Ontology highlight
ABSTRACT:
PROVIDER: PRJNA484010 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7648360.fastq.gz | Fastqsanger.gz | |||
| SRR7648361.fastq.gz | Fastqsanger.gz | |||
| SRR7648362.fastq.gz | Fastqsanger.gz | |||
| SRR7648363.fastq.gz | Fastqsanger.gz |
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Project description:Although obesity is a modifiable risk factor for pancreatic cancer, the role of dietary changes that lead to weight loss in pancreatic carcinogenesis remains unknown. Thus, we determined the effects of weight normalization via dietary switch on pancreatic carcinogenesis and the associated mechanisms. Five-week-old male and female LSL-KrasG12D/+; p48Cre/+ (KC) mice (8-12/diet group/sex) were fed a high-fat, diet-induced obesity diet (DIO; 60 kCal% energy from fat) or a low-fat, control diet (CD; 11 kCal% energy from fat) for 21 weeks. A subset of mice was fed the DIO for 8 weeks, then switched to a CD for 13 additional weeks (DIO→CD). Cancer incidence was evaluated by histology. Lipidomics and RNAseq followed by bioinformatic analysis were conducted to identify possible mechanisms. The gut microbiome was characterized using 16s rRNA amplicon sequencing. After 21 weeks, DIO-fed mice had significantly higher body weight, fat mass, and pancreatic acinar-to-ductal metaplasia compared to the other 2 groups. While none of the 21 mice fed a CD developed cancer, 2 out of 21 DIO-fed mice did. Switching from a DIO to a CD normalized body weight and composition, reduced acinar-to-ductal metaplasia and prevented cancer incidence with no mice developing cancer. Mechanistically, the DIO affected the expression of genes regulating cellular metabolism, immune function, and cell-signaling, while CD and DIO→CD had similar global gene expression. Moreover, DIO increased epoxy metabolites of linoleic acid, which were mitigated by the dietary switch. Finally, compared to a CD, DIO altered the gut microbiome and switching from a DIO to a CD restored the gut microbiome profile to one close to the mice fed a CD. Body weight normalization mitigates obesity-accelerated pancreatic carcinogenesis, in part, by affecting inflammatory and cell signaling pathways, reducing epoxy metabolites, and modulating the gut microbiome.
2025-08-30 | GSE293790 | GEO
Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver. Adult male Wistar rats were fed diets with varying amounts of protein, carbohydrates and fat for 5 weeks. At the end of the experiment, rats were killed and tanscriptome analysis was performed on pooled liver samples.
2015-09-01 | E-GEOD-47570 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) continues to be a major health problem. A ketogenic diet (KD), characterized by a very low carbohydrate and high fat composition, has gained attention for its anti-tumor potential. We evaluated the effect and mechanisms of feeding a strict KD alone or in combination with gemcitabine in the autochthonous LSL-KrasG12D/+; LSL- Trp53 R172H/+; Pdx1-Cre (KPC) mouse model. For this purpose, both male and female pancreatic tumor-bearing KPC mice were allocated to a control diet (CD; %kcal: 70% carb, 14% protein, 16% fat), a KD (%kcal: 14% protein, 1% carb, 85% fat), a CD + gemcitabine (CG), or a KD + gemcitabine (KG) group. Mice fed a KD alone or in combination with gemcitabine showed significantly increased blood β-hydroxybutyrate levels compared to mice fed a CD or CG. KPC mice fed a KG had a significant increase in overall median survival compared to KPC mice fed a CD (increased overall median survival by 42%). Interestingly, when the data was disaggregated by sex, the effect of a KG was significant in female KPC mice (60% increase in median overall survival), but not in male KPC mice (28% increase in median overall survival). Mechanistically, the enhanced survival response to a KD combined with gemcitabine was multifactorial, including inhibition of ERK and AKT pathways, regulation of fatty acid metabolism and the modulation of the gut microbiota. In summary, a KD in combination with gemcitabine appears beneficial as a treatment strategy in PDAC in KPC mice, deserving further clinical evaluation.
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Project description:In this study, the minimal consortium Oligo-Mouse Microbiota (OMM)12 was used to study the function of Coriobacteriia under defined conditions in gnotobiotic mice. OMM12 mice with or without adding the dominant gut bacterium Eggerthella lenta were fed with diets varying in fat content or supplemented with primary bile acids. Changes in the host liver proteomes were studied using untargeted proteomics.
2024-01-19 | PXD047016 | Pride
Project description:Regulatory innovation is central to the evolution of species. Different nutritional sources are one environmental pressure that can select for novel regulatory elements. Dietary composition changes, including exposure to “western” diets with excess fat content, can lead to transcriptional regulatory changes in the liver. In order to investigate how transcriptional regulatory changes in response to a high fat diet diverge across species, we profiled chromatin accessibility, histone modifications and the transcriptome in livers of rhesus macaques and mice fed high fat and normal diets.
2021-04-01 | GSE160247 | GEO
Project description:Transcriptional profiling in subcutaneous adipose tissue of 48 pigs aged (132 days of age) originated from two lines divergently selected for residual feed intake (RFI) : low-RFI pigs (RFIneg), high-RFI pigs (RFIpl). Both lines were offered isocaloric and isoproteic diets with contrasted energy source and nutrients: low fat, low fiber (LF) diet or a high fat, high fiber (HF)diet during 10 weeks. Effects of RFI selection, diet and interaction between diet and line were investigated. Four experimental groups: low-RFI pigs fed high fat, high fiber diet (HF_RFIneg), high-RFI pigs fed high fat, high fiber diet(HF_RFIpl), low-RFI pigs fed low fat, low fiber diet (LF_RFIneg) and high-RFI pigs fed low fat, low fiber diet(LF_RFIpl). 12 pigs per condition. One replicate per array.
2016-07-01 | E-GEOD-70836 | biostudies-arrayexpress
Project description:High fat diet (HF) rodent models have contributed significantly to the dissection of the pathophysiology of the insulin resistance syndrome, but their phenotype varies distinctly between different studies. Here, we have analyzed gene expression patterns in livers of animals fed with different HF with varying fatty acid compositions. Experiment Overall Design: Male Wistar rats were fed with high fat diets (42 energy%, fat sources: lard, olive oil; coconut fat; cod liver oil). Weight, food intake, whole body insulin tolerance and plasma parameters of glucose and lipid metabolism were measured during a 12 week diet course. Liver histologies and hepatic gene expression profiles using AffymetrixR gene chips were obtained.
2007-10-10 | E-GEOD-3512 | biostudies-arrayexpress
Project description:Overnutrition during pregnancy inM-oM-,M-^Buences the future health of the offspring, with outcomes differing depending on the childM-bM-^@M-^Ys sex. The placenta is involved in the programming of obesity, type 2 diabetes and cardiovascular disease. Sex-specific adaptation of the placenta may be central to the differences in fetal growth and survival. The impact of diet and fetal sex on placental gene expression and epigenetic marks was investigated in mice fed a high-fat (HFD) or a control diet (CD), during the first 15 days of gestation Microarrays analysis revealed that expression was affected by maternal diet and was sexually dimorphic. We analyzed the placentae of 4 mice litters fed with an high-fat diet (HFD) and 4 with a control diet (CD). For each litter, the placenta transcriptome was analysed according to the foetus sex using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.
2012-03-31 | E-GEOD-29585 | biostudies-arrayexpress
Project description:Aging alters gastrointestinal morphology, microbiota, and functionality, and is associated with increased incidence of intestinal disease. The mechanisms that contribute to these changes are poorly described. Gene expression in dogs has been evaluated for a few select genes under pathogenic or varying dietary conditions, but global gene expression profiles of aged versus young adult dogs have not been compared previously. Thus, we used canine microarrays to compare gene expression profiles of colonic epithelial tissue from geriatric and young adult dogs fed 2 different diets. Colon tissue samples were collected from 6 geriatric (12 yr-old) and 6 young adult (1 yr-old) female beagles after being fed one of two diets (animal protein-based versus plant-protein based) for 12 months. RNA samples were hybridized to Affymetrix GeneChip Canine Genome Arrays. Statistical analyses indicated that age had the greatest impact on gene expression, with 212 genes differentially expressed in geriatric dogs. Although not as robust as age, diet affected mRNA abundance of 66 genes. The effect of age was most notable, with increased expression in genes related to inflammation, stress response, cellular metabolism and cell proliferation and decreased expression in genes associated with apoptosis and defense mechanism in senior dogs. The effect of diet on gene expression was not consistent, but appeared to have a greater response in senior dogs. Six geriatric (11.1 yr old) and 6 weanling (8 wk old) female beagles were used. Three dogs of each age were assigned to one of two dietary treatments and fed for 12 months. Diets tested in this experiment were previously shown to manipulate energy metabolism. One diet was an animal-protein based diet (APB) and was composed primarily of highly digestible ingredients and animal-derived protein and fat sources (brewer’s rice, poultry by-product meal, poultry fat) and was formulated to contain 28% protein, 23% fat, and 5% dietary fiber. The other diet was a plant-protein based diet (PPB) and was composed primarily of moderately digestible plant-derived ingredients (corn, soybean meal, wheat middlings, and meat and bone meal) and was formulated to contain 26% protein, 11% fat, and 15% dietary fiber. Although the two diets were very different in terms of ingredient and chemical composition, both were formulated to meet or exceed all nutrient requirements for canine growth according to the Association of American Feed Control Officials. Young dogs were fed ad libitum to allow for adequate growth, while geriatric dogs were fed to maintain baseline BW throughout the experiment. To produce the desired metabolic effects, the PPB diet was formulated to contain a lower caloric density (APB = 5.38 kcal/g; PPB = 4.75 kcal/g) and have a lower nutrient digestibility than the APB diet. Thus, dogs fed the PPB diet needed to consume a greater (P<0.05) quantity of food (237 g/d; 1123 kcal/d) than dogs fed the APB diet (166 g/d; 893 kcal/d) to grow (young) or maintain BW (geriatrics). Even though metabolic indices were altered, mean BW among dietary treatments was not different at any time over the course of the study for young or geriatric dogs. After 12 months on experiment, animals were fasted for 12 hr and then given a lethal dose (130 mg/kg BW) of sodium pentobarbital (Euthasol, Virbac Corp., Fort Worth, TX) intravenously into the left forearm. Death was confirmed by lack of respiration and a corneal reflex, and absence of a heartbeat detected with a stethoscope placed under the left elbow. Colon samples were collected immediately after death was confirmed, flash frozen using liquid nitrogen, and stored at -80oC. Frozen samples were placed in RNAlater-ICE until epithelial layer could be scraped off and used for microarray analysis.
2010-08-01 | E-GEOD-20557 | biostudies-arrayexpress
Project description:De novo lipogenesis (DNL) has been implicated in the development and progression of hepatic liver steatosis. Hepatic DNL is strongly influenced by dietary macronutrient composition with diets high in carbohydrate increasing DNL and diets high in fat decreasing DNL. The enzymes in the core DNL pathway have been well characterised however less is known about proteins that play accessory or regulatory roles in DNL. In the current study, we associate measured rates of hepatic DNL and liver fat content with abundance of liver proteins from liquid chromatography mass spectrometry in mice to identify known and uncharacterised proteins that may have a role in DNL. Male C57BL/6J mice were fed either a standard chow diet a semi-purified high starch diet or a high fat diet. Both semi-purified diets resulted in increased body weight, fat mass and liver triglyceride content compared to chow-fed mice while hepatic DNL was increased in the high starch fed mice and decreased in the high fat fed mice. Proteomic analysis was carried out on the livers of these mice and proteins were identified that associated with either the rate of DNL or triglyceride content in the liver. There was no overlap between DNL and triglyceride associated proteins. We identify novel proteins associated with DNL that are involved in taurine metabolism, which suggests a link between these pathways. Further analysis identified proteins that are differentially regulated when comparing a non-purified chow diet to either of the semi-purified diets to provide a set of proteins that are regulated by the degree of dietary complexity alone. Finally, we compared the liver proteome between 4 week-fed and 30-week diet-fed mice and found remarkable similarity suggesting that the majority of diet-regulated proteins change early in response to differing dietary components.
2024-10-30 | PXD054323 | Pride