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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature Inflammatory Bowel Disease (IBD) is a complex chronic inflammatory disease involving multiple genetic and environmental drivers.
More and more evidence shows that ketogenic diets (KDs) mediate the rise of circulating ketone bodies and exert potential anti-inflammatory effects.
However, the consequences of this unique diet on colitis are still unknown.
On April 23, 2021, Ma Yanlei of Fudan University, Qin Huanlong of Tongji University, and Ajay Goel of the Beckman Institute in the United States (Tongji University is the first unit) jointly published an online communication titled " Ketogenic diet alleviates colitis by reduction of colonic group 3 innate lymphoid cells through altering gut microbiome" research paper, this study compared small diets fed with ketogenic diet (KDs), low carbohydrate diet (LCD) or normal diet (ND) Changes in the intestinal microbiome and metabolism of mice.
In addition, the study used a colitis model induced by dextran sulfate sodium sulfate (DSS) to study the effects of KD on inflammation, intestinal microbiome, mucosal barrier, and immunity.
The research used transcriptome sequencing, RT2 profiler PCR array, histopathology and immunofluorescence analysis of colon tissue, analysis of serum samples through metabolic assay kits, analysis of fecal samples through 16S rRNA gene sequencing, liquid chromatography-mass spectrometry and gas chromatography-mass spectrometry .
The study observed that KD reduced colitis in a different way from LCD by changing the intestinal flora and metabolites.
Quantitative diet experiments confirmed the unique influence of KD relative to LCD.
After colitis is induced, KD protects the intestinal barrier function and reduces the production of ILC3s cells and related inflammatory cytokines (IL-17α, IL-18, IL-22, Ccl4).
Finally, transplanting fecal flora into sterile mice showed that KD-mediated colitis suppression and ILC3 regulation depend on the modification of intestinal flora.
In summary, this study puts forward an overall view of the changes in microbiome metabolism that occur during the treatment of KD colitis, and confirms that the regulation of the gut microbiome and ILC3s is a new target involving IBD diet therapy.
Inflammatory bowel disease (IBD) is a complex chronic inflammatory disease involving multiple genetic and environmental drivers.
For example, a high-salt diet exacerbates intestinal inflammation by reducing the abundance of lactobacilli and the metabolism of butyrate, while a high-fat diet contributes to IBD.
Although enteral nutrition has shown clinical promise to promote the remission of Crohn's disease, it is still unclear whether dietary therapy can help treat ulcerative colitis.
Ketogenic diet (KD) is a diet therapy characterized by high fat and low carbohydrates.
It was originally used to treat drug-resistant epilepsy, but it has recently become a promising treatment for chronic diseases and human malignancies.
universal.
In Alzheimer's disease, KD can not only protect senescent nerve cells, but also enhance mitochondrial function and down-regulate the expression of apoptotic mediators.
KD has also been shown to help reduce the blood sugar response caused by diet, so it may represent a beneficial adjuvant therapy for type 2 diabetes.
In addition, it has been found that strict KD can change the amino acid metabolism in cancer cells and enhance the efficacy of chemotherapy and radiotherapy.
Recent studies have shown that KD-related intestinal flora reduces the accumulation of intestinal Th17 cells, suggesting its potential anti-inflammatory effects.
Emerging evidence suggests that it can be used in a variety of diseases, and few studies have investigated whether KD can be used to relieve intestinal inflammation or examine its effect on the intestinal flora and immune cells in the inflammatory microenvironment.
In this study, the gut microbiome and metabolic changes of mice fed with KD, low carbohydrate diet (LCD) or normal diet (ND) were compared.
In addition, the study used a colitis model induced by dextran sulfate sodium sulfate (DSS) to study the effects of KD on inflammation, intestinal microbiome, mucosal barrier, and immunity.
Finally, the study used fecal microbiota transplantation (FMT) in a sterile (GF) mouse model to elucidate the beneficial effects of KD-modified gut microbiome on intestinal inflammation.
This finding shows that KD is a promising diet therapy for the treatment of intestinal inflammation and proves its regulating effect on the intestinal flora.
Reference message:
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature Inflammatory Bowel Disease (IBD) is a complex chronic inflammatory disease involving multiple genetic and environmental drivers.
More and more evidence shows that ketogenic diets (KDs) mediate the rise of circulating ketone bodies and exert potential anti-inflammatory effects.
However, the consequences of this unique diet on colitis are still unknown.
On April 23, 2021, Ma Yanlei of Fudan University, Qin Huanlong of Tongji University, and Ajay Goel of the Beckman Institute in the United States (Tongji University is the first unit) jointly published an online communication titled " Ketogenic diet alleviates colitis by reduction of colonic group 3 innate lymphoid cells through altering gut microbiome" research paper, this study compared small diets fed with ketogenic diet (KDs), low carbohydrate diet (LCD) or normal diet (ND) Changes in the intestinal microbiome and metabolism of mice.
In addition, the study used a colitis model induced by dextran sulfate sodium sulfate (DSS) to study the effects of KD on inflammation, intestinal microbiome, mucosal barrier, and immunity.
The research used transcriptome sequencing, RT2 profiler PCR array, histopathology and immunofluorescence analysis of colon tissue, analysis of serum samples through metabolic assay kits, analysis of fecal samples through 16S rRNA gene sequencing, liquid chromatography-mass spectrometry and gas chromatography-mass spectrometry .
The study observed that KD reduced colitis in a different way from LCD by changing the intestinal flora and metabolites.
Quantitative diet experiments confirmed the unique influence of KD relative to LCD.
After colitis is induced, KD protects the intestinal barrier function and reduces the production of ILC3s cells and related inflammatory cytokines (IL-17α, IL-18, IL-22, Ccl4).
Finally, transplanting fecal flora into sterile mice showed that KD-mediated colitis suppression and ILC3 regulation depend on the modification of intestinal flora.
In summary, this study puts forward an overall view of the changes in microbiome metabolism that occur during the treatment of KD colitis, and confirms that the regulation of the gut microbiome and ILC3s is a new target involving IBD diet therapy.
Inflammatory bowel disease (IBD) is a complex chronic inflammatory disease involving multiple genetic and environmental drivers.
For example, a high-salt diet exacerbates intestinal inflammation by reducing the abundance of lactobacilli and the metabolism of butyrate, while a high-fat diet contributes to IBD.
Although enteral nutrition has shown clinical promise to promote the remission of Crohn's disease, it is still unclear whether dietary therapy can help treat ulcerative colitis.
Ketogenic diet (KD) is a diet therapy characterized by high fat and low carbohydrates.
It was originally used to treat drug-resistant epilepsy, but it has recently become a promising treatment for chronic diseases and human malignancies.
universal.
In Alzheimer's disease, KD can not only protect senescent nerve cells, but also enhance mitochondrial function and down-regulate the expression of apoptotic mediators.
KD has also been shown to help reduce the blood sugar response caused by diet, so it may represent a beneficial adjuvant therapy for type 2 diabetes.
In addition, it has been found that strict KD can change the amino acid metabolism in cancer cells and enhance the efficacy of chemotherapy and radiotherapy.
Recent studies have shown that KD-related intestinal flora reduces the accumulation of intestinal Th17 cells, suggesting its potential anti-inflammatory effects.
Emerging evidence suggests that it can be used in a variety of diseases, and few studies have investigated whether KD can be used to relieve intestinal inflammation or examine its effect on the intestinal flora and immune cells in the inflammatory microenvironment.
In this study, the gut microbiome and metabolic changes of mice fed with KD, low carbohydrate diet (LCD) or normal diet (ND) were compared.
In addition, the study used a colitis model induced by dextran sulfate sodium sulfate (DSS) to study the effects of KD on inflammation, intestinal microbiome, mucosal barrier, and immunity.
Finally, the study used fecal microbiota transplantation (FMT) in a sterile (GF) mouse model to elucidate the beneficial effects of KD-modified gut microbiome on intestinal inflammation.
This finding shows that KD is a promising diet therapy for the treatment of intestinal inflammation and proves its regulating effect on the intestinal flora.
Reference message:
