Mouse gut metagenome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR149053_1.fastq.gz | Fastqsanger.gz | |||
| DRR149053_2.fastq.gz | Fastqsanger.gz | |||
| DRR149054_1.fastq.gz | Fastqsanger.gz | |||
| DRR149054_2.fastq.gz | Fastqsanger.gz | |||
| DRR149055_1.fastq.gz | Fastqsanger.gz |
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Project description:Ketone body receptor GPR43 regulates lipid metabolism under fasting condition
| PRJDB7362 | ENA
Project description:Interventions: Nutrition counseling We provide outpatient nutritional guidance once a month for 30 minutes. It can be calculated once a month as an outpatient nutrition dietary guidance fee. The modified MCT ketogenic diet is 2-3 meals a day, prepared under the supervision of a registered dietitian, and you can cook your own food according to the following rules, or obtain low-carbohydrate foods at the supermarket or the Internet. .. Meal purchase funds will be borne by the patient. Cooking recipes will be distributed at the start of clinical research. 7 rules of dietary intake 1. The target energy intake is 35-40 kcal per body weight. 2. Eat 1.6-2.0 g of protein-rich foods (meat, fish, eggs, soy products) per body weight. 3. Take at least 4g of EPA daily. 4. Limit the amount of sugar to 25 g or less per day (when the body weight is 50 kg). 5. Ingest 60 to 100 g of medium-chain fatty acids per day in terms of MCT oil. 6. The weight of the meal is morning: noon: evening = 4: 10: 6, and the weight is adjusted so that the person feels hungry before going to bed. 7. The target ketone ratio is 1.4 to 1.6: 1. Estimated implementation period and meal contents (see A and B below) 1. First 3 months: Super ketogenic. 2. From 3 months to 1 year: Continue to eat ketogenic diet, mainly super ketogenic. 3. After the above research period is exceeded, we will instruct them to continue ketogenic and semi-ketogenic Level of carbohydrate restriction 1. Semi-ketogenic Ketone ratio Lipid: Sugar + Protein = 1: 1 Sugar intake 80 g / day or less Lipid intake: flaxseed oil 30 g / day, MCT oil 80 mg / day (total fat 110 g) 2. Ketogenic Ketone ratio Lipid: Sugar + Protein = 1.4: 1 Sugar intake 40 g / day or less Lipid intake: flaxseed oil 30 g / day, MCT oil 80 mg / day (total fat 110
Primary outcome(s): Safety Presence or absence of diarrhea or allergic symptoms b. Dehydration, symptomatological hypoglycemia, excessive ketosis, gastrointestinal symptoms Nutritional status (body weight, body composition analysis using In Body (BIA), serum albumin, serum cholinesterase, serum transthyretin, CRP), QOL score (EORTCQLQ-CR38 Japanese version, POMS2 Japanese version)
Study Design: Single arm Non-randomized
| 2723656 | ecrin-mdr-crc
Project description:Ketone bodies are an alternate fuel source generated by the liver in response to low carbohydrate availability in neonates and after starvation and exhausting exercise in adulthood. The postnatal alternative splicing generates a highly conserved muscle-specific MEF2D⍺2 protein isoform of the transcription factor MEF2D. Here, we discovered that compared to WT mice, MEF2D⍺2 exon knockout (Eko) mice displayed reduced running capacity and muscle expression of all three ketolytic genes, BDH1, OXCT1, and ACAT1. Consistent with reduced muscle utilization of ketone bodies, MEF2D⍺2 Eko mice also showed increased ketone body levels in a tolerance test, after exercise, and upon feeding a ketogenic diet. Lastly, using mitochondria isolated from skeletal muscle, we showed reduced ketone body utilization and respiration in Eko compared to WT mice. Thus, we identified a new role of MEF2D⍺2 protein isoform in regulating skeletal muscle ketone body oxidation, exercise capacity, and its effect on systemic ketone body levels.
2025-07-18 | GSE302518 | GEO
Project description:Influenza A virus (IAV) infection-associated morbidity and mortality are a key global healthcare concern, necessitating the identification of novel therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing anti-viral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet, as neither feeding mice a high-fat high-carbohydrate diet nor providing chemical ketone body substrate that bypasses hepatic ketogenesis protected against infection. Therefore, KD mediated immune-metabolic integration represents a viable avenue towards preventing or alleviating influenza disease.
2019-08-29 | GSE136536 | GEO
Project description:The ketone body β-hydroxybutyrate (BHB) is produced during dietary restriction, fasting, and exercise. A ketogenic diet (KD) results in long-term production of BHB outside of these contexts. We sought to determine a protein-matched, non-obese ketogenic diet (KD) would affect the longevity and healthspan of C57BL/6 male mice. We find that feeding KD every-other-week to prevent obesity (cyclic KD) reduces mid-life mortality but does not affect maximum lifespan. Similar feeding of a non-ketogenic high-fat/low-carbohydrate (HF) diet may have an intermediate effect on mortality. Cyclic KD improves memory performance in old age, while modestly improving composite measures of healthspan. RNAseq gene expression analysis identifies down-regulation of insulin, TOR, and fatty acid synthesis pathways as possible longevity mechanisms common to KD and HF. However, up-regulation of fasting-related PPARα target genes is unique to KD, consistent across tissues, and preserved in old age, suggesting a mechanism for an incremental benefit from KD. In all, we show that a non-obese ketogenic diet improves survival, memory, and healthspan into old age. These gene expression studies were carried out on 12 month-old male C56BL/6 mice from the NIA Aged Rodent Colony, habituated to AIN-93M control diet and then either maintained on this diet or switched for one week to a 75% kcal fat non-ketogenic high-fat diet or a 90% kcal fat ketogenic diet (all diets with 10% kcal from carbohydrates). Tissues were harvested in the middle of the nighttime feeding period (MN-3am).
2017-09-05 | GSE101657 | GEO
Project description:Chronic neural inflammation is the key pathology of neuropathic pain. The ketogenic diet (KD) has been shown to reduce neural inflammation and hyperexcitability in Alzheimer's disease. However, the function and mechanism of KD in neuropathic pain remains unclear. In this study, we first found that the KD production was decreased upon neuropathic pain induced by chronic constriction injury (CCI). Then we demonstrated that KD effectively alleviated CCI-induced thermal hyperalgesia and mechanical allodynia and relieved neuroinflammation by reducing microglia activation and pro-inflammatory cytokines. β-hydroxybutyrate (BHB), a major component of KD, reduced ROS production by enhancing mitochondrial membrane potential in microglia, thereby decreasing microglia-induced inflammatory responses. In vivo and in vitro experiments revealed that the expression of UCP2, SIRT3 and PGC-1α expression in the spinal dorsal horn was increased by KD. SIRT3-deficiency abolished the protective function of KD on neuropathic pain. Additionally, SIRT3 deficiency decreased BHB production due to the reduced expression of ketone body synthases in the liver and ketone body-utilizing enzymes in the spinal dorsal horn. These findings suggest that SIRT3 is a promising therapeutic target for neuropathic pain, particularly in the context of a ketogenic diet, which may inspire novel therapeutic strategies and potentially improve patient prognosis and quality of life.
2025-05-29 | GSE277072 | GEO
Project description:There is currently no established treatment for Cockayne syndrome, a disease characterized by progressive early onset neurodegeneration with features of premature aging and death in childhood. Here, we tested if acetyl-CoA precursors, citrate and beta-hydroxybutyrate, could reduce features of Cockayne syndrome. We identified the gene Helicase 89B (Hel89B) as a homologue of CSB in drosophila and found that the ketone beta-hydroxybutyrate rescued features of premature aging in Hel89B deficient flies. In mammals, loss of the citrate carrier Indy exacerbated the phenotype of Csbm/m mice, rescued by a ketogenic diet. The rescue effect appeared to be mediated through ketone stimulated histone acetylation and facilitation of transcriptional resolution of non-B DNA. Notably, this appears to be a common effect of a ketogenic diet.
2024-01-01 | GSE207368 | GEO
Project description:Rationale: Sepsis patients suffer from severe metabolic and immunologic dysfunction that may be amplified by standard carbohydrate-based nutritional regimes. We therefore hypothesize that a ketogenic diet improves sepsis treatment. Objectives: We investigated the safety and feasibility of a ketogenic diet in sepsis patients. Methods: We conducted a monocentric open-labeled randomized controlled trial (DRKS00017710) enrolling adult sepsis patients randomly assigned to either ketogenic or standard high-carbohydrate diet for 14 days with follow-up until day 30. The primary outcome measure was β-hydroxybutyrate serum concentration on day 14. Secondary outcomes included safety, clinical and immunological changes. Measurements and Main Results: 40 critically ill septic patients were assigned to the study groups. Increase in β-hydroxybutyrate concentrations from baseline to day 14 was markedly greater under ketogenic diet (1.2 ±0.9) compared to controls (-0.3 ±0.4); estimated mean difference 1.4 (95%-CI 1.0-1.8; p<0.0001). During ketogenic diet, no patient required insulin treatment beyond day 4, whereas 35% to 60% of control patients did (p=0.0095). Metabolic side effects were not observed under ketogenic diet. Ventilation-free (IRR 1.7; 95%-CI: 1.5 to 2.1; p<0.0001), vasopressor-free (IRR 1.7; 95%-CI: 1.5 to 2.0; p<0.0001), dialysis-free (IRR 1.5; 95%-CI: 1.3 to 1.8; p<0.0001), and ICU-free days (IRR 1.7; 95%-CI: 1.4 to 2.1; p<0.0001) significantly increased in patients under ketogenic diet. There was no difference in 30-day mortality. Analyses indicated favorable changes towards immune homeostasis. Conclusions: Ketogenic diet is a feasible and safe nutritional regimen in septic patients promoting recovery from sepsis-related organ dysfunction and could become a new tool in modern treatment concepts.
2024-06-13 | PXD046061 | Pride
Project description:Peroxisome Proliferator-Activated receptor α (PPARα) and cAMP-Responsive Element Binding Protein 3-Like 3 (CREB3L3) are transcription factors involved in the regulation of lipid metabolism in the liver. The aim of the present study was to characterize the interrelationship between PPARα and CREB3L3 in regulating hepatic gene expression. Male wildtype, PPARα-/-, CREB3L3-/- and combined PPARα/CREB3L3-/- mice were subjected to a 16-hour fast or 4 days of ketogenic diet. Whole genome expression analysis was performed on liver samples. Under conditions of overnight fasting, the effects of PPARα ablation and CREB3L3 ablation on plasma triglyceride, plasma β-hydroxybutyrate, and hepatic gene expression were largely disparate, and showed only limited interdependence. Gene and pathway analysis underscored the importance of CREB3L3 in regulating (apo)lipoprotein metabolism, and of PPARα as master regulator of intracellular lipid metabolism. A small number of genes, including Fgf21 and Mfsd2a, were under dual control of PPARα and CREB3L3. By contrast, a strong interaction between PPARα and CREB3L3 ablation was observed during ketogenic diet feeding. Specifically, the pronounced effects of CREB3L3 ablation on liver damage and hepatic gene expression during ketogenic diet were almost completely abolished by the simultaneous ablation of PPARα. Loss of CREB3L3 influenced PPARα signalling in two major ways. Firstly, it reduced expression of PPARα and its target genes involved in fatty acid oxidation and ketogenesis. In stark contrast, the hepatoproliferative function of PPARα was markedly activated by loss of CREB3L3. These data indicate that CREB3L3 ablation uncouples the hepatoproliferative and lipid metabolic effects of PPARα. Overall, except for the shared regulation of a very limited number of genes, the roles of PPARα and CREB3L3 in hepatic lipid metabolism are clearly distinct and are highly dependent on dietary status.
2019-01-23 | GSE121096 | GEO
Project description:Targeting Ketone Body Metabolism in Mitigating Gemcitabine Resistance
| PRJNA1176263 | ENA