Similar Datasets
Project description:High fat diets (HFDs) are linked to several diseases including obesity, diabetes, insulin resistance, fatty liver, and susceptibility to inflammatory bowel disease (IBD) in both mouse and humans. RNA-seq from male mice (C57BL/6N) fed Vivarium Chow (VIV) or any one of three high fat diets (40% kcal fat) (SO+CO, PL+CO, CO) for 24 weeks was performed on four segments of the intestinal tract (Duodenum, Jejunum, Terminal Ileum and Proximal Colon).
2023-03-01 | GSE220302 | GEO
Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.
2016-02-16 | E-GEOD-67324 | biostudies-arrayexpress
Project description:The aim of this study was to characterize the metabolomic and proteomic changes in the intestinal tissue of weaned piglets fed with diets containing Spirulina as an ingredient (10% incorporation in the diet), combining such information with histomorphology data.
2022-09-20 | PXD030446 | Pride
Project description:High fat effect on mouse intestinal stem cells
| PRJNA636084 | ENA
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: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.
2015-09-01 | GSE47570 | GEO
Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors.
2016-02-16 | GSE67324 | GEO
Project description:The present study was conducted to evaluate the effects of the intake of three types of coffee (caffeinated, decaffeinated, and green unroasted coffee) on the livers of C57BL/6J mice fed a high-fat diet, and to extensively elucidate the physiological responses to coffee intake by analysing the findings obtained from a comprehensive transcriptomic analysis using DNA microarrays. The present study was conducted to evaluate the effects of the intake of three types of coffee (caffeinated, decaffeinated, and green unroasted coffee) on the livers of C57BL/6J mice fed a high-fat diet, and to extensively elucidate the physiological responses to coffee intake by analysing the findings obtained from a comprehensive transcriptomic analysis using DNA microarrays. Briefly, 7-week-old male C57BL/6J mice purchased from Charles River Laboratories Japan (Yokohama) were divided into the following five groups. The normal diet group (ND group) was fed D12450B (10 kcal% fat, Research Diets, New Brunswick, NJ, USA). The high-fat diet group (HF group) was fed D12492 (60 kcal% fat, Research Diets, New Brunswick, NJ, USA). The caffeinated coffee group (HFCC group) was fed a high-fat diet containing 2% caffeinated freeze-dried coffee. The decaffeinated coffee group (HFDC group) was fed a high-fat diet containing 2% decaffeinated freeze-dried coffee. The green unroasted coffee group (HFGC group) was fed a high-fat diet containing 2% unroasted caffeinated freeze-dried coffee. The mice had ad libitum access to their diets and drinking water. After 9 weeks, mice were sacrificed and the livers were subjected to the Affymrtix DNA microarray experiment.
2013-12-10 | E-GEOD-53131 | biostudies-arrayexpress
Project description:In this study we assessed the intestinal proteome of Atlantic salmon from four groups that were fed different diets. We employed isobaric tags for relative and absolute quantification and 2D LC-MS/MS approach for quantifying the proteins. The proteins described here can be exploited to alleviate intestinal inflammation in fish and higher vertebrates.
2022-02-14 | PXD027922 | Pride
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