Dietary Fructose Intake Research Articles

Dietary fructose and risk of metabolic syndrome in Chinese residents aged 45 and above: results from the China National Nutrition and Health Survey

BackgroundA growing number of researches supported that dietary fructose was associated with most of the key features of metabolic syndrome (MetS). However, there was no related epidemiological studies among Chinese population, despite the sharp increase in MetS cases. This study explores the relationship between dietary fructose and MetS among Chinese residents aged 45 and above.MethodsA total of 25,528 participants (11,574 males and 13,954 females) were included in this nationwide representative cross-sectional study of China National Nutrition and Health Survey. Dietary fructose intake was assessed by 3-day 24-h dietary records. MetS was defined by the International Diabetes Federation and Chinese Diabetes Society criteria.ResultsThe consumption of dietary fructose was 11.6 g/day for urban residents and 7.6 g/day for rural residents. Fruits and vegetables as well as their products were the main sources of fructose intake. There was no association between dietary fructose intake and the odds of having MetS in both urban (P = 0.315) and rural residents (P = 0.230) after adjustment for confounding factors. Moreover, for urban residents participating physical activities, the odds of having MetS in the fourth quartiles (OR: 0.67; 95%CI: 0.52-0.87) was lower than that in the first quartile. In the sensitivity analysis, a significant reduction in the odds of having MetS was also found in the fourth quartiles (OR, 95%CI: 0.68, 0.51-0.90; 0.67, 0.49-0.91; 0.74, 0.56-0.99) compared with the first quartile when excluding smokers, alcohol users, and underweight/obesity, respectively. And there was no association between dietary fructose intake and the odds of having MetS after multivariate adjustment stratified by gender, smoking and alcohol use.ConclusionsUnder the current dietary fructose intake status, there was no association between dietary fructose intake and the odds of having MetS among Chinese residents aged 45 and above. Physical activity and relatively low fructose intake may have a beneficial synergistic effect on MetS.

Dietary fructose intake is correlated with fat distribution in the Newfoundland population

Objective: Increased dietary fructose intake is associated with elevated body weight and body mass index. Few studies are available regarding the relationship between fat distribution and dietary fructose intake. The aim of this study was to investigate the association between dietary fructose intake and fat distribution in adults in a large Newfoundland cohort.Methods: We analyzed 2298 adults from CODING (Complex Diseases in the New found land Population: Environment and Genetics) study. Intake of dietary fructose was evaluated from the Willett food frequency questionnaire. Fat distribution was estimated by dual-energy x-ray absorptiometry. Partial correlation analysis was used to determine the correlations of dietary fructose intake with fat distribution adjusted for major confounding factors.Results: Daily dietary fructose intake was negatively associated with arm fat in postmenopausal women (r = –0.080, P < 0.05), but positively associated with arm fat in premenopausal women after adjusting for age, total calorie intake, and physical activity levels (r = 0.079, P < 0.05). Dietary fructose intake was negatively correlated with both arm fat (r = –0.131, P < 0.05) and visceral fat (r = –0.124 measured in mass, r = –0.124 measured in volume respectively; P < 0.05) in men <45 y of age, not in men ≥45 y.Conclusion: This study demonstrated that dietary fructose intake is significantly correlated with arm fat in both women and men, and visceral fat in men in the Newfoundland free-living population. The correlations are sex- and menopause-status dependent.

Transferrin Isoforms, Old but New Biomarkers in Hereditary Fructose Intolerance.

Hereditary Fructose Intolerance (HFI) is an autosomal recessive inborn error of metabolism characterised by the deficiency of the hepatic enzyme aldolase B. Its treatment consists in adopting a fructose-, sucrose-, and sorbitol (FSS)-restrictive diet for life. Untreated HFI patients present an abnormal transferrin (Tf) glycosylation pattern due to the inhibition of mannose-6-phosphate isomerase by fructose-1-phosphate. Hence, elevated serum carbohydrate-deficient Tf (CDT) may allow the prompt detection of HFI. The CDT values improve when an FSS-restrictive diet is followed; however, previous data on CDT and fructose intake correlation are inconsistent. Therefore, we examined the complete serum sialoTf profile and correlated it with FSS dietary intake and with hepatic parameters in a cohort of paediatric and adult fructosemic patients. To do so, the profiles of serum sialoTf from genetically diagnosed HFI patients on an FSS-restricted diet (n = 37) and their age-, sex- and body mass index-paired controls (n = 32) were analysed by capillary zone electrophoresis. We found that in HFI patients, asialoTf correlated with dietary intake of sucrose (R = 0.575, p < 0.001) and FSS (R = 0.475, p = 0.008), and that pentasialoTf+hexasialoTf negatively correlated with dietary intake of fructose (R = −0.386, p = 0.024) and FSS (R = −0.400, p = 0.019). In addition, the tetrasialoTf/disialoTf ratio truthfully differentiated treated HFI patients from healthy controls, with an area under the ROC curve (AUROC) of 0.97, 92% sensitivity, 94% specificity and 93% accuracy.

Dietary fructose promotes liver carcinogenesis by inducing the malignant transformation of hepatic progenitor cells

Abstract The incidence of nonalcoholic fatty liver disease (NAFLD)-associated liver cancer is rising particularly in western societies. Dietary fructose has been increasingly reported as a significant contributor for the onset of NAFLD. However, the association between a high-fructose diet and liver cancer incidence is not fully understood. In this study, we investigated the effect of dietary fructose on liver tumorigenesis. In a mouse model of diethylnitrosamine (DEN)-induced liver tumor initiation, high-fructose diet was found to significantly increased hepatic lipid deposition and expression of inflammatory cytokines in mouse livers. Besides, DEN administration induced the malignant transformation of hepatic progenitor cells (HPCs) into malignant tumor initiating cells, while DEN + Fructose mice had significantly enriched HPCs with enhanced proliferation, invasion, chemoresistance, and tumorigenic capabilities. This study for the first time demonstrates that fructose promotes liver carcinogenesis via increasing tumorigenic HPCs and inflammatory microenvironment, which warrants precautionary control of the excessive intake of dietary fructose.

Effects of fructose restriction on liver steatosis (FRUITLESS); a double-blind randomized controlled trial

ABSTRACTBackgroundThere is an ongoing debate on whether fructose plays a role in the development of nonalcoholic fatty liver disease.ObjectivesThe aim of this study was to investigate the effects of fructose restriction on intrahepatic lipid (IHL) content in a double-blind randomized controlled trial using an isocaloric comparator.MethodsBetween March 2017 and October 2019, 44 adult overweight individuals with a fatty liver index ≥ 60 consumed a 6-wk fructose-restricted diet (<7.5 g/meal and <10 g/d) and were randomly assigned to supplementation with sachets of glucose (= intervention group) or fructose (= control group) 3 times daily. Participants and assessors were blinded to the allocation. IHL content, assessed by proton magnetic resonance spectroscopy, was the primary outcome and glucose tolerance and serum lipids were the secondary outcomes. All measurements were conducted in Maastricht University Medical Center.ResultsThirty-seven participants completed the study protocol. After 6 wk of fructose restriction, dietary fructose intake and urinary fructose excretion were significantly lower in the intervention group (difference: −57.0 g/d; 95% CI: −77.9, −39.5 g/d; and −38.8 μmol/d; 95% CI: −91.2, −10.7 μmol/d, respectively). Although IHL content decreased in both the intervention and control groups (P < 0.001 and P = 0.003, respectively), the change in IHL content was more pronounced in the intervention group (difference: −0.7% point, 95% CI: −2.0, −0.03% point). The changes in glucose tolerance and serum lipids were not significantly different between groups.ConclusionsSix weeks of fructose restriction per se led to a small, but statistically significant, decrease in IHL content in comparison with an isocaloric control group.This trial was registered at clinicaltrials.gov as NCT03067428.

Fructose intake is not associated to the risk of hepatic fibrosis in patients with Non-Alcoholic Fatty Liver Disease (NAFLD)

Non-Alcoholic Fatty Liver Disease (NAFLD) has been linked to fructose intake (FI). The aim of this study was to evaluate whether the dietary FI from different food sources (added/industrial processing and natural/intrinsic to food) is associated with NAFLD and risk of hepatic fibrosis (HF). Cross-sectional study with 128 patients with NAFLD underwent clinical, functional, laboratory, nutritional and dietary intake by 3-day-diet-record evaluation. The proportions (in grams/milliliters) of foods and beverages in the diet for each subject was computed from the database NUTTAB and classified by their processing level according to the NOVA classification to identify the source of fructose. The mean age was 54.0±11.9 years; 72.7% were women, and BMI 32.6±5.4kg/m2. Total fructose (TF) intake was 21.6g, natural fructose (NF) 14.8g and added fructose (AF) 6.8g. TF, NF, and AF intakes not differ in patients with steatosis, steatohepatitis and cirrhosis (p-values 0.140; 0.101; 0.739, respectively), and not justify HF according NAFLD score, in view of the low correlation power found (r2 0.009; 0.040; 0.051) respectively for TF, NF and AF. Patients presented elevated cardiometabolic risk due to the prevalence of 78.0% intermediate/high risk of HF; 96.8% over waist-to-height ratio (WHtR), 79.7% of metabolic syndrome (MetS), 65.6% low hand grip strength (HGS), and 70.3% had sarcopenic obesity. Patients had low FI compared to the amounts presented in other occidental countries and studies. No association was found between FI and NAFLD or risk of HF.

Tissue-Specific Fructose Metabolism in Obesity and Diabetes.

The objective of this review is to provide up-to-date and comprehensive discussion of tissue-specific fructose metabolism in the context of diabetes, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD). Increased intake of dietary fructose is a risk factor for a myriad of metabolic complications. Tissue-specific fructose metabolism has not been well delineated in terms of its contribution to detrimental health effects associated with fructose intake. Since inhibitors targeting fructose metabolism are being developed for the management of NAFLD and diabetes, it is essential to recognize how inability of one tissue to metabolize fructose may affect metabolism in the other tissues. The primary sites of fructose metabolism are the liver, intestine, and kidney. Skeletal muscle and adipose tissue can also metabolize a large portion of fructose load, especially in the setting of ketohexokinase deficiency, the rate-limiting enzyme of fructose metabolism. Fructose can also be sensed by the pancreas and the brain, where it can influence essential functions involved in energy homeostasis. Lastly, fructose is metabolized by the testes, red blood cells, and lens of the eye where it may contribute to infertility, advanced glycation end products, and cataracts, respectively. An increase in sugar intake, particularly fructose, has been associated with the development of obesity and its complications. Inhibition of fructose utilization in tissues primary responsible for its metabolism alters consumption in other tissues, which have not been traditionally regarded as important depots of fructose metabolism.

Hepatic cholesterol synthesis and lipoprotein levels impaired by dietary fructose and saturated fatty acids in mice: Insight on PCSK9 and CD36.

The aim of this study was to investigate the uncertain effects of high saturated fatty acids (SFAs) or fructose intake on cholesterol and lipoproteins with an insight of proprotein convertase subtilisin/kexin type 9 (PCSK9)- and cluster of differentiation 36 (CD36)-induced mechanisms. Forty male C57 BL/6 mice (8 wks of age) were divided into four groups and fed ad libitum with standard chow or three isocaloric diets containing high SFAs (SFA group), monounsaturated fatty acids (MUFA group, vehicle), or fructose for 15 wks. Subsequently, mice were sacrificed and blood, liver, and heart were collected for further analysis. Consequently, fructose or SFA intake resulted in higher plasma and liver total cholesterol (TC) levels, plasma low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein (Apo)-B levels, TC/HDL-C, and LDL-C/HDL-C ratios, and lower plasma levels of HDL-C and Apo-A1 (P < 0.05). Levels of 3-hydroxy-3-methylglutaryl-CoA reductase and acetyl-CoA acetyltransferase 1 enzymes in liver and CD36 levels in plasma were elevated by high SFAs and fructose intake (P < 0.05), whereas plasma PCSK9 levels were not significantly changed. Fructose and SFA intake increased PCSK9 and CD36 levels in the heart, along with increased CD36 levels in the liver (P < 0.05). Furthermore, plasma LDL-C was found to be positively correlated with liver PCSK9 (r=0.85, P=0.02), and CD36 (r=0.70, P=0.02) in the SFA and fructose groups. High intakes of dietary SFAs and fructose might induce dysregulations in the cholesterol synthesis and blood lipoprotein levels via proposed nutrient-sensitive biomarkers PCSK9 and CD36 in liver and extrahepatic tissues involved in cholesterol homeostasis.

Dietary Fructose Intake and Hippocampal Structure and Connectivity during Childhood.

In rodent literature, there is evidence that excessive fructose consumption during development has a detrimental impact on hippocampal structure and function. In this study of 103 children ages 7–11 years old, we investigated whether dietary fructose intake was related to alterations in hippocampal volume and connectivity in humans. To examine if these associations were specific to fructose or were related to dietary sugars intake in general, we explored relationships between dietary intake of added sugars and the monosaccharide, glucose, on the same brain measures. We found that increased dietary intake of fructose, measured as a percentage of total calories, was associated with both an increase in the volume of the CA2/3 subfield of the right hippocampus and increased axial, radial, and mean diffusivity in the prefrontal connections of the right cingulum. These findings are consistent with the idea that increased fructose consumption during childhood may be associated with an inflammatory process, and/or decreases or delays in myelination and/or pruning. Increased habitual consumption of glucose or added sugar in general were associated with an increased volume of right CA2/3, but not with any changes in the connectivity of the hippocampus. These findings support animal data suggesting that higher dietary intake of added sugars, particularly fructose, are associated with alterations in hippocampal structure and connectivity during childhood.

Associations of dietary carbohydrate and fatty acid intakes with cognition among children.

To investigate the cross-sectional associations of dietary carbohydrate and fatty acid intakes with cognition in mid-childhood. Dietary carbohydrate and fatty acid intakes were assessed using 4-d food records, and cognition was evaluated using the Raven's Coloured Progressive Matrices (RCPM) score. The cross-sectional associations of dietary carbohydrate and fatty acid intakes with cognition were investigated using linear regression analyses adjusted for age, sex, body fat percentage, household income, parental education and daily energy intake. The baseline examinations of the Physical Activity and Nutrition in Children study. A population-based sample of 487 children (250 boys, 237 girls) aged 6-8 years living in the city of Kuopio, Finland. A higher dietary intake of fructose (standardised regression coefficient, β = 0·24, P < 0·001), total fibre (β = 0·16, P = 0·02) and soluble fibre (β = 0·15, P = 0·02) was associated with a higher RCPM score in boys. Other dietary carbohydrates and fatty acids, including total carbohydrates, glucose, sucrose, starch, insoluble fibre, total fat, SFAs, MUFAs, PUFAs, palmitic acid (C16), stearic acid (C18), linoleic acid (C18:2), α-linoleic acid (C18:3), arachidonic acid (C20:4), EPA (C20:5n-3) and DHA (C22:6n-6), were not associated with the RCPM score in boys. Dietary carbohydrates or fatty acids were not associated with the RCPM score in girls. Higher dietary fructose and fibre intakes were associated with better cognition in boys, but not in girls. Dietary fatty acids were not related to cognition in boys or in girls.

Dietary Sugars: Not as Sour as They Are Made Out to Be.

Over the course of evolution, Mother Nature preserved the ability of humans to make every sugar they need for metabolic functions. Glucose is the almost exclusive fuel preferred by the human brain. Human infants are born with sweet taste receptors, sugars are a significant energy source in human milk, and mammals have a direct gut-to-brain sugar-sensing system that enhances development of a preference for sugars. If sugars are as toxic as many postulate, what species advantage was conferred by this evolutionary progression? Observational studies have reported that sugar consumption is associated with various adverse health risks. However, observational studies can never prove causality, dietary intake records are known to be highly problematic, and the huge number of correlation interdependencies among environmental "exposome" variables makes it impossible to attribute causality to individual dietary components. Additionally, these studies overall have been graded as low quality, and many reported the small effect sizes are likely within the propagated methodological "noise." With several exceptions, data from randomized controlled trials that ensured isocaloric energy intakes have failed to confirm the causal implications of the observational data. Likewise, the comprehensive UK Scientific Committee on Nutrition Report on Carbohydrates and Health also failed to confirm the vast majority of widely postulated detrimental effects of sugar consumption per se. Current data on intakes of sugar-sweetened beverages and on the risks associated with high intakes of dietary fructose remain under debate.

Stearoyl CoA desaturase is a gatekeeper that protects human beta cells against lipotoxicity and maintains their identity

Aims/hypothesisDuring the onset of type 2 diabetes, excessive dietary intake of saturated NEFA and fructose lead to impaired insulin production and secretion by insulin-producing pancreatic beta cells. The majority of data on the deleterious effects of lipids on functional beta cell mass were obtained either in vivo in rodent models or in vitro using rodent islets and beta cell lines. Translating data from rodent to human beta cells remains challenging. Here, we used the human beta cell line EndoC-βH1 and analysed its sensitivity to a lipotoxic and glucolipotoxic (high palmitate with or without high glucose) insult, as a way to model human beta cells in a type 2 diabetes environment.MethodsEndoC-βH1 cells were exposed to palmitate after knockdown of genes related to saturated NEFA metabolism. We analysed whether and how palmitate induces apoptosis, stress and inflammation and modulates beta cell identity.ResultsEndoC-βH1 cells were insensitive to the deleterious effects of saturated NEFA (palmitate and stearate) unless stearoyl CoA desaturase (SCD) was silenced. SCD was abundantly expressed in EndoC-βH1 cells, as well as in human islets and human induced pluripotent stem cell-derived beta cells. SCD silencing induced markers of inflammation and endoplasmic reticulum stress and also IAPP mRNA. Treatment with the SCD products oleate or palmitoleate reversed inflammation and endoplasmic reticulum stress. Upon SCD knockdown, palmitate induced expression of dedifferentiation markers such as SOX9, MYC and HES1. Interestingly, SCD knockdown by itself disrupted beta cell identity with a decrease in mature beta cell markers INS, MAFA and SLC30A8 and decreased insulin content and glucose-stimulated insulin secretion.Conclusions/interpretationThe present study delineates an important role for SCD in the protection against lipotoxicity and in the maintenance of human beta cell identity.Data availabilityMicroarray data and all experimental details that support the findings of this study have been deposited in in the GEO database with the GSE130208 accession code.

Fructose-mediated effects on gene expression and epigenetic mechanisms associated with NAFLD pathogenesis.

Nonalcoholic fatty liver disease (NAFLD) is a chronic, frequently progressive condition that develops in response to excessive hepatocyte fat accumulation (i.e., steatosis) in the absence of significant alcohol consumption. Liver steatosis develops as a result of imbalanced lipid metabolism, driven largely by increased rates of de novo lipogenesis and hepatic fatty acid uptake and reduced fatty acid oxidation and/or disposal to the circulation. Fructose is a naturally occurring simple sugar, which is most commonly consumed in modern diets in the form of sucrose, a disaccharide comprised of one molecule of fructose covalently bonded with one molecule of glucose. A number of observational and experimental studies have demonstrated detrimental effects of dietary fructose consumption not only on diverse metabolic outcomes such as insulin resistance and obesity, but also on hepatic steatosis and NAFLD-related fibrosis. Despite the compelling evidence that excessive fructose consumption is associated with the presence of NAFLD and may even promote the development and progression of NAFLD to more clinically severe phenotypes, the molecular mechanisms by which fructose elicits effects on dysregulated liver metabolism remain unclear. Emerging data suggest that dietary fructose may directly alter the expression of genes involved in lipid metabolism, including those that increase hepatic fat accumulation or reduce hepatic fat removal. The aim of this review is to summarize the current research supporting a role for dietary fructose intake in the modulation of transcriptomic and epigenetic mechanisms underlying the pathogenesis of NAFLD.

Fructose Consumption is Associated with Non-Alcoholic Fatty Liver Disease Risk: A Case-Control Study from Iran

Objectives: This study aimed is to evaluate the association between dietary fructose intake and risk of nonalcoholic fatty liver disease (NAFLD). Methods: Newly diagnosed patients with NAFLD and age matched controls were asked about their dietary intakes. Fructose consumption was assessed using a reliable and valid food frequency questionnaire and fructose intake was calculated using food composition table. Results: In the crude model, subjects in the highest quartile had more than 3.08 times higher risk of NAFLD in comparison to those in the lowest quartile of the fructose intake (OR: 3.08; 95 percent CI: 1.87 - 5.06), (P < 0.001). Also, adjustment for age, sex, physical activity (MET-h/wk), body mass index (kg/m2), energy intake (kcal/d) and simple sugar strengthened this association (OR: 3.54; 95 percent CI: 1.81 - 6.93) (P = 0.003). Conclusions: Our results indicate that higher intake of fructose is significantly associated with the higher risk of NAFLD; this association remained significant after adjustment for known confounding factors. Further studies are required to find the cut point for safe daily fructose consumption alone or in combination with dietary fiber sources.

Farklı Miktarlarda Tüketilen Fruktozun, Vücut Ağırlığı ve Bazı Biyokimyasal Parametreler Üzerine Etkisi

Amaç: Bireylerin doğal ve/veya yüksek fruktozlu mısır şurubu olarak günlük diyetle tükettikleri farklı fruktoz miktarlarının antropometrik ölçümler, kan biyokimyasal bulguları ve diğer beslenme parametreleri ile ilişkisinin incelenmesidir.Bireyler ve Yöntem: Çalışma, 90 (41 erkek, 49 kadın) sağlıklı birey (18-65 yıl) üzerinde yürütülmüştür. Bireylerin kişisel özellikleri, fruktoz alımlarını da içeren bazı beslenme alışkanlıkları, beslenme durumları ve fiziksel aktivite durumları belirlenmiş, antropometrik ölçümleri alınmış, bazı biyokimyasal parametreleri analiz edilmiştir.Bulgular: Bireylerin günlük diyetle fruktoz alım ortalaması 42.3±22.73 g’dır ve erkeklerin (49±26.13 g), kadınlara (36.7±17.85 g) göre daha fazla fruktoz tükettikleri belirlenmiştir (p&lt;0.05). Bireylerin ortalama %33.3’ünün (erkeklerin %39’u, kadınların %28.6’sı) günlük fruktoz alımının 50 g ve üzerinde olduğu belirlenirken, ortalama %18.9’unda (erkeklerin %14.6’sı, kadınların %22.4’ü) fruktoz alımının, toplam enerji alımının %10’undan daha fazla olduğu bulunmuştur. Günlük fruktoz alımı en yüksek olan grubun obez bireyler (BKİ= ≥30 kg/m2) olduğu görülmüştür. Bireylerin cinsiyete, günlük diyetle fruktoz alım miktarlarına ve günlük diyetle alınan fruktozun toplam enerjiden gelen oranlarına göre kan biyokimyasal bulgularının ortalamaları karşılaştırıldığında da, glukoz, ürik asit, total, yüksek yoğunluklu lipoprotein, düşük yoğunluklu lipoprotein kolesterol, trigliserit, serum glutamik oksaloasetik transaminaz, serum glutamik pirüvik transaminaz ve insülin değerleri açısından gruplar arası istatistiksel açıdan önemli bir farkın olmadığı saptanmıştır (p&gt;0.05).Sonuç: Yüksek miktarda fruktoz alımının başta obezite olmak üzere insülin direnci, bozulmuş glukoz toleransı, tip 2 diyabet, hiperlipidemi, kardiyovasküler hastalıklar, hiperürisemi, gut ve metabolik sendrom gibi hastalıklar için risk oluşturabileceği göz önünde bulundurulmalı ve günlük diyet enerjisinin %10’dan daha azı meyve gibi doğal fruktoz kaynaklarından sağlanmalıdır.

High intake of dietary fructose in overweight/obese teenagers associated with depletion of Eubacterium and Streptococcus in gut microbiome

ABSTRACT Background A western high fat, high carbohydrate diet has been shown to be associated with decreased gut bacterial diversity and reductions in beneficial bacteria. This gut bacteria dysbiosis could develop in early life and contribute to chronic disease risk such as obesity, type 2 diabetes and non-alcoholic fatty liver disease. Objective To determine how dietary macronutrients are associated with the relative abundance of gut bacteria in healthy adolescents. Methods Fifty-two obese participants (12–19 years) from two studies, many who were primarily of Hispanic background, provided fecal samples for 16S rRNA gene sequencing. Dietary macronutrients were assessed using 24-hour diet recalls and body composition was assessed using DEXA. General regression models assuming a negative binomial distribution were used to examine the associations between gut bacteria and dietary fiber, saturated fat, unsaturated fats, protein, added sugar, total sugar and free fructose after adjusting for age, gender, race/ethnicity, body fat percentage, study and caloric intake. Results The genera Eubacterium (Benjamini-Hochberg (BH) corrected p-value = 0.10) and Streptococcus (BH corrected p-value = 0.04) were inversely associated with dietary fructose intake. There were no other significant associations between abundances of gut microbes and other dietary macronutrients, including fiber, fat, protein, total sugar or added sugar. Conclusions High dietary fructose was associated with lower abundance of the beneficial microbes Eubacterium and Streptococcus, which are involved with carbohydrate metabolism.

Dietary Sources of Fructose and Its Association with Fatty Liver in Mexican Young Adults.

Fructose intake has been associated with non-alcoholic fatty liver disease (NAFLD). The objective of this study was to assess the consumption of dietary fructose according to: 1) classification of hepatic steatosis by two indexes and 2) diagnosis of NAFLD by MRI. We conducted a cross-sectional analysis among 100 young adults from Mexico City. The Hepatic Steatosis Index (HSI) and the Fatty Liver Index (FLI) were estimated using Body Mass Index (BMI), waist circumference, and fasting concentrations of glucose, triglycerides, and hepatic enzymes (ALT, AST, GGT). A semi-quantitative food frequency questionnaire was administered to obtain dietary sources of fructose. We estimated the concordance between the hepatic indices and NAFLD and the correlation between the index scores and the percentage of liver fat. Eighteen percent presented NAFLD; 44% and 46% were classified with hepatic steatosis according to HSI and FLI, respectively. We compared dietary intake of fructose by each outcome: HSI, FLI, and NAFLD. Sugar-sweetened beverages (SSB) and juices were consumed significantly more by those with steatosis by FLI and NAFLD suggesting that SSB intake is linked to metabolic alterations that predict the risk of having NAFLD at a young age.

Lactobacillus helveticus and Lactobacillus plantarum modulate renal antioxidant status in a rat model of fructose-induced metabolic syndrome

High dietary fructose intake causes a metabolic disorder and augments the risk of chronic kidney disease most likely due to oxidative stress. Probiotics could have antioxidant, antiinflammatory and immunoregulatory properties. The present study examined the influence of Lactobacillus helveticus and Lactobacillus plantarum supplementation on dietary fructose-induced metabolic changes and renal antioxidant/oxidant status of rats. Male Wistar rats were divided into four groups as follows: control; fructose; fructose plus L. helveticus; fructose plus L. plantarum. Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. The probiotic supplementation was applied by gastric gavage once a day for six weeks. Several metabolic parameters in the plasma, gene and protein expressions of the main antioxidant enzymes in renal tissues of rats were measured. Dietary fructose-induced elevations in plasma insulin, triglyceride, VLDL, creatinine as well as renal urea levels were alleviated after treatment with L. helveticus and L. plantarum. Moreover, L. helveticus and L. plantarum supplementation recovered the changes in renal protein expression level of SOD1, SOD2 and CAT. In conclusion, supplementation with L. helveticus and L. plantarum has an improving effect on specific metabolic parameters and renal antioxidative enzymes in a fructose-induced metabolic disorder.

The negative impact of fructose overconsumption on health

An epidemic of metabolic disorders nowadays, may be partially explained by fructose overconsumption. Experimental and human studies suggest that high dietary intake of fructose is an important nutritional factor in the development of metabolic syndrome and its associated complications. The aim of this article is to increase the awareness by negative impact of fructose overconsumption on health and how to avoid it.

Dietary fat stimulates development of NAFLD more potently than dietary fructose in Sprague\u2013Dawley rats

BackgroundIn humans and animal models, excessive intake of dietary fat, fructose and cholesterol has been linked to the development of non-alcoholic fatty liver disease (NAFLD). However, the individual roles of the dietary components remain unclear. To investigate this further, we compared the effects of a high-fat diet, a high-fructose diet and a combination diet with added cholesterol on the development of NAFLD in rats.MethodsForty male Sprague–Dawley rats were randomized into four groups receiving either a control-diet (Control: 10% fat); a high-fat diet (HFD: 60% fat, 20% carbohydrate), a high-fructose diet [HFr: 10% fat, 70% carbohydrate (mainly fructose)] or a high-fat/high-fructose/high-cholesterol-diet (NASH: 40% fat, 40% carbohydrate (mainly fructose), 2% cholesterol) for 16 weeks.ResultsAfter 16 weeks, liver histology revealed extensive steatosis and inflammation in both NASH- and HFD-fed rats, while hepatic changes in HFr-rats were much more subtle. These findings were corroborated by significantly elevated hepatic triglyceride content in both NASH- (p < 0.01) and HFD-fed rats (p < 0.0001), elevated hepatic cholesterol levels in NASH-fed rats (p < 0.0001), but no changes in HFr-fed rats, compared to Control. On the contrary, only HFr-fed rats developed dyslipidemia as characterized by higher levels of plasma triglycerides compared to all other groups (p < 0.0001). Hepatic dysfunction and inflammation was confirmed in HFD-fed rats by elevated levels of hepatic MCP-1 (p < 0.0001), TNF-alpha (p < 0.001) and plasma β-hydroxybutyrate (p < 0.0001), and in NASH-fed rats by elevated levels of hepatic MCP-1 (p < 0.01), increased hepatic macrophage infiltration (p < 0.001), and higher plasma levels of alanine aminotransferase (p < 0.0001) aspartate aminotransferase (p < 0.05), haptoglobin (p < 0.001) and TIMP-1 (p < 0.01) compared to Control.ConclusionThese findings show that dietary fat and cholesterol are the primary drivers of NAFLD development and progression in rats, while fructose mostly exerts its effect on the circulating lipid pool.