Associations between Intake of Dietary Sugars and Diet Quality: A Systematic Review of Recent Literature.

Understanding the relationship between the intake of sugars and diet quality can inform public health recommendations. This systematic review synthesized recent literature on associations between sugar intake and diet quality in generally healthy populations aged 2 years or older. We searched databases from 2010 to 2022 for studies of any design examining associations between quantified sugar intake in the daily diet and dietary indexes (DIs) or micronutrient intakes. Different sugar types and diet quality measures were analyzed separately. We converted DI results to Pearson's r correlations and grouped indexes with or without a free or added sugar component to facilitate cross-study comparisons. Meta-analysis was deemed inappropriate. From 13,869 screened records, we included 27 cross-sectional studies. NUQUEST risk of bias ratings were neutral (n = 18 studies) or poor (n = 9), and strength of evidence by the GRADE approach was very low due to study design. Most studies reported negative associations for added and free sugars with diet quality indexes (r ranging from -0.13 to -0.42) and nutrients of public health concern (fiber, vitamin D, calcium, potassium), while associations with total sugars were mixed. Due to cross-sectional study designs, the clinical relevance of these findings is unclear. Prospective studies are needed to minimize confounding and inform causal relationships.

Free sugar intake is associated with reduced proportion of circulating invariant natural killer T cells among women experiencing overweight and obesity.

Background: Higher prevalence of obesity has been observed among women compared to men, which can be explained partly by the higher consumption of sweets and physical inactivity. Obesity can alter immune cell infiltration, and therefore increase the susceptibility to develop chronic inflammation and metabolic disorders. In this study, we aimed to explore the association between free sugar intake and other unhealthy lifestyle habits in relation to the proportion of circulating iNKT cells among women with healthy weight and women experiencing overweight and obesity. Methods: A cross-sectional study was conducted on 51 Saudi women > 18 years, wherein their daily free sugar intake was assessed using the validated Food Frequency Questionnaire. Data on smoking status, physical activity, and supplement use were also collected. Anthropometric data including height, weight, waist circumference were objectively measured from each participants. The proportion of circulating iNKT cells was determined using flow cytometry. Results: Smoking, physical activity, supplement use, and weight status were not associated with proportion of circulating iNKT cells. Significant association was found between proportion of circulating iNKT cells and total free sugar intake and free sugar intake coming from solid food sources only among women experiencing overweight and obesity (Beta: -0.10: Standard Error: 0.04 [95% Confidence Interval: -0.18 to -0.01], p= 0.034) and (Beta: -0.15: Standard Error: 0.05 [95% Confidence Interval: -0.25 to -0.05], p= 0.005), respectively. Conclusion: Excessive free sugar consumption may alter iNKT cells and consequently increase the risk for chronic inflammation and metabolic disorders.

High sugar diet alters immune function and the gut microbiome in juvenile green iguanas (Iguana iguana).

The present work aimed to study whether a high sugar diet can alter immune responses and the gut microbiome in green iguanas. Thirty-six iguanas were split into four treatment groups using a 2×2 design. Iguanas received either a sugar-supplemented diet or a control diet, and either a lipopolysaccharide (LPS) injection or a phosphate-buffered saline (PBS) injection. Iguanas were given their respective diet treatment through the entire study (∼3 months) and received a primary immune challenge 1 and 2 months into the experiment. Blood samples and cloacal swabs were taken at various points in the experiment and used to measure changes in the immune system (bacterial killing ability, lysis and agglutination scores, LPS-specific IgY concentrations), and alterations in the gut microbiome. We found that a sugar diet reduces bacterial killing ability following an LPS challenge, and sugar and the immune challenge temporarily alters gut microbiome composition while reducing alpha diversity. Although sugar did not directly reduce lysis and agglutination following the immune challenge, the change in these scores over a 24-h period following an immune challenge was more drastic (it decreased) relative to the control diet group. Moreover, sugar increased constitutive agglutination outside of the immune challenges (i.e. pre-challenge levels). In this study, we provide evidence that a high sugar diet affects the immune system of green iguanas (in a disruptive manner) and alters the gut microbiome.

Association of added sugar intake and its forms and sources with handgrip strength decline among middle-aged and older adults: A prospective cohort study.

PURPOSE: The consumption of added sugar has increased rapidly in recent years. Limited knowledge exists regarding the association between added sugar intake and muscle strength, although the latter is a predictor of physical disability in older adults. This study aimed to investigate the association between added sugar intake and longitudinal changes in handgrip strength among middle-aged and elderly Chinese adults. METHODS: This prospective cohort study included 5298 adults aged 40 years and older (62.6% men) from the TCLSIH (Tianjin Chronic Low-grade Systemic Inflammation and Health) cohort study. Added sugar intake was obtained through a frequency questionnaire containing 100 items of food. Handgrip strength is measured annually using a handheld digital dynamometer. Multivariate linear regression models were used to examine the association between added sugars intake and the annual changes in handgrip strength and weight-adjusted handgrip strength. RESULTS: In the fully adjusted model, the annual change in handgrip strength for one unit increase in total added sugar, solid added sugar, and liquid added sugar intake was -0.0353 kg, (95% confidence intervals (CI) -0.000148, -0.0000164; P = 0.01), -0.0348 kg (95% CI: -0.000227, -0.0000269; P = 0.01) and -0.0189 kg (95% CI -0.000187, 0.0000338; P = 0.17), respectively. Added sugar from bread and biscuits sources were remarkably associated with a decline in handgrip strength (ß = -0.0498; 95%CI -0.00281, -0.000787) and (ß = -0.0459; 95%CI 0.00158, 0.00733) (P < 0.01). CONCLUSIONS: Our data suggest that the higher the intake of solid added sugars, but not liquid sugars, were associated with the declined handgrip strength in the Chinese middle-aged and elderly population. In addition, the consumption of added sugars from bread and biscuits sources was also associated with a decline in grip strength.

Sugar types, genetic predictors of the gut microbiome, and the risk of chronic kidney disease: a prospective cohort study.

Background: Emerging studies suggest that focusing on the intake of specific types or sources of sugars may yield greater benefits in preventing chronic kidney disease (CKD). Objective: We aimed to investigate the associations between free and non-free sugar intakes and CKD risk as well as the potential sugar type-gut microbiome interactions. Methods: A total of 138 064 participants from the UK Biobank were included in this prospective study. The free and non-free sugar intakes were assessed using repeated web-based 24-hour dietary recalls. A cause-specific competing risk model was used to estimate hazard ratios (HRs) and the corresponding confidence intervals (CIs) of incident CKD, treating deaths before incident CKD as competing events. Results: During a median follow-up of 10.5 years, 2,923 participants (2.1%) developed CKD. The free sugar intake was positively associated with the risk of CKD (HRquartile 4 vs. quartile 1 = 1.32, 95% CI = 1.18, 1.47), with a nonlinear relationship (P for nonlinearity = 0.01, the risk increased rapidly after free sugars made up 10% of the total energy). The non-free sugar intake was inversely associated with CKD risk (HRquartile 4 vs. quartile 1 = 0.68, 95% CI = 0.60, 0.77), with an L-shaped nonlinear curve (p for nonlinearity = 0.01, the turning point was at 13.5% of the total energy). We found that the associations between free sugar and non-free sugar intakes and CKD risk were more pronounced in participants with high genetically predicted gut microbial abundance. Furthermore, a significant interaction was observed between the genetically predicted gut microbial abundance and non-free sugar intake (P for interaction = 0.04). Conclusion: A higher intake of free sugars was associated with an elevated risk of CKD, whereas a higher intake of non-free sugars was associated with a reduced risk of CKD. The impact of free sugar intake and non-free sugar intake may be modified by the gut microbial abundance.

Use of table sugar and non-caloric sweeteners in Brazil: associated factors and changes across a decade.

This study evaluated changes in the use of sweeteners over one decade and the relationship between socio-demographics, diet and weight status with the type of sweetener. Data came from the Brazilian National Dietary Surveys of 2008-2009 and 2017-2018, including ≥ 10-year-old individuals (n 32 749; n 44 744, respectively, after excluding pregnant and lactating women). The use of table sugar, non-caloric sweeteners (NCS), both or none was reported through a specific question. Food consumption was assessed using two non-consecutive food records (2008-2009) and 24-h recalls (2017-2018). For the last survey, means of energy, macro and micronutrient intake, food groups' contribution (%) to daily energy intake and age- and energy-adjusted nutrient intake were estimated according to the type of sweetener used. Differences in means and proportions across the categories of sweeteners used were evaluated based on the 95 % CI. All analyses were stratified by sex and considered sample design and weights. Over 10 years, the use of table sugar decreased by 8 %, while the habit of not using any sweetener increased almost three times, and the use of NCS remained stable. Larger reductions in the use of table sugar were observed in the highest income level and among men. Regardless of sex, compared with NCS users, table sugar users had greater mean intake of energy, carbohydrates and added sugar and lower micronutrient intake means. Although table sugar is still the most used sweetener, the increased choice of 'no sweetener' is noteworthy in Brazil.

Is the Consumption of Added Sugar from Common Beverages Associated with the Presence of Attention Deficit Hyperactivity Disorder Symptoms in Thai Medical Students?

Attention deficit hyperactivity disorder (ADHD) significantly affects the well-being of medical students in various aspects. Sugar-sweetened beverages (SSBs) pose a potential risk of ADHD. Our study aimed to determine the prevalence of ADHD symptoms and the association between consumption of added sugar in common beverages and ADHD symptoms in Thai medical students. An online cross-sectional survey was conducted among medical students at Chiang Mai University from May 2022 to April 2023. The consumption of added sugar from common beverages in Thailand was assessed using the Thai Adolescence Sugar Sweetened Beverage Intake (THASSI) questionnaire. An Adult ADHD Self-Report Scale (ASRS) score ≥ 3 identified the presence of ADHD symptoms. Multivariable logistic regression was used for the analysis. Of 441 participants, 29.9% had ADHD symptoms. Daily consumption of added sugar from beverages higher than 25 g/day showed an increased risk of ADHD symptoms (adjusted odds ratio (OR) 1.80, 95%CI 1.15 to 2.84, p = 0.011). The same trend was observed when using the sex-specific cutoff points (adjusted OR 1.73, 95%CI 1.10 to 2.73, p = 0.018). Higher consumption of added sugar from beverages may increase the risk of ADHD symptoms in Thai medical students. This finding supports the implementation of health policies that promote healthy consumption behaviors among medical students.

Associations between Total and Added Sugar Intake and Diabetes among Chinese Adults: The Role of Body Mass Index.

Sugar intake has been linked to the global rise in diabetes. However, the unique diabetogenic effect of sugar, independent of weight gain, remains controversial. This study aimed to investigate the associations between total and added sugar intake and diabetes status, and to test whether the sugar-diabetes associations were moderated or mediated by the body mass index (BMI). We performed a nationwide cross-sectional study on 12,889 Chinese adults who were enrolled in the China Health and Nutrition Survey (CHNS) 2011. The data for the total and added sugar intake were measured using three consecutive 24 h recalls, and determined based on the U.S. Department of Agriculture (USDA) National Nutrient Database for Standard Reference, Release 28 (SR28), the Food Patterns Equivalents Database (FPED) 2015-2016, and the labeled ingredients and nutrient contents. A multivariable logistic regression model was used to analyze the associations between the total and added sugar intake and diabetes. A nutrient density model was used to adjust for the total energy intake. A mediation analysis for significant sugar-diabetes associations shown in multivariable logistic analysis (p < 0.05), and a subgroup analysis according to the BMI category were performed, to examine the mediating and moderating effects of the BMI on the sugar-diabetes association, respectively. We included 12,800 individuals, with a mean age of 50.5, in the final analysis. The means of the total and added sugar intake, total sugar (%E), and added sugar (%E) were 28.2 ± 0.2 g/d, 5.0 ± 0.1 g/d, 6.0 ± 0.0%, and 1.0 ± 0.0%, respectively. The overall prevalence of self-reported physician-diagnosed diabetes was 4.0%. A significant association between the total sugar intake and an increased risk of diabetes was found (odds ratio [OR] =1.008, 95% CI 1.001-1.016). The mediation analysis showed a significant mediation effect through the BMI of the effect of the total sugar on diabetes status (p < 0.001), where 11.7% (95% CI: 4.7-35.7%) of the effect of the total sugar on diabetes was mediated through the BMI. The total sugar intake had a significant direct effect on diabetes around the BMI (estimated coefficient = 0.0004, p < 0.001). The overall total-sugar-intake-diabetes association remained significant in normal-weight participants in the subgroup analysis (OR =1.012, 1.000-1.024). In conclusion, although the BMI moderated and mediated the association between the total sugar intake and diabetes, the total sugar still showed some unique weight-independent diabetogenic effects. Our findings call for efforts to prevent and control diabetes by reducing sugar intake, and losing weight appropriately.

Nutrient pattern analysis of mineral based, simple sugar based, and fat based diets and risk of metabolic syndrome: a comparative nutrient panel.

BACKGROUND: Although there is growing evidence on the association between nutrient patterns and metabolic risk factors, very little is known about the relationship between nutrient patterns and metabolic syndrome (MetS). The aim of this study was to examine the associations of nutrient patterns with MetS among apparently healthy obese adults living in Tabriz, Iran. METHODS: Three hundred and forty-seven apparently healthy obese (BMI ≥ 30 kg/m2) adults aged 20-50 years were included in this cross-sectional study. Dietary intake of 38 nutrients was assessed by a validated semi-quantitative food frequency questionnaire (FFQ) of 132 food items. Nutrient patterns were determined using factor analysis. The MetS was defined based on the guidelines of the National Cholesterol Education Program Adult Treatment Panel III (ATP III). RESULTS: Three major nutrient patterns were extracted: "Mineral based pattern", "Simple sugar based pattern" and "Fat based pattern". There was no significant association between nutrient patterns and MetS, in the crude model even after adjusting for confounders. There was a significant difference between quartiles in the mineral based pattern for free mass (FFM), diastolic blood pressure (DBP), large Waist circumference (WC) and Waist-to-hip ratio (WHR). In the simple sugar based pattern, we observed a significant association for SBP, DBP, and triglyceride (TG) levels. In addition, the fat based pattern was positively associated with BMI, and weight. CONCLUSIONS: We did not observe any significant association of nutrient patterns with the risk of MetS amongst the apparently healthy obese adult's population. Whereas we confirmed the deleterious effect of the simple sugar and fat based patterns on several metabolic risk factors, our findings also showed that the mineral based pattern is related to healthier metabolic factors in an Iranian population. These results should be approved by future studies to recognize any causal relationship between adherence to specific nutrient patterns and MetS.

Dietary curcumin restores insulin homeostasis in diet-induced obese aged mice.

Although aging is a physiological process to which all organisms are subject, the presence of obesity and type 2 diabetes accelerates biological aging. Recent studies have demonstrated the causal relationships between dietary interventions suppressing obesity and type 2 diabetes and delaying the onset of age-related endocrine changes. Curcumin, a natural antioxidant, has putative therapeutic properties such as improving insulin sensitivity in obese mice. However, how curcumin contributes to maintaining insulin homeostasis in aged organisms largely remains unclear. Thus, the objective of this study is to examine the pleiotropic effect of dietary curcumin on insulin homeostasis in a diet-induced obese (DIO) aged mouse model. Aged (18-20 months old) male mice given a high-fat high-sugar diet supplemented with 0.4% (w/w) curcumin (equivalent to 2 g/day for a 60 kg adult) displayed a different metabolic phenotype compared to mice given a high-fat high-sugar diet alone. Furthermore, curcumin supplementation altered hepatic gene expression profiling, especially insulin signaling and senescence pathways. We then mechanistically investigated how curcumin functions to fine-tune insulin sensitivity. We found that curcumin supplementation increased hepatic insulin-degrading enzyme (IDE) expression levels and preserved islet integrity, both outcomes that are beneficial to preserving good health with age. Our findings suggest that the multifaceted therapeutic potential of curcumin can be used as a protective agent for age-induced metabolic diseases.

Influence of a Nutrigenetic Intervention on Self-Efficacy, Emotions, and Rewarding Behaviors in Unhealthy Eating among Mexicans: An Exploratory Pilot Study.

The Genome-based Mexican (GENOMEX) diet is a strategy for preventing and managing obesity. Emotion and eating behavior in the context of a nutrigenetic intervention have not been thoroughly studied. We aimed to explore the influence of the GENOMEX diet on emotions, self-efficacy, and rewarding behaviors in unhealthy eating among subjects with risk factors for obesity-related chronic diseases. Twenty-eight subjects included in the six-month GENOMEX intervention answered questions regarding emotions that influence food consumption. Additionally, the Patient Health Questionnaire (PHQ-9) and the Reward-based eating drive scale (RED) were applied. In the study, minimal, mild, moderate, and severe depression were present in 46.4%, 39.3%, 10.7%, and 3.6%, respectively. RED did not change, but it correlated with a higher intake of fats (r2 = 0.684, ß = 2.066, p = 0.003). Mood influenced unhealthy eating in 71.7% of subjects, and 76.9% experienced binge episodes triggered by anxiety. Sugars were the most consumed foods during binge episodes (42.2%). Both low self-efficacy levels and binge episodes were associated with high consumption of unhealthy foods. After the intervention, 10.7% of subjects reported a high level of self-efficacy. In conclusion, a culturally acceptable and genetically compatible regional Mexican food diet reduced negative emotions and unhealthy eating while increasing self-efficacy.

High fructose diet-induced obesity worsens post-ischemic brain injury in the hippocampus of female rats.

Objectives: Cerebral ischemia is caused by a reduction of the blood flow in a specific area in the brain, triggering cellular cascades in the tissue that result in neuronal death. This phenomenon leads to neurological decline in patients with stroke. The extent of the injury after stroke could be related to the condition of obesity. Thus, we aim to analyze the effect of obesity induced by a high fructose diet (HFD) on the brain after cerebral ischemia in rats.Methods: We induced the obesity model in female Wistar rats with 20% fructose in water for 11 weeks. We then performed cerebral ischemia surgery (2-vessel occlusion), carried out the neurological test 6, 24 and 48 h post-ischemia and analyzed the histological markers.Results: The HFD induced an obese phenotype without insulin resistance. The obese rats exhibited worse neurological performance at 6 h post-ischemia and showed neuronal loss and astroglial and microglial immunoreactivity changes in the caudate putamen, motor cortex, amygdala and hippocampus at 48 h post-ischemia. However, the most commonly affected area was the hippocampus, where we found an increase in interleukin 1ß in the blood vessels of the dentate gyrus, a remarkable disruption of MAP-2+ dendrites, a loss of brain-derived neurotrophic factor and the presence of PHF-tau. In conclusion, a HFD induces an obese phenotype and worsens the neuronal loss, inflammation and plasticity impairment in the hippocampus after cerebral ischemia.

Ten-week high fat and high sugar diets in mice alter gut-brain axis cytokines in a sex-dependent manner.

Diets high in fat and sugar induce inflammation throughout the body, particularly along the gut-brain axis; however, the way these changes in immune signaling mediate one another remains unknown. We investigated cytokine changes in the brain and colon following prolonged high fat or sugar diet in female and male adult C57BL/6 mice. Ten weeks of high fat diet increased levels of TNFα, IL-1ß, IL-6, IFNγ, and IL-10 in the female hippocampus and altered cytokines in the frontal cortex of both sexes. High sugar diet increased hippocampal cytokines and decreased cytokines in the diencephalon and frontal cortex. In the colon, high fat diet changed cytokine expression in both sexes, while high sugar diet only increased TNFα in males. Causal mediation analysis confirmed that colon IL-10 and IL-6 mediate high fat diet-induced neuroimmune changes in the female hippocampus and male frontal cortex. Additionally, high fat diet increased food consumption and weight gain in both sexes, while high sugar diet decreased male weight gain. These findings reveal a novel causal link between gut and brain inflammation specific to prolonged consumption of high fat, not high sugar, diet. Importantly, this work includes females which have been under-represented in diet research, and demonstrates that diet-induced neuroinflammation varies by brain region between sexes. Furthermore, our data suggest female brains are more vulnerable than males to inflammatory changes following excessive fat and sugar consumption, which may help explain the increased risk of inflammation-associated psychiatric conditions in women who eat a Western Diet rich in both dietary components.

Dietary sugar restriction reduces hepatic de novo lipogenesis in adolescent boys with fatty liver disease.

BACKGROUNDHepatic de novo lipogenesis (DNL) is elevated in nonalcoholic fatty liver disease (NAFLD). Improvements in hepatic fat by dietary sugar reduction may be mediated by reduced DNL, but data are limited, especially in children. We examined the effects of 8 weeks of dietary sugar restriction on hepatic DNL in adolescents with NAFLD and correlations between DNL and other metabolic outcomes.METHODSAdolescent boys with NAFLD (n = 29) participated in an 8-week, randomized controlled trial comparing a diet low in free sugars versus their usual diet. Hepatic DNL was measured as percentage contribution to plasma triglyceride palmitate using a 7-day metabolic labeling protocol with heavy water. Hepatic fat was measured by magnetic resonance imaging-proton density fat fraction.RESULTSHepatic DNL was significantly decreased in the treatment group (from 34.6% to 24.1%) versus the control group (33.9% to 34.6%) (adjusted week 8 mean difference: -10.6% [95% CI: -19.1%, -2.0%]), which was paralleled by greater decreases in hepatic fat (25.5% to 17.9% vs. 19.5% to 18.8%) and fasting insulin (44.3 to 34.7 vs. 35.5 to 37.0 µIU/mL). Percentage change in DNL during the intervention correlated significantly with changes in free-sugar intake (r = 0.48, P = 0.011), insulin (r = 0.40, P = 0.047), and alanine aminotransferase (ALT) (r = 0.39, P = 0.049), but not hepatic fat (r = 0.13, P = 0.532).CONCLUSIONOur results suggest that dietary sugar restriction reduces hepatic DNL and fasting insulin, in addition to reductions in hepatic fat and ALT, among adolescents with NAFLD. These results are consistent with the hypothesis that hepatic DNL is a critical metabolic abnormality linking dietary sugar and NAFLD.TRIAL REGISTRYClinicalTrials.gov NCT02513121.FUNDINGThe Nutrition Science Initiative (made possible by gifts from the Laura and John Arnold Foundation, Ambrose Monell Foundation, and individual donors), the UCSD Altman Clinical and Translational Research Institute, the NIH, Children's Healthcare of Atlanta and Emory University's Children's Clinical and Translational Discovery Core, Children's Healthcare of Atlanta and Emory University Pediatric Biostatistical Core, the Georgia Clinical and Translational Science Alliance, and the NIH National Institute of Diabetes, Digestive, and Kidney Disease.

Acute Metabolic Responses to Glucose and Fructose Supplementation in Healthy Individuals: A Double-Blind Randomized Crossover Placebo-Controlled Trial.

The aim of this study was to investigate the impact of glucose (Glu), fructose (Fru), glucose and fructose (GluFru) and sucralose on blood glucose response in healthy individuals. Fifteen healthy individuals (five females, age of 25.4 ± 2.5 years, BMI of 23.7 ± 1.7 kg/m2 with a body mass (BM) of 76.3 ± 12.3 kg) participated in this double-blind randomized crossover placebo-controlled trial. Participants received a mixture of 300 mL of water with 1 g/kg BM of Glu, 1 g/kg BM of Fru, 0.5 g/kg BM of GluFru (each), and 0.2 g sucralose as a placebo. Peak BG values Glu were reached after 40 ± 13 min (peak BG: 141 ± 20 mg/dL), for Fru after 36 ± 22 min (peak BG: 98 ± 7 mg/dL), for GluFru after 29 ± 8 min (BG 128 ± 18 mg/dL), and sucralose after 34 ± 27 min (peak BG: 83 ± 5 mg/dL). Significant differences regarding the time until peak BG were found only between Glu and GluFru supplementation (p = 0.02). Peak blood glucose levels were significantly lower following the ingestion of Fru compared to the supplementation of Glu and GluFru (p < 0.0001) while Glu and GluFru supplementation showed no difference in peak values (p = 0.23). All conditions led to a significantly higher peak BG value compared to sucralose (p < 0.0001). Blood lactate increased in Glu (p = 0.002), Fru and GluFru (both p < 0.0001), whereas sucralose did not increase compared to the baseline (p = 0.051). Insulin levels were significantly higher in all conditions at peak compared to sucralose (p < 0.0001). The findings of this study prove the feasibility of combined carbohydrate supplementations for many applications in diabetic or healthy exercise cohorts.

Kombuchas from green and black teas reduce oxidative stress, liver steatosis and inflammation, and improve glucose metabolism in Wistar rats fed a high-fat high-fructose diet.

The aim of this study was to evaluate the effect of green and black tea kombuchas consumption on adiposity, lipid and glucose metabolism, liver steatosis, oxidative stress, and inflammation in Wistar rats fed a high-fat high-fructose (HFHF) diet. Wistar rats, after 8 weeks to induce metabolic alterations, were divided into an AIN-93M control group, HFHF control group, green tea kombucha + HFHF diet (GTK group), and black tea kombucha + HFHF diet (BTK group), for 10 weeks. The kombuchas improved glucose metabolism, plasma total antioxidant capacity, superoxide dismutase activity, and decreased nitric oxide concentration. Moreover, both kombuchas reduced systemic inflammation by decreasing the neutrophil/lymphocyte ratio (NLR), reduced the total adipose tissue and blood triglyceride, and reverted liver steatosis (from grade 2 to 1), besides the modulation of genes related to adipogenesis and ß-oxidation. Therefore, kombuchas from green and black teas have bioactive properties that can help control metabolic alterations induced by the HFHF diet.

Maternal high fructose diet exacerbates white adipose tissue thermogenic process in offspring upon exposure to cold temperature.

AIM: An adverse endogenous environment during early life predisposes to metabolic disorder development. We previously reported adverse metabolic and adipose tissue effects in adult male rats born to dams fed with a fructose-rich diet (FRD). The aim of this work was to determine the effect of a FRD consumed by the pregnant mother on the white adipose tissue (WAT) browning capacity of male offspring at adulthood. MAIN METHODS: Adult SD male offspring from control (C) and FRD-fed mothers were exposed during one week to a cold stimulus. WAT browning capacity was studied through in vivo and in vitro approaches. KEY FINDINGS: After cold exposure, WAT browning was higher in fructose-programmed animals as evidenced by an increase in ucp-1 gene expression, protein levels, and higher UCP-1 positive foci. Moreover, pgc1-α gene expression was increased. In vitro studies showed a lower adipogenic capacity in cells of prenatally fructose-exposed animals differentiated with a white differentiation cocktail, while a higher ucp-1 expression was noted when their cells were treated with a pro-beige differentiation cocktail. SIGNIFICANCE: For the first time we demonstrate that pre-natal fructose exposure predisposes programmed male rats to a higher WAT browning-induced response, under stimulated conditions, despite an apparent lower basal thermogenic capacity. These results should be considered in future studies to generate new therapeutic approaches to deal with adverse programming malnutrition effects.

Post-oral sensing of fat increases food intake and attenuates body weight defense.

In mammals, changes in weight elicit responses that favor a return to one's previous weight and promote weight stability. It has been hypothesized that palatable sweet and high-fat foods disturb the defense of body weight, leading to weight gain. We find that increasing sweetness or percent calories from fat increases diet palatability but that only increases in nutritive fat content increase caloric intake and body weight. In a mouse model of overfeeding that activates weight defense, high-fat diets, but not sweetened diets, attenuate the defense of body weight, leading to weight gain. The ability of a palatable, high-fat diet to increase food intake does not require tasting or smelling the food. Instead, the direct infusion of a high-fat diet into the stomach increases the ad libitum intake of less palatable, low-fat food. Post-oral sensing of percent calories from fat modulates feeding behavior to alter weight stability.

Isorhamnetin attenuates high-fat and high-fructose diet induced cognitive impairments and neuroinflammation by mediating MAPK and NFκB signaling pathways.

Isorhamnetin (ISO), a flavonoid compound isolated from sea-buckthorn (Hippophae rhamnoides L.) fruit, has anti-inflammatory effects. However, the effects of ISO on neuroinflammation and cognitive function are still unclear. The purpose of this study was to evaluate the protective effect of ISO on cognitive impairment in obese mice induced by a high-fat and high fructose diet (HFFD). It has been found that oral administration of ISO (0.03% w/w and 0.06% w/w) for 14 weeks significantly reduced the body weight, food intake, liver weight, liver lipid level, and serum lipid level of HFFD-fed mice. ISO can also significantly prevent HFFD-induced neuronal working, spatial, and long-term memory impairment. Notably, the ISO treatment activated the CREB/BDNF pathway and increased neurotrophic factors in the brains of mice. Furthermore, ISO inhibited HFFD-induced microglial overactivation and down-regulated inflammatory cytokines in both serum and the brain. It can also inhibit the expression of p-JNK, p-p38, and p-NFκB protein in the mouse brain. In conclusion, these results indicated that ISO mitigated HFFD-induced cognitive impairments by inhibiting the MAPK and NFκB signaling pathways, suggesting that ISO might be a plausible nutritional intervention for metabolic syndrome-related cognitive complications.