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High-fat diet-derived microbial metabolome induces an inflammatory phenotype in intestinal epithelial cells [colon]

ABSTRACT: We investigated transcriptomic changes in the colon of diet-induced obese rats. Colon tissue samples were collected after eight weeks on the special diet. Our findings revealed induction of local inflammatory processes under a high-fat diet (HFD).

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE302243 | GEO | 2026/03/31

REPOSITORIES: GEO

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High-fat diet-derived microbial metabolome induces an inflammatory phenotype in intestinal epithelial cells [organoids]

Project description:We investigated transcriptomic changes in mouse organoids treated with colonic contents from diet-induced obese and normal-weight rats. 2D Mouse organoids were harvested after 40 h of treatment with 10% solutions of rat colonic content. Our findings revealed induction of local inflammatory processes under treatment with content derived from rats fed a high-fat diet.

2026-03-31 | GSE302244 | GEO

Investigation of microbial community composition in a rat model of obesity [16S rRNA-seq]

Project description:We investigated the microbial composition in the colon of rats with diet-induced obesity. Fecal samples were collected after eight weeks on the special diet, and 16S rRNA sequencing was employed to analyze microbial communities. Our findings revealed distinct microbial profiles between rats fed a LFD and HFD.

2026-03-31 | GSE302254 | GEO

Expression data from murine colon tumors induced by azoxymethane. Tumors from control, obese, formerly obese, or sulindac-treated mice.

Project description:Obesity is associated with an increased risk of colon cancer. Our current study examines whether weight loss and/or treatment with the non-steroidal anti-inflammatory drug (NSAID) sulindac suppresses the protumor effects of obesity in a mouse model of colon cancer. Azoxymethane-treated male FVB/N mice were fed a low-fat diet (LFD) or high-fat diet (HFD) for 15 weeks, then HFD mice were randomized to remain on HFD (obese) or switch to LFD (formerly obese (FOb-LFD)). Within the control (LFD), obese, and FOb-LFD groups, half the mice were also randomized to start sulindac treatment (140 ppm in the diet). All mice were euthanized seven weeks later. FOb-LFD mice had intermediate levels of body weight, lower than obese but higher than control mice (P<0.05). Sulindac did not affect body weight. Obese mice had greater tumor multiplicity and burden than all other groups (P<0.05). Transcriptomic profiling indicated that both weight loss and sulindac modulate the expression of tumor genes related to invasion and may promote a more anti-tumor immune landscape. Furthermore, the fecal microbes Prevotella and Akkermansia muciniphila, both known to be elevated in colorectal cancer patients, were positively correlated with tumor multiplicity and reduced by sulindac in obese mice. In sum, either moderate weight loss or sulindac treatment completely reversed the effects of chronic obesity on colon tumorigenesis. Our findings suggest that an investigation regarding the effects of NSAID treatment on colon cancer risk and/or progression in obese individuals is warranted, particularly for those unable to achieve moderate weight loss.

2022-08-10 | GSE197846 | GEO

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined colon transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

2025-07-02 | GSE293222 | GEO

Organic vegetable juice supplement modulates microbial community in continuous colon simulation system

Project description:In this study, we investigated the effects of organic vegetable juice supplementation on modulating the microbial community, and how its consumption ameliorates blood lipid profiles in diet-induced obese mice. Here, we analyzed the effect of organic vegetable juice on the microbial community and fatty acid synthesis via animal experiments using diet-induced obese mice and continuous colon simulation system. Organic vegetable juice supplement influenced intestinal bacterial composition from phylum to genus level, including decreased Proteobacteria in the ascending colon in the phylum. At the family level, Akkermansia which are associated with obesity, were significantly augmented in the transverse colon and descending colon compared to the control juice group. In addition, treatment with organic vegetable juice affected predicted lipid metabolism function genes related to lipid synthesis. Organic vegetable juice consumption did not have a significant effect on weight loss but helped reduce epididymis fat tissue and adipocytes. Additionally, blood lipid profiles, such as triglyceride, high-density lipoprotein, and glucose, were improved in the organic vegetable juice-fed group. Expression levels of genes related to lipid synthesis, including SREBP-1, PPARγ, C/EBPα, and Fas, were significantly decreased. Analysis of antioxidant markers, including 8-OHdG and MDA, in the vegetable juice group, indicated that blood lipid profiles were improved by the antioxidant effect. These results suggest that organic vegetable juice supplementation may modulate gut microbial community and reduce the potential role of hyperlipidemia in diet-obese mice.

