Association of consumption of sugar-sweetened beverages with elevated blood pressure among college students in Yunnan Province, China.

OBJECTIVE: Although some studies have examined the association between eating behaviour and elevated blood pressure (EBP) in adolescents, current data on the association between sugar-sweetened beverages (SSB) and EBP in adolescents in Yunnan Province, China, are lacking. SETTING: Cluster sampling was used to survey freshmen at a college in Kunming, Yunnan Province, from November to December. Data on SSB consumption were collected using an FFQ measuring height, weight and blood pressure. A logistic regression model was used to analyse the association between SSB consumption and EBP, encompassing prehypertension and hypertension with sex-specific analyses. PARTICIPANTS: The analysis included 4781 college students. RESULTS: Elevated systolic blood pressure (SBP) and diastolic blood pressure (DBP) were detected in 35·10 % (1678/4781) and 39·34 % (1881/4781) of patients, respectively. After adjusting for confounding variables, tea beverage consumption was associated with elevated SBP (OR = 1·24, 95 % CI: 1·03, 1·49, P = 0·024), and carbonated beverage (OR = 1·23, 95 % CI: 1·04, 1·45, P = 0·019) and milk beverage (OR = 0·81, 95 % CI: 0·69, 0·95, P = 0·010) consumption was associated with elevated DBP in college students. Moreover, fruit beverage (OR = 1·32, 95 % CI: 1·00, 1·75, P = 0·048) and milk beverage consumption (OR = 0·69, 95 % CI: 0·52, 0·93, P = 0·014) was associated with elevated DBP in males. CONCLUSION: Our findings indicated that fruit and milk beverage consumption was associated with elevated DBP in males, and no association was observed with EBP in females.

Determining the metabolic effects of dietary fat, sugars and fat-sugar interaction using nutritional geometry in a dietary challenge study with male mice.

The metabolic effects of sugars and fat lie at the heart of the "carbohydrate vs fat" debate on the global obesity epidemic. Here, we use nutritional geometry to systematically investigate the interaction between dietary fat and the major monosaccharides, fructose and glucose, and their impact on body composition and metabolic health. Male mice (n = 245) are maintained on one of 18 isocaloric diets for 18-19 weeks and their metabolic status is assessed through in vivo procedures and by in vitro assays involving harvested tissue samples. We find that in the setting of low and medium dietary fat content, a 50:50 mixture of fructose and glucose (similar to high-fructose corn syrup) is more obesogenic and metabolically adverse than when either monosaccharide is consumed alone. With increasing dietary fat content, the effects of dietary sugar composition on metabolic status become less pronounced. Moreover, higher fat intake is more harmful for glucose tolerance and insulin sensitivity irrespective of the sugar mix consumed. The type of fat consumed (soy oil vs lard) does not modify these outcomes. Our work shows that both dietary fat and sugars can lead to adverse metabolic outcomes, depending on the dietary context. This study shows how the principles of the two seemingly conflicting models of obesity (the "energy balance model" and the "carbohydrate insulin model") can be valid, and it will help in progressing towards a unified model of obesity. The main limitations of this study include the use of male mice of a single strain, and not testing the metabolic effects of fructose intake via sugary drinks, which are strongly linked to human obesity.

High Fructose Corn Syrup Accelerates Kidney Disease and Mortality in Obese Mice with Metabolic Syndrome.

The presence of obesity and metabolic syndrome is strongly linked with chronic kidney disease (CKD), but the mechanisms responsible for the association are poorly understood. Here, we tested the hypothesis that mice with obesity and metabolic syndrome might have increased susceptibility to CKD from liquid high fructose corn syrup (HFCS) by favoring the absorption and utilization of fructose. We evaluated the pound mouse model of metabolic syndrome to determine if it showed baseline differences in fructose transport and metabolism and whether it was more susceptible to chronic kidney disease when administered HFCS. Pound mice have increased expression of fructose transporter (Glut5) and fructokinase (the limiting enzyme driving fructose metabolism) associated with enhanced fructose absorption. Pound mice receiving HFCS rapidly develop CKD with increased mortality rates associated with intrarenal mitochondria loss and oxidative stress. In pound mice lacking fructokinase, the effect of HFCS to cause CKD and early mortality was aborted, associated with reductions in oxidative stress and fewer mitochondria loss. Obesity and metabolic syndrome show increased susceptibility to fructose-containing sugars and increased risk for CKD and mortality. Lowering added sugar intake may be beneficial in reducing the risk for CKD in subjects with metabolic syndrome.

