expression of several markers associated with immune cells, inflammation, oxidative and ER stress in several organs/tissues. In addition, HF diet feeding resulted in a decreased microbial load at the end of the experiment. When analyzing the gut microbiota composition, we found that HS, HF/HS, and HF diets induced specific changes in the abundance of certain bacterial taxa. This was not associated with a specific change in systemic inflammatory markers, but HS mice exhibited higher FGF21 plasma levels compared with HF diet-fed mice. Taken together, our results highlight that dietary intake of different macronutrients distinctively impacts the development of an obese/diabetic state and the regulation of metabolic inflammation in specific organs. We propose that these differences are not only obesity-driven but that changes in the gut microbiota composition may play a key role in this context.NEW & NOTEWORTHY To our knowledge, this study is the first to demonstrate that dietary macronutrients (i.e., sugar and fat) have an impact on fecal bacterial cell counting and quantitative microbiome profiling in mice. Yet, we demonstrate that dietary fat is the determining factor to promote obesity and diabetes progression, and local inflammation in different body sites. These observations can help to disentangle the conundrum of the detrimental effects of fat and sugar in our dietary habits.

Sugar Consumption Pattern among Cardiometabolic Risk Individuals: A Scoping Review.

BACKGROUND: The global prevalence of noncommunicable diseases has risen rapidly over the past decade. Research has focused on dietary management, particularly dietary sugar, to prevent and treat noncommunicable diseases. OBJECTIVE: This study undertakes a scoping review of research on the impacts of dietary sugar on cardiometabolic related health outcomes. METHODS: Ovid Medline, Scopus and Web of Science Core collection databases were used to identify papers published from January 1, 2010 onwards. The included studies had to be cross-sectional or cohort studies, peered review, published in English and in adults, aged 18 years old and above. Articles had to determine the impacts of sugar intake on cardiometabolic related health outcomes. Study quality was measured using the Quality Assessment Tool for Observational Cohort and Cross-sectional Studies. In addition, a narrative synthesis of extracted information was conducted. RESULTS: Thirty-one articles were included in this review. All studies had a large sample size, and the exposure measure was clearly defined, valid and applied consistently across all study participants. Exposure was measured using validated questionnaires. All data were statistically analysed and adjusted for critical potential confounding variables. Results showed that dietary sugar intake was significantly associated with metabolic syndrome, blood pressure, blood glucose, blood lipids, and body weight. CONCLUSION: Dietary sugar intake significantly increased cardiometabolic risks through mechanisms dependent and independent of weight gain. It is essential to create public awareness on the topics of cardiometabolic risk management and dietary sugars intake.

The Effect of Unrefined Sugar on Inflammation: A Systematic Review of Intervention Studies.

Background: It is well established that unrefined sugarcane products have antioxidant activity due to phytochemicals, polyphenols, and total antioxidant capacity, which may decrease inflammation and oxidative stress. Therefore, we conducted a systematic review to evaluate the association of unrefined sugar consumption with inflammatory biomarkers. Methods: Google Scholar, ScienceDirect, Scopus, Cochrane Library, and ProQuest databases were searched up to December 2021 for studies that report the effect of unrefined sugar on inflammation according to inflammatory cytokines, chemokine, and adhesion molecules as outcome measures. Results: Thirty-six studies were evaluated. Across all research, five studies (two in vitro and three animal studies) reported the effect of unrefined sugar on levels of cytokines, including IL-6, TNF-α, IL-10, IL-1ß, and IFN-γ. Additionally, the quality of the studies was assessed for risk of bias. Conclusions: it is possible to affirm that unrefined sugarcane products, including jaggery, may have a protective effect on inflammation via regulating some of the inflammatory pathways and a favorable impact on cytokines secretion according to the results of in vitro and animal model studies. However, since the findings are still insufficient, more scientific research, especially well-designed human trials, is highly recommended to conclude the outcomes confidently. Human data may encourage industries and the public to replace purified sugar with unrefined sugarcane in sugar-based food and for further health-care policy decisions.

Crossbred Sows Fed a Western Diet during Pre-Gestation, Gestation, Lactation, and Post-Lactation Periods Develop Signs of Lean Metabolic Syndrome That Are Partially Attenuated by Spirulina Supplementation.

Excessive dietary intake of fats and sugars ("Western diet", WD) is one of the leading causes of obesity. The consumption of the microalga Arthrospira platensis (spirulina, Sp) is increasing due to its presumed health benefits. Both WD and Sp are also consumed by pregnant and breastfeeding women. This study investigated if gestating and lactating domestic pigs are an appropriate model for WD-induced metabolic disturbances similar to those observed in humans and if Sp supplementation may attenuate any of these adverse effects. Pigs were fed a WD high in fat, sugars, and cholesterol or a control diet. Half of the animals per diet group were supplemented with 20 g Sp per day. The WD did not increase body weight or adipose tissue accumulation but led to metabolic impairments such as higher cholesterol concentration in plasma, lower IGF1 plasma levels, and signs of hepatic damage compared to the control group. Spirulina supplementation could not reduce all the metabolic impairments observed in WD-fed animals. These findings indicate limited suitability of gestating and lactating domestic pigs as a model for WD but a certain potential of low-dose Sp supplementation to partially attenuate negative WD effects.

"What Should I Eat?"-Addressing Questions and Challenges Related to Nutrition in the Integrative Oncology Setting.

PURPOSE OF REVIEW: This review aims to assess how nutrition can be addressed in the integrative oncology setting, taking into account cancer patients' unmet needs as they relate to nutrition in cancer care and the evidence-based information that is available on this topic. RECENT FINDINGS: During and after cancer treatment, nutrition is an important component of supportive care, for patients and their family members. Current scientific data consistently show that poor nutrition can reduce survival and decrease adherence to cancer treatments. Unfortunately, the limited availability of dietitians makes access to individualized nutrition counseling challenging, and many cancer patients still do not receive adequate nutritional support. As a result, one of the main unmet needs of patients and their families through the whole cancer trajectory is accessible and up-to-date evidence-based nutritional counseling that emphasizes basic healthy nutrition. The popularity of complementary and integrative medicine among patients with cancer makes the integrative oncology setting an excellent avenue for providing such support. A suggested simple approach that utilizes World Cancer Research Fund/American Institute for Cancer Research and American Cancer Society basic information is described. This approach can be easily incorporated into integrative oncology settings, while reserving the role for the registered dietician to address underweight patients, patients with malnutrition, and patients with more complicated dietary situations. The integrative oncology setting is in a unique place in oncology that can be utilized for enhancing dissemination of healthy nutrition information and addressing the unmet needs expressed by patients and families.

Neurosecretory Protein GL Accelerates Liver Steatosis in Mice Fed Medium-Fat/Medium-Fructose Diet.

Sugar consumption can readily lead to obesity and metabolic diseases such as liver steatosis. We previously demonstrated that a novel hypothalamic neuropeptide, neurosecretory protein GL (NPGL), promotes fat accumulation due to the ingestion of sugar by rats. However, differences in lipogenic efficiency of sugar types by NPGL remain unclear. The present study aimed to elucidate the obesogenic effects of NPGL on mice fed different sugars (i.e., sucrose or fructose). We overexpressed the NPGL-precursor gene (Npgl) in the hypothalamus of mice fed a medium-fat/medium-sucrose diet (MFSD) or a medium-fat/medium-fructose diet (MFFD). Food intake and body mass were measured for 28 days. Body composition and mRNA expression of lipid metabolic factors were measured at the endpoint. Npgl overexpression potently increased body mass with fat accumulation in the white adipose tissue of mice fed MFFD, although it did not markedly affect food intake. In contrast, we observed profound fat deposition in the livers of mice fed MFFD but not MFSD. In the liver, the mRNA expression of glucose and lipid metabolic factors was affected in mice fed MFFD. Hence, NPGL induced liver steatosis in mice fed a fructose-rich diet.

Simple sugar intake and cancer incidence, cancer mortality and all-cause mortality: A cohort study from the PREDIMED trial.

OBJECTIVE: To examine associations between intake of simple sugars and cancer incidence, cancer mortality, and total mortality in a prospective cohort study based on the PREDIMED trial conducted from 2003 to 2010. METHODS: Participants were older individuals at high cardiovascular risk. Exposures were total sugar, glucose and fructose from solid or liquid sources, and fructose from fruit and 100% fruit juice. Cancer incidence was the primary outcome; cancer mortality and all-cause mortality were secondary outcomes. Multivariable-adjusted, time-dependent Cox proportional hazard models were used. RESULTS: Of 7447 individuals enrolled, 7056 (94.7%) were included (57.6% women, aged 67.0 ± 6.2 years). 534 incident cancers with 152 cancer deaths and 409 all-cause deaths were recorded after a median follow-up of 6 years. Intake of simple sugars in solid form was unrelated to outcomes. Higher cancer incidence was found per 5 g/day increase in intake of liquid sugars, with multivariable-adjusted HR of 1.08 (95% CI, 1.03-1.13) for total liquid sugar, 1.19 (95% CI, 1.07-1.31) for liquid glucose, 1.14 (95% CI, 1.05-1.23) for liquid fructose, and 1.39 (95% CI, 1.10-1.74) for fructose from fruit juice. Cancer and all-cause mortality increased to a similar extent with intake of all sugars in liquid form. In categorical models, cancer risk was dose-related for all liquid sugars. CONCLUSIONS: Simple sugar intake in drinks and fruit juice was associated with an increased risk of overall cancer incidence and mortality and all-cause mortality. This suggests that sugary beverages are a modifiable risk factor for cancer and all-cause mortality.

Obesity and Dietary Added Sugar Interact to Affect Postprandial GLP-1 and Its Relationship to Striatal Responses to Food Cues and Feeding Behavior.

It has been hypothesized that the incretin hormone, glucagon-like peptide-1 (GLP-1), decreases overeating by influencing mesolimbic brain regions that process food-cues, including the dorsal striatum. We previously showed that habitual added sugar intake was associated with lower glucose-induced circulating GLP-1 and a greater striatal response to high calorie food cues in lean individuals. Less is known about how dietary added sugar and obesity may interact to affect postprandial GLP-1 and its relationship to striatal responses to food cues and feeding behavior. The current study aimed to expand upon previous research by assessing how circulating GLP-1 and striatal food cue reactivity are affected by acute glucose consumption in participants with varied BMIs and amounts of habitual consumption of added sugar. This analysis included 72 participants from the Brain Response to Sugar Study who completed two study visits where they consumed either plain water or 75g glucose dissolved in water (order randomized; both drinks were flavored with non-caloric cherry flavoring) and underwent repeated blood sampling, a functional magnetic resonance imaging (fMRI) based food-cue task, and an ad-libitum buffet meal. Correlations between circulating GLP-1 levels, striatal food-cue reactivity, and food intake were assessed, and interactions between obesity and added sugar on GLP-1 and striatal responses were examined. An interaction between BMI and dietary added sugar was associated with reduced post-glucose GLP-1 secretion. Participants who were obese and consumed high levels of added sugar had the smallest increase in plasma GLP-1 levels. Glucose-induced GLP-1 secretion was correlated with lower dorsal striatal reactivity to high-calorie versus low-calorie food-cues, driven by an increase in reactivity to low calorie food-cues. The increase in dorsal striatal reactivity to low calorie food-cues was negatively correlated with sugar consumed at the buffet. These findings suggest that an interaction between obesity and dietary added sugar intake is associated with additive reductions in postprandial GLP-1 secretion. Additionally, the results suggest that changes to dorsal striatal food cue reactivity through a combination of dietary added sugar and obesity may affect food consumption.

Degradation of the low-calorie sugar substitute 5-ketofructose by different bacteria.

There is an increasing public awareness about the danger of dietary sugars with respect to their caloric contribution to the diet and the rise of overweight throughout the world. Therefore, low-calorie sugar substitutes are of high interest to replace sugar in foods and beverages. A promising alternative to natural sugars and artificial sweeteners is the fructose derivative 5-keto-D-fructose (5-KF), which is produced by several Gluconobacter species. A prerequisite before 5-KF can be used as a sweetener is to test whether the compound is degradable by microorganisms and whether it is metabolized by the human microbiota. We identified different environmental bacteria (Tatumella morbirosei, Gluconobacter japonicus LMG 26773, Gluconobacter japonicus LMG 1281, and Clostridium pasteurianum) that were able to grow with 5-KF as a substrate. Furthermore, Gluconobacter oxydans 621H could use 5-KF as a carbon and energy source in the stationary growth phase. The enzymes involved in the utilization of 5-KF were heterologously overproduced in Escherichia coli, purified and characterized. The enzymes were referred to as 5-KF reductases and belong to three unrelated enzymatic classes with highly different amino acid sequences, activities, and structural properties. Furthermore, we could show that 15 members of the most common and abundant intestinal bacteria cannot degrade 5-KF, indicating that this sugar derivative is not a suitable growth substrate for prokaryotes in the human intestine. KEY POINTS: • Some environmental bacteria are able to use 5-KF as an energy and carbon source. • Four 5-KF reductases were identified, belonging to three different protein families. • Many gut bacteria cannot degrade 5-KF.

