Environmental Enrichment Prevents Gut Dysbiosis Progression and Enhances Glucose Metabolism in High-Fat Diet-Induced Obese Mice
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ABSTRACT:
SUBMITTER: Manzo R
PROVIDER: S-EPMC11241766 | biostudies-literature | 2024 Jun
REPOSITORIES: biostudies-literature
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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
Project description:Abnormal fat accumulation with gut microbiota dysbiosis results in hepatic inflammation by upregulating the release of lipopolysaccharide (LPS) and inflammatory cytokine. Gochujang, a traditional fermented condiment, has beneficial effects, such as anti-colonic inflammatory effects. However, Gochujang has been controversial because of its high salt content (the Korean Paradox). Thus, the present study aimed to investigate the preventative effects of Gochujang on hepatic inflammation and related gut microbiota through discussing the Korean Paradox. The mice were divided into groups including a normal diet (ND), high-fat diet (HD), HD with salt (SALT), HD with a high percentage of beneficial microbiota Gochujang (HBM), and HD with diverse beneficial microbiota Gochujang (DBM). Gochujang markedly reduced lipid accumulation, hepatic injury, and inflammation response. Furthermore, Gochujang attenuated protein expression involved in the JNK/IκB/NF-κB pathway. Additionally, Gochujang regulated the gut microbiota-derived LPS production and Firmicutes/Bacteroidetes ratio. Gochujang regulated the levels of gut microbiota such as Bacteroides, Muribaculum, Lactobacillus, and Enterorhabdus, which were correlated with hepatic inflammation. Salt did not have foregoing effects, meaning that the salt content in Gochujang did not affect its anti-inflammatory effect. In conclusion, Gochujang showed anti-hepatic inflammation effects via reduced lipid accumulation, hepatic injury, and inflammatory response together with reorganization of gut microbiota dysbiosis regardless of salt content and the difference of micro bacteria composition.
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Project description:BackgroundC1q/tumor necrosis factor-related protein 1 (CTRP1) is an adipokine secreted by adipose tissue, related to chondrocyte proliferation, inflammation, and glucose homeostasis. However, the therapeutic effects on metabolic disorders and the underlying mechanism were unclear. Here, we investigated the functions and mechanisms of CTRP1 in treating obesity and diabetes.MethodsThe plasmid containing human CTRP1 was delivered to mice by hydrodynamic injection, which sustained expression of CTRP1 in the liver and high protein level in the blood. High-fat diet (HFD) fed mice and STZ-induced diabetes model were used to study the effects of CTRP1 on obesity, glucose homeostasis, insulin resistance, and hepatic lipid accumulation. The lipid accumulation in liver and adipose tissue, glucose tolerance, insulin sensitivity, food intake, and energy expenditure were detected by H&E staining, Oil-Red O staining, glucose tolerance test, insulin tolerance test, and metabolic cage, respectively. The metabolic-related genes and signal pathways were determined using qPCR and western blotting.ResultsWith high blood circulation, CTRP1 prevented obesity, hyperglycemia, insulin resistance, and fatty liver in HFD-fed mice. CTRP1 also improved glucose metabolism and insulin resistance in obese and STZ-induced diabetic mice. The metabolic cage study revealed that CTRP1 reduced food intake and enhanced energy expenditure. The mechanistic study demonstrated that CTRP1 upregulated the protein level of leptin in blood, thermogenic gene expression in brown adipose tissue, and the gene expression responsible for lipolysis and glycolysis in white adipose tissue (WAT). CTRP1 also downregulated the expression of inflammatory genes in WAT. Overexpression of CTRP1 activated AMPK and PI3K/Akt signaling pathways and inhibited ERK signaling pathway.ConclusionThese results demonstrate that CTRP1 could improve glucose homeostasis and prevent HFD-induced obesity and fatty liver through upregulating the energy expenditure and reducing food intake, suggesting CTRP1 may serve as a promising target for treating metabolic diseases.
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Project description:Background: Concerns are emerging that a high-fat diet rich in n-6 PUFA (n-6HFD) may alter gut microbiome and increase the risk of intestinal disorders. Research is needed to model the relationships between consumption of an n-6HFD starting at weaning and development of gut dysbiosis and colonic inflammation in adulthood. We used a C57BL/6J mouse model to compare the effects of exposure to a typical American Western diet (WD) providing 58.4%, 27.8%, and 13.7% energy (%E) from carbohydrates, fat, and protein, respectively, with those of an isocaloric and isoproteic soybean oil-rich n-6HFD providing 50%E and 35.9%E from total fat and carbohydrates, respectively on gut inflammation and microbiome profile. Methods: At weaning, male offspring were assigned to either the WD or n-6HFD through 10-16 weeks of age. The WD included fat exclusively from palm oil whereas the n-6HFD contained fat exclusively from soybean oil. We recorded changes in body weight, cyclooxygenase-2 (COX-2) expression, colon histopathology, and gut microbiome profile. Results: Compared to the WD, the n-6HFD increased plasma levels of n-6 fatty acids; colonic expression of COX-2; and the number of colonic inflammatory and hyperplastic lesions. At 16 weeks of age, the n-6HFD caused a marked reduction in the gut presence of Firmicutes, Clostridia, and Lachnospiraceae, and induced growth of Bacteroidetes and Deferribacteraceae. At the species level, the n-6HFD sustains the gut growth of proinflammatory Mucispirillum schaedleri and Lactobacillus murinus. Conclusions: An n-6HFD consumed from weaning to adulthood induces a shift in gut bacterial profile associated with colonic inflammation.
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Project description:PurposeCommensal microbiome secretes various metabolites that can exert important effects on the host immunity and inflammation and can alter cellular functions. However, little is known regarding the effect of microbiome on corneal immunity and genetic expression. The purpose of this study is to describe the effect of diet-induced gut dysbiosis on corneal immunity and corneal gene expression after wounding.MethodsThis study is approved by the Animal Care and Use of the University of Illinois. Six-week-old female C57BL6 mice were fed on a normal chow diet (ND), isocaloric low-fat control diet (LFD), or a 21% milk high-fat diet (HFD) for six weeks. 2 mm corneal epithelial debridement was performed (n = 10). Fecal samples from mice were used for microbial diversity analysis (n > 3). Immunofluorescence staining of corneal wholemount tissue post-debridement was used to visualize immune cell distribution. RNA Seq was performed on tissue samples from corneas following debridement.ResultsMice fed differing diets had significant alterations in gut microbial diversities. After corneal debridement, HFD mice experienced delayed wound healing in comparison to LFD mice and ND mice groups. However, fecal transplantation led to normalization of wound closure rates. Increased γδTCR staining was observed in the LFD group, and decreased LY6G was observed in HFD group (p < 0.05). Gene Ontology terms of differentially expressed genes included response to external stimulus, cell proliferation, migration, adhesion, defense response and leukocyte migration. Top over-represented pathways included ECM-receptor interaction, Cytokine-cytokine receptor interaction, Focal adhesion and Leukocyte trans-endothelial migration.ConclusionsGut microbial dysbiosis alters corneal immune cell distribution, corneal response to injury, and genes related to epithelial function and corneal immunity.
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