Ramadan fasting shift the human gut microbiota with influence of diet changes
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ABSTRACT:
PROVIDER: PRJEB38231 | ENA |
REPOSITORIES: ENA
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Project description:To investigate whether the fasting-mimicking diet (FMD) affects intratumor immunity, we assessed the impact of one FMD cycle before surgery in matched tumor tissue specimens from 22 early-stage breast cancer patients. At the tumor level, FMD activated antitumor immune programs in early-stage breast cancer patients.
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Project description:The metabolic syndrome represents a cluster of well-documented risk factors for the development of type 2 diabetes and cardiovascular disease. Next to visceral obesity, dyslipidemia and insulin resistance, excessive triglyceride accumulation in the liver has been implicated to play a role in the development of the metabolic syndrome. To investigate the underlying molecular changes leading to hepatic steatosis we performed microarray analysis on livers of mice either fasted over night or fed a high fat diet for 2 Weeks. We analysed 7 500 genes and subsequently performed a pathway analysis to identify changes in hepatic genes in both models. Fasting induced a high number of differentially expressed hepatic genes, resulting in an change towards an energy saving phenotype. In contrast only a small number of genes were differentially expressed after high fat diet. Fasting promoted gluconeogenesis and b-oxidation, strongly suppressed cholesterol synthesis and activated pathways to preserve hepatic function. High fat diet induced steatosis was accompanied by the activation of the stearoyl-CoA desaturase and the lipogenic transcription factor Srebp-1c, both implicated in the development of hepatic insulin resistance. These changes reflect the activation of different gene expression programs in response to plasma lipid overload. Keywords: Diet intervention Two conditions, fasting and high fat diet. 5 biological replicates for comparison of high fat diet versus fasting and controls versus high fat diet, 4 biological replicates for the comparison of controls versus fasting. All biological replicates are performed as technical replicates in the form of a dye-swap. Total number of arrays hybridises is therefore 28.
2011-04-02 | E-GEOD-8576 | biostudies-arrayexpress
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Project description:Background & Aims: The complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis. Methods: To examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or dextran sodium sulfate colitis model. Results: Diet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other. Conclusions: Our results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation. Keywords: IBD; Diet; Microbiota; Mouse Models; Systems Biology
2017-10-30 | GSE104461 | GEO
Project description:To understand the transcriptional effect of fasting and feeding a ketogenic diet on mouse CNS astrocytes, we performed translating ribosomal affinity purification (TRAP) of mRNAs immunoprecipitated from hippocampus. TRAP mice express a ribosomal epitope tag upon Cre-induced recombination that can be immunoprecipitated following activation. We measured the abundance of actively translating mRNAs from a ribosomal pull-down that came from adult astrocyte (Aldh1l1-Cre)-specific TRAP mice that were subjected to one of three dietary conditions: four weeks of normal chow diet, four weeks of ketogenic diet (high-fat, low-carbohydrate)43, or an 18-hour fast. Immediately following the respective diets, forebrain and hippocampus was harvested from all groups, ribosomes were immunoprecipitated, and actively translating mRNAs in the ribosomes were purified.
2021-05-24 | GSE169625 | GEO
Project description:Diet-induced obesity is the central cause of diabetes, cardiovascular disease as well as metabolic syndrome. Here, we have studied the efficacy of cycles of a 4-5 day fasting mimicking diet (FMD) in inhibiting high-fat, high calorie diet (HFCD) -induced obesity in mature female C57BL/6 mice. We show that a monthly 5-day cycle of FMD inhibit HFCD-mediated obesity by causing a reduction in calorie intake and accumulation of visceral and subcutaneous fat depots without lean body mass loss. FMD cycles also increase cardiac vascularity, function and stress resistance, and reverse the hypercholesterolemia caused by the HFCD. The sustained activation of adipocyte genes associated with mitochondrial metabolism and biogenesis and the sustained ketogenesis in the HFCD-fed mice subjected to monthly cycles of FMD indicate a reprogramming of fat cell metabolism that is likely to be at the center of obesity reversal. All these improvements could explain the protection from early mortality elicited by the high-fat, high calorie diet.
2021-08-19 | GSE163060 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is most prevalent form of liver disease, affecting over 30% of Americans. Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and their potential role in the increasing global incidence of NAFLD. Male C57BL/6 mice were fed with either a low-fat diet (11% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42g/L) diet with or without PFOS or PFHxS in feed (0.0003% w/w) for 29 weeks. Proteomic, lipidomic, and gene expression measurement techniques were utilized to explore mechanistic pathways. With administration of a high fat high carbohydrate (HFHC) diet, PFOS and PFHxS augmented macrovesicular steatosis, indicative of fatty liver. There was a clear shift in the lipidome of the serum phosphatidylcholines, phosphatidylethanolamines, and triglycerides with PFAS exposure. Finally, chain length exerted significant influence on tissue partitioning and the resulting hepatic gene and protein signatures of PFHxS and PFOS in vivo.
2020-09-15 | PXD015976 | Pride
Project description:The metabolic syndrome represents a cluster of well-documented risk factors for the development of type 2 diabetes and cardiovascular disease. Next to visceral obesity, dyslipidemia and insulin resistance, excessive triglyceride accumulation in the liver has been implicated to play a role in the development of the metabolic syndrome. To investigate the underlying molecular changes leading to hepatic steatosis we performed microarray analysis on livers of mice either fasted over night or fed a high fat diet for 2 Weeks. We analysed 7 500 genes and subsequently performed a pathway analysis to identify changes in hepatic genes in both models. Fasting induced a high number of differentially expressed hepatic genes, resulting in an change towards an energy saving phenotype. In contrast only a small number of genes were differentially expressed after high fat diet. Fasting promoted gluconeogenesis and b-oxidation, strongly suppressed cholesterol synthesis and activated pathways to preserve hepatic function. High fat diet induced steatosis was accompanied by the activation of the stearoyl-CoA desaturase and the lipogenic transcription factor Srebp-1c, both implicated in the development of hepatic insulin resistance. These changes reflect the activation of different gene expression programs in response to plasma lipid overload. Keywords: Diet intervention
2011-04-02 | GSE8576 | GEO