The role of sugar-rich diet and salivary proteins in dental plaque formation and oral health.

BACKGROUND: Dental plaque is a complex colorless film of bacteria that develops on the surfaces of teeth. Different mechanisms of microbial adhesion to tooth surfaces exist. Both non-specific and specific types of adherence have been anticipated. HIGHLIGHT: The present review evaluated the effect of sugar-rich diet and salivary proteins on oral hygiene and dental plaque development. CONCLUSION: The oral microbiota is essential for maintaining and reestablishing a healthy oral cavity. Different types of sugars have different effects on the inhibition and formation of dental plaque. The peptides, proteins, and amino acids secreted by parotid glands in the oral cavity facilitate neutralizing the acidity in dental plaque and preventing dental caries. A properly balanced diet is crucial for both a healthy oral cavity and the oral microbiome.

World trends in sugar-sweetened beverage and dietary sugar intakes in children and adolescents: a systematic review.

OBJECTIVE: To provide a systematic overview of world dietary sugar and sugar-sweetened beverage (SSB) intake trends in children and adolescents. DATA SOURCES: Medline, Embase, and the Cochrane Central Register of Controlled Trials in the Cochrane Library were searched through January 2019 to identify longitudinal follow-up studies with time-trend data and repeated cross-sectional studies. DATA EXTRACTION: Data from studies reporting ≥ 2 measurements (sugars, SSB, or sweets/candy) over ≥ 2 years and included ≥ 20 healthy, normal- or overweight children or adolescents aged 1-19 years. DATA ANALYSIS: Data from 43 articles (n = 4 prospective cohort studies; n = 39 repeated cross-sectional studies) from 15 countries (n = 8 European countries plus Australia, Canada, China, South Korea, Mexico, Russia, and the United States) are presented narratively. According to the risk of bias in nonrandomized studies of interventions tool, 34 studies were judged to have a moderate risk of bias, and 5 to have a serious risk of bias. CONCLUSIONS: Consumption among US children and adolescents increased substantially in the decades preceding 2000, followed by a faster and continued decline. As a whole, other international intake trends did not reveal drastic increases and decreases in SSB and dietary sugars; they tended to change only slightly across 3 decades.

Ribosylation induced structural changes in Bovine Serum Albumin: understanding high dietary sugar induced protein aggregation and amyloid formation.

Non-enzymatic glycation of proteins is believed to be the root cause of high dietary sugar associated pathophysiological maladies. We investigated the structural changes in protein during progression of glycation using ribosylated Bovine Serum Albumin (BSA). Non enzymatic attachment of about 45 ribose molecules to BSA resulted in gradual reduction of hydrophobicity and aggregation as indicated by red-shifted tryptophan fluorescence, reduced ANS binding and lower anisotropy of FITC-conjugated protein. Parallely, there was a significant decrease of alpha helicity as revealed by Circular Dichroism (CD) and Fourier transformed-Infra Red (FT-IR) spectra. The glycated proteins assumed compact globular structures with enhanced Thioflavin-T binding resembling amyloids. The gross structural transition affected by ribosylation led to enhanced thermostability as indicated by melting temperature and Transmission Electron Microscopy. At a later stage of glycation, the glycated proteins developed non-specific aggregates with increase in size and loss of amyloidogenic behaviour. A parallel non-glycated control incubated under similar conditions indicated that amyloid formation and associated changes were specific for ribosylation and not driven by thermal denaturation due to incubation at 37 °C. Functionality of the glycated protein was significantly altered as probed by Isothermal Titration Calorimetry using polyphenols as substrates. The studies demonstrated that glycation driven globular amyloids form and persist as transient intermediates during formation of misfolded glycated adducts. To the best of our knowledge, the present study is the first systematic attempt to understand glycation associated changes in a protein and provides important insights towards designing therapeutics for arresting dietary sugar induced amyloid formation.