Dataset Information

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases.

ABSTRACT: High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota are still largely unknown. We therefore examined the effect of short-term high-fructose consumption on the human intestinal microbiota. Twelve healthy adult women were enrolled in a pilot intervention study. All study participants consecutively followed four different diets, first a low fructose diet (< 10 g/day fructose), then a fruit-rich diet (100 g/day fructose) followed by a low fructose diet (10 g/day fructose) and at last a high-fructose syrup (HFS) supplemented diet (100 g/day fructose). Fecal microbiota was analyzed by 16S rRNA sequencing. A high-fructose fruit diet significantly shifted the human gut microbiota by increasing the abundance of the phylum Firmicutes, in which beneficial butyrate producing bacteria such as Faecalibacterium, Anareostipes and Erysipelatoclostridium were elevated, and decreasing the abundance of the phylum Bacteroidetes including the genus Parabacteroides. An HFS diet induced substantial differences in microbiota composition compared to the fruit-rich diet leading to a lower Firmicutes and a higher Bacteroidetes abundance as well as reduced abundance of the genus Ruminococcus. Compared to a low-fructose diet we observed a decrease of Faecalibacterium and Erysipelatoclostridium after the HFS diet. Abundance of Bacteroidetes positively correlated with plasma cholesterol and LDL level, whereas abundance of Firmicutes was negatively correlated. Different formulations of high-fructose diets induce distinct alterations in gut microbiota composition. High-fructose intake by HFS causes a reduction of beneficial butyrate producing bacteria and a gut microbiota profile that may affect unfavorably host lipid metabolism whereas high consumption of fructose from fruit seems to modulate the composition of the gut microbiota in a beneficial way supporting digestive health and counteracting harmful effects of excessive fructose.

SUBMITTER: Beisner J

PROVIDER: S-EPMC7697676 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases.

Beisner Julia J Gonzalez-Granda Anita A Basrai Maryam M Damms-Machado Antje A Bischoff Stephan C SC

Nutrients 20201110 11

High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota are still largely unknown. We therefore examined the effect of short-term high-fructose consumption on the human intestinal microbiota. Twelve healthy adult women were enrolled in a pilot intervention study. All study participants consecutively ...[more]

PMID: 33182700

Similar Datasets

Project description:Caries development is associated with shifts in the oral biofilm microbiota and primarily linked to frequent simple carbohydrate consumption. Different nutritional ingredients can either promote or prevent caries development. To investigate the effects of selected ingredients on the oral biofilm microbiota in situ, 11 study participants underwent 3-month-long dietary phases with intake of a regular diet (PI), additional frequent sucrose (PII), milk and yoghurt (PIII), and a diet rich in dietary fiber (PIV) and then returned to their regular diet (PV). Oral biofilm was sampled and analyzed applying 16S rRNA Illumina MiSeq sequencing. Additionally, the effect on the enamel was analyzed by measuring enamel surface roughness with laser scanning microscopy. The beta-diversity results showed that the microbiota in all the following phases differed significantly from PI and that the microbial community in PII was significantly different from all other phases. The abundance of the genus Streptococcus fluctuated over the course of the five phases, with a significant increase in PII (P = 0.01), decreasing in PIII and PIV (PIII and PIV versus PII: P < 0.00001) and increasing again toward PV. Other taxa showed various fluctuations of their abundances, with PV returning approximately to the levels of PI. In conclusion, while elevated sucrose consumption favored caries-promoting non-mutans streptococci, frequent milk and yoghurt intake caused a significant decrease in the abundance of these microbial taxa and in addition reduced enamel surface roughness. These results indicate that modulations of the oral biofilm microbiota can be attained even in adults through dietary changes and corresponding recommendations can be made for the prevention of caries development.IMPORTANCE Caries affects a large proportion of the population worldwide, resulting in high treatment costs. Its etiology can be ascribed to shifts of the microbiota in dental biofilms primarily driven by dietary factors. It is unclear how diet affects the microbial community of plaque biofilm in situ and whether it can be modulated to help prevent caries development. To address these issues, we analyzed changes of the in situ plaque microbiota following 3-month-long dietary changes involving elevated sucrose, dairy, and dietary fiber consumption over a period of 15 months. Applying high-throughput sequencing, we found non-mutans streptococci, a taxonomic group involved in the beginning stages toward microbial dysbiosis, in decreased abundance with elevated dairy and dietary fiber intake. Through analysis of the enamel surface roughness, these effects were confirmed. Therefore, correspondent dietary measures can be recommended for children as well as adults for caries prevention.

Project description:BackgroundAn alkalescent (pH 8.3) mineral water (AMW) of Hita basin, located in the northwestern part of Kyushu island in Japan, has been recognized for the unique quality of ingredients including highly concentrated silicic acid, sodium, potassium, and hydrogen carbonate. The biological effects of AMW intake were evaluated with a particular focus on its "antiobesity" properties through its modulation of the gut microbiota population.MethodsTwo groups of C57BL6/J mice (8-week-old male) were maintained with a standard diet and tap water (control: TWC group) or AMW (AMW group) for 6 months and the following outputs were quantitated: (1) food and water intake, (2) body weight (weekly), (3) body fat measurements by CT scan (monthly), (4) sera biochemical values (TG, ALT, AST, and ALP), and (5) UCP-1 mRNA in fat tissues (terminal point). Two groups of ICR mice (7-week-old male) were maintained with the same method and their feces were collected at the 0, 1st, 3rd, and 6th month at which time the population rates of gut microbiota were quantitated using metagenomic sequencing analysis of 16S-rRNA.ResultsAmong all antiobesity testing items, even though a weekly dietary consumption was increased (p=0.012), both ratios of weight gain (p=1.21E - 10) and visceral fat accumulation (p=0.029) were significantly reduced in the AMW group. Other criteria including water intake (p=0.727), the amounts of total (p=0.1602), and subcutaneous fat accumulation (p=0.052) were within the margin of error and UCP-1 gene expression level (p=0.171) in the AMW group was 3.89-fold higher than that of TWC. Among 8 major gut bacteria families, Lactobacillaceae (increased, p=0.029) and Clostridiaceae (decreased, p=0.029) showed significant shift in the whole population.ConclusionWe observed significantly reduced (1) weight gaining ratio (average -1.86%, up to -3.3%), (2) visceral fat accumulation ratio (average -4.30%, up to -9.1%), and (3) changes in gut microbiota population. All these consequences could support the "health benefit" functionality of AMW.

Project description:BackgroundOral vancomycin remains the mainstay of therapy for severe infections produced by Clostridium difficile, the most prevalent cause of healthcare-associated infectious diarrhoea in developed countries. However, its short- and long-term effects on the human intestinal microbiota remain largely unknown.MethodsWe utilized high-throughput sequencing to analyse the effects of vancomycin on the faecal human microbiota up to 22 weeks post-antibiotic cessation. The clinical relevance of the observed microbiota perturbations was studied in mice.ResultsDuring vancomycin therapy, most intestinal microbiota genera and operational taxonomic units (OTUs) were depleted in all analysed subjects, including all baseline OTUs from the phylum Bacteroidetes. This was accompanied by a vast expansion of genera associated with infections, including Klebsiella and Escherichia/Shigella. Following antibiotic cessation, marked differences in microbiota resilience were observed among subjects. While some individuals recovered a microbiota close to baseline composition, in others, up to 89% of abundant OTUs could no longer be detected. The clinical relevance of the observed microbiota changes was further demonstrated in mice, which developed analogous microbiota alterations. During vancomycin treatment, mice were highly susceptible to intestinal colonization by an antibiotic-resistant pathogen and, upon antibiotic cessation, a less-resilient microbiota allowed higher levels of pathogen colonization.ConclusionsOral vancomycin induces drastic and consistent changes in the human intestinal microbiota. Upon vancomycin cessation, the microbiota recovery rate varied considerably among subjects, which could influence, as validated in mice, the level of susceptibility to pathogen intestinal colonization. Our results demonstrate the negative long-term effects of vancomycin, which should be considered as a fundamental aspect of the cost-benefit equation for antibiotic prescription.

Project description:Obesity is closely associated with adipose tissue inflammation and insulin resistance. Dysglycemia and type 2 diabetes results when islet β cells fail to maintain appropriate insulin secretion in the face of insulin resistance. To clarify the early transcriptional events leading to β-cell failure in the setting of obesity, we fed male C57BL/6J mice an obesogenic, high-fat diet (60% kcal from fat) or a control diet (10% kcal from fat) for one week, and islets from these mice (from four high-fat- and three control-fed mice) were subjected to single-cell RNA sequencing (sc-RNAseq) analysis. Islet endocrine cell types (α cells, β cells, δ cells, PP cells) and other resident cell types (macrophages, T cells) were annotated by transcript profiles and visualized using Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) plots. UMAP analysis revealed distinct cell clusters (11 for β cells, 5 for α cells, 3 for δ cells, PP cells, ductal cells, endothelial cells), emphasizing the heterogeneity of cell populations in the islet. Collectively, the clusters containing the majority of β cells showed the fewest gene expression changes, whereas clusters harboring the minority of β cells showed the most changes. We identified that distinct β-cell clusters downregulate genes associated with the endoplasmic reticulum stress response and upregulate genes associated with insulin secretion, whereas others upregulate genes that impair insulin secretion, cell proliferation, and cell survival. Moreover, all β-cell clusters negatively regulate genes associated with immune response activation. Glucagon-producing α cells exhibited patterns similar to β cells but, again, in clusters containing the minority of α cells. Our data indicate that an early transcriptional response in islets to an obesogenic diet reflects an attempt by distinct populations of β cells to augment or impair cellular function and/or reduce inflammatory responses as possible harbingers of ensuing insulin resistance.

Dataset Information

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases.

Publications

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets