Effects of Allulose and Erythritol Consumption on a High-Fat Diet
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ABSTRACT: Long-term consumption of erythritol, a widely used sugar substitute, has been associated with increased risks of thrombosis and cardiometabolic diseases. In this study, we investigated the effects and mechanisms of allulose in mitigating these risks compared to erythritol using the clusterProfiler tool. Since a high-fat diet (HFD) is known to enhance platelet aggregation, we compared the pathways related to these processes between groups of mice treated with allulose and those treated with erythritol. While erythritol exacerbated HFD-induced increased platelet aggregation, allulose treatment significantly reduced it. The groups consisted of a normal diet group (ND, with 10% of calories derived from fat), a high-fat diet group (HFD, with 40% of calories from fat), a high-fat diet with 5% allulose supplementation (ALLU), and a high-fat diet with 5% erythritol supplementation (ERY).
Project description:Carotenoids are naturally occurring pigments in plants responsible for the orange, yellow, and red color of fruits and vegetables. Carrots are one of the primary dietary sources of carotenoids. The biological activities of carotenoids in higher organisms are well documented in most tissues but not the large intestine. The gastrointestinal barrier acts as a line of defense against the systemic invasion of pathogenic bacteria, especially at the colonic level. Proteins involved in tight junction assembly between epithelial cells and mucus secretion from goblet cells are essential for maintaining intestinal barrier homeostasis. A high-fat diet can cause gut impairment by inducing barrier permeability, leading to low-grade chronic inflammation via metabolic endotoxemia. Our hypothesis for this study is that the dietary intake of carotenoid-rich foods can alleviate obesity-associated gut inflammation and strengthen the intestinal barrier function. Male C57BL/6J mice were randomized to one of four experimental diets for 20 weeks (n = 20 animals/group): Low-fat diet (LFD, 10% calories from fat), high-fat diet (HFD, 45% calories from fat), HFD with white carrot powder (HFD + WC), or HFD with orange carrot powder (HFD + OC). Colon tissues were harvested to analyze the biochemical effects of carotenoids in carrots. The distal sections were subjected to isobaric labeling-based quantitative proteomics in which tryptic peptides were labeled with tandem mass tags, followed by fractionation and LC-MS/MS analysis in an Orbitrap Eclipse Tribrid instrument. High-performance liquid chromatography results depicted that the HFD+WC pellets were carotenoid-deficient, and the HFD+OC pellets contained high concentrations of provitamin A carotenoids, specifically α-carotene and β-carotene. As a result of the quantitative proteomics, a total of 4410 differentially expressed proteins were identified. Intestinal barrier-associated proteins were highly upregulated in the HFD+OC group, particularly mucin-2 (MUC-2). Upon closer investigation into mucosal activity, other proteins related to MUC-2 functionality and tight junction management were upregulated by the HFD+OC dietary intervention. Carotenoid-rich foods may prevent high-fat diet-induced intestinal barrier disruption by promoting colonic mucus synthesis and secretion in mammalian organisms.
Project description:Using a C57BL6/J mouse model of diet-induced obesit,we observed that mannose supplementation of high fat diet (HFD)-fed mice prevents weight gain,lowers adiposity, reduces liver steatosis, and improves glucose tolerance and insulin sensitivity. We used microarrays to determine the gene expression pattern in epididymal fat frommice weaned on Normal diet (ND), HFD and HFD with mannose (HFDM)
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of wild-type C57BL-6 mice exposed to a high-fat diet that might have been caused by the oral consumption of the probiotic B. pseudocatenulatum CECT 7765. The aim of this work was to determine whether the daily intake (by oral gavage) of the probiotic (P) B. pseudocatenulatum for seven weeks exerted any modulatory effects, at the level of gene expression, in the liver of C57BL-6 male mice exposed to a high-fat diet (HFD). Male mice were randomly assigned to four experimental groups (n= 5 animals per group) as follows: (1) control group, fed a standard diet (SD); (2) obese group, fed a high-fat diet (HFD); (3) a group that received the SD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (SD+P); and (d) an obese group that was fed the HFD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (HFD+P). At the end of the experimental procedure total RNA was extracted from the liver to compare differential gene expression between the groups. Liver differential gene expression after 7 weeks of supplementation between: 1) the HFD group and the SD group (effects of the high-fat diet); 2) the HFD+P and the HFD (effects of the probiotic on the consumption of a high-fat diet) and 3) the SD+P group and the SD (direct effects of the probiotic on the liver of animals consuming a normal diet).
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
Project description:Microarray analyses were performed in order to determine the effect of galectin-3 ablation on the endothelial transcriptional response in a mouse model of type 2 diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed a high-fat diet (60% fat calories) or standard chow for 8 weeks. CD105+/CD45- endothelial cells were isolated from the aortae and skeletal muscles of these mice by FACS. Whole genome microarray expression profiling revealed greater transcriptional dysregulation in the endothelium of the KO after high-fat feeding compared to WT. Transcripts dysregulated in the KO endothelium after HFD include those involved in glucose uptake and insulin signaling, oxidative stress, vasoregulation, coagulation, and atherogenesis. Real-time PCR confirmed transcriptional downregulation of the glucose transporter, Glut4, and immunofluorescence staining confirmed reduced GLUT4 protein in the endothelium and mudcle of the KO compared to WT. The transcriptional and histological data was consistent with physiological studies showing exacerbated hyperglycemia and coagulation in the KO. These results suggest that galectin-3 serves a protective role against metabolic dysregulation and endothelial dysfunction in diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed either a high-fat diet (60% fat calories) or standard chow diet (12% fat calories) for 8 weeks. Three independent experiments were performed. For each experiment, the aorta and skeletal muscle from 3-4 animals per diet/genotype group were excised and pooled for each tissue. Live, CD105+/CD45- endothelial cells were isolated from the aortic and muscle suspensions by FACS.
Project description:From a long time ago, supplementation of fermented enzyme foods could have worked health effects on the body in the east nevertheless, only a few studies reported functions of them such as weight loss and metabolic syndrome. Thus, it is necessary to be verified whether supplementation of fermented enzyme foods can act in the body as a functional material. Therefore, we investigated the anti-obesity effects of fermented mixed grain with digestive enzymes (FMG) in high-fat diet induced mice. Sixty C57BL/6J mice were divided into six dietary groups and fed a normal diet (ND), a high-fat diet (HFD), Bacilus Coagulans group, steamed grain group, low-dose fermented mixed grain group(L-FMG), high-dose fermented mixed grain group (H-FMG) supplement for 12 weeks. After sacrificing, body weight and body fat mass in H-FMG group were significantly decreased compared to HFD group with a simultaneous decrease in plasma lipids. Also, H-FMG significantly decreased the blood glucose and improved the glucose tolerance compared to HFD group. Moreover high-dose FMG supplementation dramatically decreased the levels of inflammatory cytokines which secreted from adipocyte. Taken together, our findings suggest that H-FMG ameliorate high fat-diet induced obesity and its complication and could be used as a potential preventive agent for obesity.
Project description:To systemically evaluate the comprehensive alterations under the supplements of quercetin and/or resveratrol in high fat diet (HFD) fed mice, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that differentially altered by different treatments. Gene expression profiles were significantly altered by long term HFD feeding. However, quercetin, resveratrol and their combination could effectively attenuate this alteration. Especially, combination use of quercetin and resveratrol showed more signifcant benefits on the changes of genes, involved in metabolic disorders, induced by HFD, which revealed a synergistic effect of quercetin and resveratrol supplementation in high fat diet fed mice.
Project description:ackground/Objectives: The aim of the current study was to elucidate the effects of long-term supplementation with D-allulose on obesity and associated comorbidities by analyzing transcriptional and metabolic responses. Subjects/Methods: C57BL/6J mice were divided into three groups and fed a normal diet, high-fat diet (HFD), or high-fat + 5% (w/w) D-allulose diet for 16 weeks. Results: Body weight and body fat mass were significantly decreased in HFD-fed with D-allulose supplemented mice and their levels were similar to that of the normal diet. Also, major symptoms of obesity, such as high plasma lipid profiles and cytokine levels, were attenuated by D-allulose supplementation. D-allulose supplement induced the alteration of mRNA expression in epididymal white adipose tissue (eWAT) and hepatic tissue. D-allulose normalized mRNA expression related lipid metabolism in eWAT and hepatic tissue. In Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapper analyses, D-allulose supplementation were down regulated the “cytokine-cytokinereceptor interaction”, “chemokinesignaling pathway”, “MAPK signaling pathway”and“toll-like receptor signaling pathway” in eWAT and hepatic tissue.
Project description:Activation of Sirt1, the mammalian homolog of an NAD+-dependent deacetylase known to modulate lifespan in lower organisms, is thought to hold promise as a strategy for delaying aging in mammals. SRT1720, a novel compound developed as a specific and potent activator of Sirt1, has shown promising effects to glucose homeostasis in short-term studies of rats and mice. Here we show SRT1720 extends both mean and maximum lifespan of mice fed a high-fat diet and has concrete benefits to health including reduced liver steatosis and increased insulin sensitivity and locomotor activity. Gene expression profiles and markers of inflammation and apoptosis were also restored to levels more reflective of standard diet controls. Furthermore, the benefits incurred by SRT1720 occurred in the absence of any observable toxicity. The current findings provide hope that safe and effective treatments may be developed to mitigate age-related diseases and enhance lifespan in humans. Male C57BL/6J mice obtained at 12 weeks of age were maintained on a standard purified mouse diet (AIN-93G) until 56 weeks of age prior to the start of the experiment. Beginning at 56 weeks of age, the SD group was fed a standard AIN-93G diet for the duration of the study. Three separate groups were placed on a high-fat diet (HFD) (AIN-93G modified by the addition of hydrogenated coconut oil to provide 60% of calories from fat) or HFD + 30mg/kg body weight SRT1720 (HFD-L) or 100mg/kg body weight SRT1720 (HFD-H) and remained on those diets throughout the study. All mice were fed ad libitum. Food intake and body weight were measured biweekly for the duration of the study.
Project description:Liver is an important organ for fat metabolism. Excessive intake of a high-fat/energy diet is a major cause of hepatic steatosis and its complications such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Supplementation with lycopene, a natural compound, is effective in lowering triglyceride levels in the liver, although the underlying mechanism at the translational level is unclear. In this study, mice were fed a high-fat diet (HFD) to induce hepatic steatosis and treated with or without lycopene. Translation omics and transcriptome sequencing were performed on the liver to explore the regulatory mechanism of lycopene in liver steatosis induced by HFD, and identify differentially expressed genes (DEGs).