Trajectories of child free sugars intake and dental caries - a population-based birth cohort study.

OBJECTIVES: To investigate the association between trajectories of free sugars intake during the first five years of life and dental caries experience at five years. METHODS: Data from the SMILE population-based prospective birth cohort study, collected at one, two and five years old, were used. A 3-days dietary diary and food frequency questionnaire were used to estimate free sugars intake (FSI) in grams. The primary outcomes were dental caries prevalence and experience (dmfs). The Group-Based Trajectory Modelling method was used to characterize three FSI trajectories ('Low and increasing'; 'Moderate and increasing'; and 'High and increasing'), which were the main exposures. Multivariable regression models were generated to compute adjusted prevalence ratios (APR) and rate ratios (ARR) for the exposure, controlling for socioeconomic factors. RESULTS: The prevalence of caries was 23.3%, with a mean dmfs of 1.4, and a median of 3.0 among those who had caries. There were clear gradients of caries prevalence and experience by the FSI trajectories. The 'High and increasing' had an APR of 2.13 (95%CI 1.23-3.70) and ARR of 2.77 (95%CI 1.45-5.32) against the 'Low and increasing'. The 'Moderate and increasing' group had intermediate estimates. A quarter of the caries cases could have been prevented if the whole study sample had been in the 'Low and increasing' FSI trajectory. CONCLUSION: A sustained, high trajectory of FSI from a young age was positively associated with child dental caries. Measures to minimise consumption of free sugars must commence early in life. CLINICAL SIGNIFICANCE: The study has provided high level evidence to inform clinicians' decisions in promoting a healthy dietary pattern for young children.

High-fat, high-sucrose, and combined high-fat/high-sucrose diets effects in oxidative stress and inflammation in male rats under presence or absence of obesity.

The study examines the influence of three types of hypercaloric diets on metabolic parameters, inflammatory markers, and oxidative stress in experimental model. Male Wistar rats (n = 40) were randomized in control (C), high-sucrose (HS), high-fat (HF), and high-fat with sucrose (HFHS) for 20 weeks. Nutritional, metabolic, hormonal, and biochemical profiles, as well as histological analysis of adipose and hepatic tissues were performed. Inflammation and oxidative stress were determined. HF model caused obesity and comorbidities as glucose intolerance and arterial hypertension. In relation to hormonal and biochemical parameters, there was no significant difference between the groups. All groups showed increased deposition of fat droplets in the hepatic tissue, even though adipocyte areas were similar. Biomarkers of oxidative stress in serum and adipose tissues were similar among the groups. HF model was effective in triggering associated obesity and comorbidities in male rats, but all hypercaloric diets were unable to promote oxidative stress and inflammation.

Consumption of Added Sugars by States and Factors Associated with Added Sugars Intake among US Adults in 50 States and the District of Columbia-2010 and 2015.

Purpose: The high intake of added sugars from foods or beverages increases the risk of obesity, hypertension, dyslipidemia, and cardiovascular disease. Because state-level data are lacking, we estimated dietary intake of added sugars by state and factors associated with intake among US adults. Design: Nationally representative, cross-sectional, in-person, household survey. Setting: 50 states and DC. Sample: 52,279 US adults from pooled data from 2010 and 2015 National Health Interview Surveys. Measures: Estimated total added sugars intake (tsp/day) using the National Cancer Institute's scoring algorithm that converts responses from the Dietary Survey Questionnaire screener to estimated total added sugars intake (tsp/day). Analysis: Mean dietary-added sugars intake estimates and standard error were calculated for adults' characteristics and by state for all 50 states and the District of Columbia. Differences by adult's characteristics were assessed by pairwise t-tests (p < 0.05). All analyses accounted for complex survey design and sampling weights. Results: Overall, US adults consumed 17.0 tsp of added sugars/day (range: 14.8 tsp/day in Alaska to 1.2 tsp/day in Kentucky). Added sugars intake varied by states and sociodemographic characteristics. Conclusion: Findings may inform efforts to reduce added sugars intake to lower the high burden of chronic disease.

High-fat/high-sucrose diet worsens metabolic outcomes and widespread hypersensitivity following early-life stress exposure in female mice.

Exposure to stress early in life has been associated with adult-onset comorbidities such as chronic pain, metabolic dysregulation, obesity, and inactivity. We have established an early-life stress model using neonatal maternal separation (NMS) in mice, which displays evidence of increased body weight and adiposity, widespread mechanical allodynia, and hypothalamic-pituitary-adrenal axis dysregulation in male mice. Early-life stress and consumption of a Western-style diet contribute to the development of obesity; however, relatively few preclinical studies have been performed in female rodents, which are known to be protected against diet-induced obesity and metabolic dysfunction. In this study, we gave naïve and NMS female mice access to a high-fat/high-sucrose (HFS) diet beginning at 4 wk of age. Robust increases in body weight and fat were observed in HFS-fed NMS mice during the first 10 wk on the diet, driven partly by increased food intake. Female NMS mice on an HFS diet showed widespread mechanical hypersensitivity compared with either naïve mice on an HFS diet or NMS mice on a control diet. HFS diet-fed NMS mice also had impaired glucose tolerance and fasting hyperinsulinemia. Strikingly, female NMS mice on an HFS diet showed evidence of hepatic steatosis with increased triglyceride levels and altered glucocorticoid receptor levels and phosphorylation state. They also exhibited increased energy expenditure as observed via indirect calorimetry and expression of proinflammatory markers in perigonadal adipose. Altogether, our data suggest that early-life stress exposure increased the susceptibility of female mice to develop diet-induced metabolic dysfunction and pain-like behaviors.

Sugar-sweetened beverages and periodontal disease: A systematic review.

This systematic review aims to determine the association between the consumption of sugar-sweetened beverages (SSBs) and periodontal disease. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed to conduct a literature search on five electronic databases till January 2022. Systemically healthy individuals consuming SSBs and presenting periodontal disease (gingivitis/periodontitis) were included. The modified Newcastle-Ottawa Scale and the Grading of Recommendation Assessment Development and Evaluation criteria were respectively used to assess the risk of bias and the evidence's quality. Of the 1303 eligible records identified in the initial search, ten studies (nine cross-sectional and one case-control) were selected for the final review. Among the included articles, five reported SSBs intake in the form of carbonated soft drinks, two as sugary drinks, two as soft drinks, and one as coffee with added sugar. Four studies reported gingivitis as an outcome, while the remaining six studies reported periodontitis using validated indices. The included studies were of medium to high quality. Consumption of SSBs may increase gingival bleeding, thereby gingivitis and the risk of periodontitis. Intake of added sugars like SSBs should be considered as a potential factor during gingival/periodontal risk assessment. Further studies are warranted to establish additional evidence of association.

Chronic intake of high dietary sucrose induces sexually dimorphic metabolic adaptations in mouse liver and adipose tissue.

Almost all effective treatments for non-alcoholic fatty liver disease (NAFLD) involve reduction of adiposity, which suggests the metabolic axis between liver and adipose tissue is essential to NAFLD development. Since excessive dietary sugar intake may be an initiating factor for NAFLD, we have characterized the metabolic effects of liquid sucrose intake at concentrations relevant to typical human consumption in mice. We report that sucrose intake induces sexually dimorphic effects in liver, adipose tissue, and the microbiome; differences concordant with steatosis severity. We show that when steatosis is decoupled from impairments in insulin responsiveness, sex is a moderating factor that influences sucrose-driven lipid storage and the contribution of de novo fatty acid synthesis to the overall hepatic triglyceride pool. Our findings provide physiologic insight into how sex influences the regulation of adipose-liver crosstalk and highlight the importance of extrahepatic metabolism in the pathogenesis of diet-induced steatosis and NAFLD.

Effects of the Long-Term Consumption of a High-Sucrose Diet on microRNA Expression in Visceral Adipose Tissue of Rats.

Noncoding microRNAs are involved in lipid and carbohydrate metabolism pathways and are powerful regulators of gene expression. The goals of this study were to evaluate the temporal expression profiles of miRNAs in rat adipose tissue and predict mRNA−microRNA interactions. Newly weaned Wistar rats were divided into groups fed a standard diet and high-sucrose diet (HSD). The HSD contains 66.86% carbohydrates (40.45% standard diet, 40.45% condensed milk, and 8.58% crystal sugar), and the HSD was provided for 4, 8 and 15-week periods to investigate the expression levels of miRNAs in visceral adipose tissue using RT−qPCR. Target selection, enriched pathways and networks were analyzed in silico. The factor consumption time significantly was associated to decreases (p < 0.05) in the expression levels of the following miRNAs: 124-5p, 125-5p, 126-5p, 200c-3p, and 212-3p in all experimental groups. The factor diet significantly influenced rno-miR-124-5p, 200c-3p, and 212-3p expression (p < 0.05). A significant reduction (p < 0.05) in rno-miR-27a-3p expression was observed. The biological processes involved key pathways regulating fat deposition. Our findings provide important insights into downregulated miRNA expression patterns in visceral adipose tissue, adiposity level, hyperinsulinemia and increased VLDL-c and triglyceride levels.

Current WHO recommendation to reduce free sugar intake from all sources to below 10% of daily energy intake for supporting overall health is not well supported by available evidence.

Sugar is widely consumed over the world. Although the mainstream view is that high added or free sugar consumption leads to obesity and related metabolic diseases, controversies exist. This narrative review aims to highlight important findings and identify major limitations and gaps in the current body of evidence in relation to the effect of high sugar intakes on health. Previous animal studies have shown that high sucrose or fructose consumption causes insulin resistance in the liver and skeletal muscle and consequent hyperglycemia, mainly because of fructose-induced de novo hepatic lipogenesis. However, evidence from human observational studies and clinical trials has been inconsistent, where most if not all studies linking high sugar intake to obesity focused on sugar-sweetened beverages (SSBs), and studies focusing on sugars from solid foods yielded null findings. In our opinion, the substantial limitations in the current body of evidence, such as short study durations, use of supraphysiological doses of sugar or fructose alone in animal studies, and a lack of direct comparisons of the effects of solid compared with liquid sugars on health outcomes, as well as the lack of appropriate controls, seriously curtail the translatability of the findings to real-world situations. It is quite possible that "high" sugar consumption at normal dietary doses (e.g., 25% daily energy intake) per se-that is, the unique effect of sugar, especially in the solid form-may indeed not pose a health risk for individuals apart from the potential to reduce the overall dietary nutrient density, although newer evidence suggests "low" sugar intake (<5% daily energy intake) is just as likely to be associated with nutrient dilution. We argue the current public health recommendations to encourage the reduction of both solid and liquid forms of free sugar intake (e.g., sugar reformulation programs) should be revised due to the overextrapolation of results from SSBs studies.

The role of dietary sugars, overweight, and obesity in type 2 diabetes mellitus: a narrative review.

Nowadays, there is still a popular belief that dietary sugars, in particular sucrose, are directly linked to the development of type 2 diabetes mellitus (T2DM). Furthermore, since insulin action is impaired in T2DM, it is still believed that excluding dietary sugars from the diet can adequately treat T2DM. This might be based on the assumption that dietary sugars have a stronger impact on blood glucose levels than other carbohydrates. Therefore, the aim of this review is to discuss the effects of dietary sugars intake, including sugar-sweetened beverages (SSBs) against the background of overall energy intake and weight gain in the development of T2DM. Furthermore, the effect of dietary sugars, including SSBs on glycemic control will be discussed. Results from various systematic reviews and meta-analyses do not support the idea that the intake of sucrose and other dietary sugars is linked to T2DM. Long-chain or complex carbohydrates can have a greater impact on postprandial glycemic response than sucrose. SSBs do not affect glycemic control if substituted for other calorie sources. Current scientific evidence clearly points toward excess energy intake followed by excess body fat gain being most relevant in the development of T2DM.

Loss of Sucrase-Isomaltase Function Increases Acetate Levels and Improves Metabolic Health in Greenlandic Cohorts.

BACKGROUND & AIMS: The sucrase-isomaltase (SI) c.273_274delAG loss-of-function variant is common in Arctic populations and causes congenital sucrase-isomaltase deficiency, which is an inability to break down and absorb sucrose and isomaltose. Children with this condition experience gastrointestinal symptoms when dietary sucrose is introduced. We aimed to describe the health of adults with sucrase-isomaltase deficiency. METHODS: The association between c.273_274delAG and phenotypes related to metabolic health was assessed in 2 cohorts of Greenlandic adults (n = 4922 and n = 1629). A sucrase-isomaltase knockout (Sis-KO) mouse model was used to further elucidate the findings. RESULTS: Homozygous carriers of the variant had a markedly healthier metabolic profile than the remaining population, including lower body mass index (ß [standard error], -2.0 [0.5] kg/m2; P = 3.1 × 10-5), body weight (-4.8 [1.4] kg; P = 5.1 × 10-4), fat percentage (-3.3% [1.0%]; P = 3.7 × 10-4), fasting triglyceride (-0.27 [0.07] mmol/L; P = 2.3 × 10-6), and remnant cholesterol (-0.11 [0.03] mmol/L; P = 4.2 × 10-5). Further analyses suggested that this was likely mediated partly by higher circulating levels of acetate observed in homozygous carriers (ß [standard error], 0.056 [0.002] mmol/L; P = 2.1 × 10-26), and partly by reduced sucrose uptake, but not lower caloric intake. These findings were verified in Sis-KO mice, which, compared with wild-type mice, were leaner on a sucrose-containing diet, despite similar caloric intake, had significantly higher plasma acetate levels in response to a sucrose gavage, and had lower plasma glucose level in response to a sucrose-tolerance test. CONCLUSIONS: These results suggest that sucrase-isomaltase constitutes a promising drug target for improvement of metabolic health, and that the health benefits are mediated by reduced dietary sucrose uptake and possibly also by higher levels of circulating acetate.

Como dosar as quantidades corretas de óleos, gorduras, sal e açúcar?

O uso de ingredientes culinários processados como óleos, gorduras, sal e açúcar são comumente utilizados ao temperar e cozinhar alimentos e criar preparações culinárias. Em uma alimentação adequada e saudável, esperamos que esses produtos sejam utilizados com moderação para não trazer prejuízos à saúde.

Assessment of the Effects of Dietary Vitamin D Levels on Olanzapine-Induced Metabolic Side Effects: Focus on the Endocannabinoidome-Gut Microbiome Axis.

Vitamin D deficiency is associated with poor mental health and dysmetabolism. Several metabolic abnormalities are associated with psychotic diseases, which can be compounded by atypical antipsychotics that induce weight gain and insulin resistance. These side-effects may be affected by vitamin D levels. The gut microbiota and endocannabinoidome (eCBome) are significant regulators of both metabolism and mental health, but their role in the development of atypical antipsychotic drug metabolic side-effects and their interaction with vitamin D status is unknown. We studied the effects of different combinations of vitamin D levels and atypical antipsychotic drug (olanzapine) exposure on whole-body metabolism and the eCBome-gut microbiota axis in female C57BL/6J mice under a high fat/high sucrose (HFHS) diet in an attempt to identify a link between the latter and the different metabolic outputs induced by the treatments. Olanzapine exerted a protective effect against diet-induced obesity and insulin resistance, largely independent of dietary vitamin D status. These changes were concomitant with olanzapine-mediated decreases in Trpv1 expression and increases in the levels of its agonists, including various N-acylethanolamines and 2-monoacylglycerols, which are consistent with the observed improvement in adiposity and metabolic status. Furthermore, while global gut bacteria community architecture was not altered by olanzapine, we identified changes in the relative abundances of various commensal bacterial families. Taken together, changes of eCBome and gut microbiota families under our experimental conditions might contribute to olanzapine and vitamin D-mediated inhibition of weight gain in mice on a HFHS diet.

High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats.

BACKGROUND/AIMS: Oxidative stress is associated with cardiometabolic alterations, and the involvement of excess glucose and fatty acids has been demonstrated in this process. Thus, the aim of this study was to investigate the effects of different hypercaloric diets on cardiac oxidative stress. METHODS: Wistar rats were randomized into four groups: control (C), high-sucrose (HS), high-fat (HF), and high-fat with sucrose (HFS). Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Cardiac oxidative stress was analyzed by malondialdehyde (MDA) and carbonylated proteins, and the cardiac protein expression levels of type 1 angiotensin receptor (AT-1), nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2), superoxide dismutase (SOD 1 e 2), glutathione peroxidase (GPX), and catalase (CAT) were determined by western blot. RESULTS: The HF group showed an increase in adiposity; however, it did not present adipocyte hypertrophy and comorbidities. Cardiac MDA and carbonylated protein levels were higher in the HF and HFS compared with the C group. The levels of oxidant and antioxidant proteins showed no difference between the groups. CONCLUSION: HF and HFS dietary interventions promoted cardiac oxidative stress, in the presence and absence of obesity, respectively. However, this process was neither mediated by the pro-oxidants AT1 and Nox2, nor by the quantitative reduction of antioxidant enzymes.

Distinct mechanisms involving diacylglycerol, ceramides, and inflammation underlie insulin resistance in oxidative and glycolytic muscles from high fat-fed rats.

This study investigated whether oxidative and glycolytic rat skeletal muscles respond differently to a high-fat (HF) sucrose-enriched diet with respect to diacylglycerol (DAG) and ceramides accumulation, protein kinase C (PKC) activation, glucose metabolism, and the expression of inflammatory genes. HF diet (8 weeks) suppressed insulin-stimulated glycogen synthesis and glucose oxidation in soleus (Sol), extensor digitorum longus (EDL) and epitrochlearis (Epit) muscles. However, DAG and ceramides levels increased in Sol and EDL, but not in Epit muscles of HF-fed rats. Additionally, membrane-bound PKC-delta and PKC-theta increased in Sol and EDL, whereas in Epit muscles both PKC isoforms were reduced by HF diet. In Epit muscles, HF diet also increased the expression of tumor necrosis factor-α (TNF-α) receptors (CD40 and FAS), toll-like receptor 4 (TLR4), and nuclear factor kappa light polypeptide gene enhancer in B cells (NF-kB), whereas in Sol and EDL muscles the expression of these inflammatory genes remained unchanged upon HF feeding. In conclusion, HF diet caused DAG and ceramides accumulation, PKC activation, and the induction of inflammatory pathways in a fiber type-specific manner. These findings help explain why oxidative and glycolytic muscles similarly develop insulin resistance, despite major differences in their metabolic characteristics and responsiveness to dietary lipid abundance.

Obesity, not a high fat, high sucrose diet alone, induced glucose intolerance and cardiac dysfunction during pregnancy and postpartum.

Cardiovascular disease is the leading cause of death in women during pregnancy and the postpartum period. Obesity is an independent risk factor for cardiovascular diseases. Nearly 60% of women of reproductive age are considered overweight or obese, cardiovascular disease morbidity and mortality continue to be pervasive. The objective of this study was to determine the effects of an obesogenic diet on the cardiometabolic health of dams during pregnancy and postpartum. Female mice were fed either a high-fat, high-sucrose diet (HFHS) or a refined control diet (CON) for 8 weeks before initiation of pregnancy and throughout the study period. Mice in the HFHS showed two distinct phenotypes, obesity-prone (HFHS/OP) and obesity resistance (HFHS/OR). Pre-pregnancy obesity (HFHS/OP) induced glucose intolerance before pregnancy and during postpartum. Systolic function indicated by the percent fractional shortening (%FS) was significantly decreased in the HFHS/OP at late pregnancy (vs. HFHS/OR) and weaning (vs. CON), but no differences were found at 6 weeks of postpartum among groups. No induction of pathological cardiac hypertrophy markers was found during postpartum. Plasma adiponectin was decreased while total cholesterol was increased in the HFHS/OP. Our results suggested that obesity, not the diet alone, negatively affected cardiac adaptation during pregnancy and postpartum.