Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from livers of C57BL/6J mice fed a high-fat diet and coffee

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Shoko Takahashi

PROVIDER: E-GEOD-53131 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

An integrated multi-omics study revealed metabolic alterations underlying the effects of coffee consumption.

Takahashi Shoko S Saito Kenji K Jia Huijuan H Kato Hisanori H

PloS one 20140311 3

Many epidemiological studies have indicated that coffee consumption may reduce the risks of developing obesity and diabetes, but the underlying mechanisms of these effects are poorly understood. Our previous study revealed the changes on gene expression profiles in the livers of C57BL/6J mice fed a high-fat diet containing three types of coffee (caffeinated, decaffeinated and green unroasted coffee), using DNA microarrays. The results revealed remarkable alterations in lipid metabolism-related m ...[more]

PMID: 24618914

Similar Datasets

Project description:Obesity and diabetes associated visual impairment and vascular dysfunctions are increasing reasons for vision loss. The detailed mechanisms in these diseases are still largely unknown, but mice models have been useful to study these mechanisms and explore the detailed effects of potential compounds. Such compounds usually have antioxidant and anti-inflammatory properties. These properties are found in anthocyanins and a major source of dietary anthocyanins in Nordic diet is bilberries (European wild blueberries, Vaccinium myrtillus). In this explorative study we show results with differentially expressed genes in retina using a high-fat diet (HFD) mouse model. Our findings displayed differential regulation of genes in pathways for apoptosis, inflammation and oxidative stress, especially systemic lupus erythematosus (SLE), mitogen activated protein kinase (MAPK) and glutathione metabolism. Mice fed with HFD had increased retinal gene expression of several crystallins, which was reduced in the retina of mice fed with bilberries. Bilberries seem to reduce the expression of genes in MAPK and to increase the expression of genes in glutathione metabolism pathway. All together despite minor effects in the mouse phenotype, a diet rich in bilberries may prevent the retinal gene expression changes in the early stages of obesity. Mice were fed ad libitum with normal control diet (NCD, 10% kcal fat), high-fat diet (HFD, 45% kcal fat), 5% (w/w) freeze-dried biberries (Vaccinium myrtillus) in NCD (NCD+BB) or HFD (HFD+BB) for 12 weeks. Diets were prepared in Research Diets Inc. Feed consumption and weight gain were measured during the feeding trial, and blood pressure and serum markers of obesity at the end. Retinas were collected and RNA extracted from all 24 mice samples, and pooled retinas from 4 mice per group were hybridized with standard Illumina protocols. The expression in retinas was analyzed using R, Pathvisio and DAVID to screen for differences between high-fat and berry induced changes to control diets and further bilberry induced changes to HFD up- or downregulated transcripts. diet: NCD, HFD, NCD+BB, HFD+BB

Project description:How signals from fatty acid metabolism are translated into changes in food intake remains unclear. Previously we reported that mice with a genetic inactivation of Acads (short-chain acyl-CoA dehydrogenase), encoding the enzyme responsible for mitochondrial beta-oxidation of C4-C6 short-chain fatty acids (SCFAs), shift consumption away from fat and toward carbohydrate when offered a choice. This finding demonstrated that the loss of a specific enzyme in fatty acid oxidation alters the choice of diet intake. To our knowledge, there are no reports of studies on the effects of dietary fat on the brain transcriptome in genetic models of fatty acid oxidation deficiency. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. We performed a transcriptional screen for gene expression in brain tissue of Acads-/- and Acads+/+ mice fed either high-fat (HF) or low-fat (LF) diet for 2 d. Ingenuity Pathway Analysis revealed three top-scoring pathways significantly modified by genotype or diet: oxidative phosphorylation, mitochondrial dysfunction, and CREB signaling in neurons. A comparison of statistically significant responses in HF Acads-/- vs. HF Acads+/+ (3917) and Acads+/+ HF vs. LF Acads+/+ (3879) revealed 2551 genes or approximately 65% in common between the two experimental comparisons. All but one of these genes were expressed in opposite direction with similar magnitude, demonstrating that Acads-deficient mice fed HF diet display transcriptional responses that mimic those of wildtype Acads+/+ mice fed LF diet. Intriguingly, genes involved in energy sensing and metabolism followed this pattern. Quantitative RT-PCR in hypothalamus confirmed the dysregulation of several genes in these pathways. Western blotting showed that the combination of Acads deficiency and HF diet increased hypothalamic AMP-kinase, a key protein in an energy-sensing cascade that responds to depletion of ATP. Our results suggest that the decreased beta oxidation of short-chain fatty acids in Acads-deficient mice fed HF diet produces a state of energy deficiency in the brain and that AMP-kinase is the cellular energy-sensing mechanism linking fatty acid oxidation to feeding behavior in this model. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from whole brain tissue was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in brain was compared between strains and between diets. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from liver was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in liver was compared between strains and diets.

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.

Dataset Information

Expression data from livers of C57BL/6J mice fed a high-fat diet and coffee

Publications

An integrated multi-omics study revealed metabolic alterations underlying the effects of coffee consumption.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets