Effect of High-Fat Diet on Mouse Liver Gene Expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Zhibo Gai
PROVIDER: E-GEOD-83700 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Microarray analyses were performed in order to determine the effect of galectin-3 ablation on the endothelial transcriptional response in a mouse model of type 2 diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed a high-fat diet (60% fat calories) or standard chow for 8 weeks. CD105+/CD45- endothelial cells were isolated from the aortae and skeletal muscles of these mice by FACS. Whole genome microarray expression profiling revealed greater transcriptional dysregulation in the endothelium of the KO after high-fat feeding compared to WT. Transcripts dysregulated in the KO endothelium after HFD include those involved in glucose uptake and insulin signaling, oxidative stress, vasoregulation, coagulation, and atherogenesis. Real-time PCR confirmed transcriptional downregulation of the glucose transporter, Glut4, and immunofluorescence staining confirmed reduced GLUT4 protein in the endothelium and mudcle of the KO compared to WT. The transcriptional and histological data was consistent with physiological studies showing exacerbated hyperglycemia and coagulation in the KO. These results suggest that galectin-3 serves a protective role against metabolic dysregulation and endothelial dysfunction in diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed either a high-fat diet (60% fat calories) or standard chow diet (12% fat calories) for 8 weeks. Three independent experiments were performed. For each experiment, the aorta and skeletal muscle from 3-4 animals per diet/genotype group were excised and pooled for each tissue. Live, CD105+/CD45- endothelial cells were isolated from the aortic and muscle suspensions by FACS.
2015-08-01 | E-GEOD-57329 | biostudies-arrayexpress
Project description:Male C57BL/6J mice were housed in cages and maintained on a 12-hour light-dark cycle. STD (NMF; Oriental Yeast) and HFHS chow (D12331; Research Diet, New Brunswick, NJ) were used, the mice were sacrificed at 20 weeks of age. Total RNAs from serum, liver and epididymal fat were subjected to Illumina TruSeq Small RNA preparation and sequencing.
2014-10-02 | E-GEOD-61959 | biostudies-arrayexpress
Project description:The goal of this study was to identify and characterize of miRNA in the regulation of inflammatory responses of high-fat induced inflammation mouse model. In this study, we established a mouse model of high-fat-diet-induced inflammation to gain understanding on the biological functions deregulated by aberrant gene expression based on miRNA and mRNA expression profiling analysis. And then we looked for direct miRNA targets by performing pair-wise correlation coefficient analysis on expression levels of mRNAs and by comparing these results with predicted miRNA targets from TargetScan5.1. A subset of the mice from the Chow and HFD groups were killed after 3 months and 9 months. All animals were weighed and anesthetized with ether. Serum was then obtained from the retro-orbital cavity, and mice were killed before liver tissue collection.
2015-06-22 | E-GEOD-59042 | biostudies-arrayexpress
Project description:While the phenomenon linking the early nutritional environment to disease susceptibility exists in many mammalian species, the underlying mechanisms are unknown. We hypothesized that nutritional programming is a variable quantitative state of gene expression, fixed by the state of energy balance in the neonate, that waxes and wanes in the adult animal in response to changes in energy balance. We tested this hypothesis with an experiment, based upon global gene expression, to identify networks of genes in which expression patterns in inguinal fat of mice have been altered by the nutritional environment during early post-natal development. Gene expression patterns in inguinal fat was assessed at 5, 10, 21 days of age and as adults fed chow (56 days of age) followed by high fat diet for 8 weeks (112 days of age) for C57BL/6J mice reared by lactating dams fed either a control diet (CONT), lactating dams fed a diet in which food intake was restricted to cause under-nourishment (lactation under-nutrition; LUN); and, lactating dams fed a high fat diet in where the number of progeny was limited to four (lactation over-nutrition; LON) . 15 samples with 3 technical replicates of each sample. Each of the 15 samples consisted of pooled total RNA from 12 male mice. Dietary control samples are included for each time period.
2011-01-01 | E-GEOD-19809 | biostudies-arrayexpress
Project description:C57BL/6 mice were fed ad libitum for the first 5 days of the experiments with high fat high cholesterol (HFC) diet only. The next 7 days of the experiments mice were continuously fed on a HFC diet and simultaneously vehicle (control group), fenofibrate (100 mg/kg) or lovastatin (30 mg/kg) were orally daily administered. At the end of the experiment (day 12) fenofibrate and lovastatin significantly decreased plasma LDL levels, while plasma cholesterol levels were significantly decreased by lovastatin only. Gene expression analysis of hyperlipidemic mouse liver revealed 391 significantly modulated genes when compared to standard diet fed mice. KEGG pathways related to modulated genes were identified and the most significant were biosynthesis of steroids, metabolism of xenobiotics by cytochrome P450 and linoleic acid metabolism. These pathways were modulated in a way, which increased the clearance of lipids and decreased endogenous synthesis of fatty acids and cholesterol. Additionally, genes involved in the regulation of detoxification pathways were significantly upregulated. The hepatic gene expression profiles of fenofibrate and lovastatin-treated HFC diet fed mice were compared to the vehicle-treated HFC diet fed mice. In the fenofibrate-treated group 124 genes and in the lovastatin-treated group 38 genes were significantly modulated. In the fenofibrate-treated group the top three significantly modulated pathways are fatty acid metabolism, propanoate metabolism and ascorbate and aldarate metabolism. While in the lovastatin-treated group the top three significantly modulated pathways are glycosphingolipid biosynthesis, tyrosine metabolism and metabolism of xenobiotics by cytochrome P450. Expert based classification revealed that both fenofibrate an lovastatin significantly down-regulated genes encoding sterol-C4-methyl oxidase like and 7-dehydrocholesterol reductase. Additionally, the regulation of cholesterol at the transcriptional level was also significantly augmented by fenofibrate and lovastatin, as judged by increased expression of -1 and decreased expression of INSIG-2. Experiment Overall Design: 24 seven week old mice were randomly divided in four experimental groups. Control group (n = 6) was fed on a standard chow diet (diet 3430, Provimi Kliba AG, Kaiseraugst, Switzerland) and treated orally once daily with vehicle for 12 days. Remaining 18 mice were fed on HFC diet for 12 days. On day five HFC diet fed mice were treated orally once daily either with vehicle (HFC group, n=6), lovastatin (HFC lovastatin group, 30mg/kg, n=6) or fenofibrate (HFC fenofibrate group, 100mg/kg, n=6). Doses of lovastatin and fenofibrate were choosen according to the literature review. On day 12 liver were excised and immediately frozen in liquid nitrogen and stored at -80°C for the subsequent transriptome analyses
2008-06-15 | E-GEOD-6652 | biostudies-arrayexpress
Project description:Bile acids are not only physiological detergents facilitating nutrient absorption, but also signaling molecules regulating metabolic homeostasis. We reported recently that transgenic expression of CYP7A1 in mice stimulated bile acid synthesis and prevented Western diet-induced obesity, insulin resistance and hepatic steatosis. The aim of this experiment is to determine the impact of induction of hepatic bile acid synthesis on liver metabolism by determining hepatic gene expression profile in CYP7A1 transgenic mice. CYP7A1 transgenic mice and wild type control mice were fed either standard chow diet or high fat high cholesterol Western diet for 4 month. Hepatic gene expressions were measured by microarray analysis. Our results indicate that hepatic bile acid synthesis is closely linked to cholesterogenesis and lipogenesis, and maintaining bile acid homeostasis is improtant in hepatic metabolic homeostasis. Male aged matched (~ 12-14 weeks) CYP7A1 transgenic mice and their wild type control littermates were fed a standard chow diet or a high fat (42%) high cholesterol (0.2%) diet (Harlan Teklad #88137) for 4 month Four groups (4 mice/group) are included in the experiments: Group 1: WT _ Chow Group 2: CYP7A1-tg + chow Group 3: WT + Western diet Group 4: CYP7A1-tg _ Western diet Total liver mRNA was isolated with a RNeasy kit (Qiagen) and used for microarray analysis.
2013-08-15 | E-GEOD-38872 | biostudies-arrayexpress
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.
2012-12-20 | E-GEOD-35180 | biostudies-arrayexpress
Project description:To determine effects of hyperglycemia and insulin resistance on arterial wall biology, gene expression profiles were generated using aortas from mice on high fat (35% fat) diet and their respective non diabetic regular chow fed controls. Keywords: Chip Experiment was done in triplicate with three independent pools from test mice on high fat diet and control mice on regular chow diet. For RNA isolation aortas were striped of adventitia and periaortic fat. RNA from three aortas was pooled for the synthesis of probe for affymetrix array analysis.
2011-12-23 | E-GEOD-6735 | biostudies-arrayexpress
Project description:The underlying mechanism of how the atopic lipids in skeletal muscle affect muscle growth remains elusive. Here we chose miniature Bama swine as our model to mimick human obesity and co-associated metabolic disorders by long time diet induction and study how the atopic fat accumulation in skeletal muscle influence muscle function. After 23 months high-fat high-sucrose diet (HFHSD) fed, the model minipig model of obesity accompanied with metabolic disorders like human, and they had increased body weight and extensive lipids deposition in adipose tissues (AT) and non-AT, especially in skeletal muscle. Further more, the mass of skeletal reduced greatly and the small area (0-2000μm2) muscle reduced after diet induced. The average fiber area of Gastroc reduced 25.2%, but no significant changes appeared in the other skeletal muscles. Antioxidant capacity of skeletal muscle also reduced. Microarray profiles showed genes related to fat deposition promotion (Peroxisome proliferator activated receptor γ, CCAAT/enhancer-binding protein α and apolipoprotein E), muscle growth inhibition (myostatin and p21) up regulated, and some other muscle cell differentiation related genes (myoD) down regulated. Meanwhile, adipokines like adiponectin and 11b-hydroxysteroid dehydrogenase type 1 (11βHSD1) which partake in the crosstalk between AT and skeletal muscles rose up. We draw a clear potential crosstalk pathway that, increased 11βHSD1 secreted by excess AT will promote the expression of the major inhibitor MSTN by activating corticosterone to cortisol, leading to the growth inhibition of skeletal muscle. Overall, this research announces how obesity affects skeletal muscle growth in a crosstalk sight. Male and female Bama minipigs, aged 6 months at the start of the study, were divided into the following two groups for 23 months of treatment. Bama minipigon control (CD group, N=3) were fed standard pig chow. The experimental group (N=6) were fed high-fat high-sucrose diet (53% basal diet, 37% sucrose, 10% lard, HFHSD).
2014-10-15 | E-GEOD-62312 | biostudies-arrayexpress
Project description:Lean male mice were fed a high fat diet (HFD, lard 24% w/w) for 16 weeks. At 9 weeks, when all hallmarks of prediabetes were established, groups of mice were treated with drug (metformin, glibenclamide, sitagliptin, rosiglitazone, pioglitazone, fenofibrate, T0901317, atorvastatin, salicylate or rofecoxib) for another 7 weeks together with the high fat diet. An additional group was switched back to a chow diet (dietary lifestyle intervention) after the first 9 weeks of high fat diet. All groups were compared to a control group receiving HFD alone and to a reference group fed chow (baseline reference) for the entire experimental period (16 weeks).
2013-04-18 | E-MTAB-1063 | biostudies-arrayexpress