2021-12-31 | GSE171609 | GEO

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High fat diet mice intestinal epithelial exosomal proteins were analyzed by MSMS.

Project description:High-fat diet (HFD) decreases insulin sensitivity. How high-fat diet causes insulin resistance is largely unknown. Here, we show that lean mice become insulin resistant after being administered exosomes isolated from the feces of obese mice fed a high-fat diet (HFD) or from human type II diabetic patients with diabetes. HFD altered the lipid composition of exosomes from predominantly PE in exosomes from lean animals (L-Exo) to PC in exosomes from obese animals (H-Exo). Mechanistically, we show that intestinal H-Exo is taken up by macrophages and hepatocytes, leading to inhibition of the insulin signaling pathway. Moreover, exosome-derived PC binds to and activates AhR, leading to inhibition of the expression of genes essential for activation of the insulin signaling pathway, including IRS-2, and its downstream genes PI3K and Akt. Together, our results reveal HFD-induced exosomes as potential contributors to the development of insulin resistance. Intestinal exosomes thus have potential as broad therapeutic targets.

2021-03-23 | PXD022641 | Pride

Metabolic effects of cesarean section induced gut microbial dysbiosis in high-fat diet induced obese mice

Project description:The aim of this study was to investigate the causative effect of CS induced dysbiosis on obesity and insulin resistance in a high-fat diet induced obese (DIO) mouse model. Male germ-free BALB/c mice were humanized by fecal microbiota transfer using samples from children born by CS or VD and fed HFD for 16 weeks. Adipose tissue was sampled for RNAseq at study termination.

2024-08-01 | GSE254801 | GEO

Quantitative proteomic analysis of oocytes from high-fat diet (HFD)-fed and normal diet mice

Project description:In order to establish an obese mouse model, female mice were continuously fed with a high-fat diet (HFD) or a normal diet (control) for 16 weeks beginning at three weeks of age. In this paper, these mice are termed ‘HFD mice’ and ‘control mice’, respectively. Accordingly, we call their oocytes ‘HFD oocytes’ and ‘control oocytes’. Substantial evidence indicates that the effects of maternal obesity on embryo/offspring development can be attributed to factors within the oocyte (9). To identify such potential effectors, we performed a comparative proteomic analysis of ovulated MII oocytes from control and HFD mice.

2018-05-24 | PXD006641 | Pride

Prior High Fiber Intake Impinges on the Cellular Responses of Mesenteric Adipose and Intestinal Tissues to Subsequent High Fat Feeding

Project description:Dietary modification by consuming plant-based food with high fiber content is a primary strategy to induce weight loss in obese individuals. However, long-term usage of such fiber-enriched dieting is challenging and rapid weight regain often occurs once the high-fat dietary habit resumes. Currently, how do adipose and intestinal tissues respond to a switch between high-fiber and high-fat diet remains unknown. Here, we applied C57BL/6J mice to chow diet (CD)/high-fiber diet (HfiD)-to-high-fat diet (HFD) switching paradigms and collected mesenteric white adipose tissue (mWAT), duodenum and colon tissue sections at different time points for single-nucleus profiling and spatially resolved transcriptomic analysis, respectively. We show that the progenitors and adipocytes of HfiD-fed mWAT are more sensitive to HFD-induced molecular changes. In addition, HfiD feeding prevents the subsequent HFD-induced expansion of immune-related enterocytes in duodenum and reverses the HFD-induced enterocyte-to-goblet cell conversion in colon. Moreover, HfiD-induced microbiome changes are mostly abrogated upon HFD feeding. Our results indicate that prior HfiD feeding can alter the cellular response of adipose and intestinal tissues to subsequent HFD feeding, which highlights the impact of dietary interventions with fiber-rich food for obesity treatment from a different perspective. Our data provide a spatiotemporal resource for future hypothesis-driven studies on the mechanisms of adipose and intestinal tissue plasticity in response to diet switches.

2025-11-30 | GSE283007 | GEO

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