Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311048 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3147420.fastq.gz | Fastqsanger.gz | |||
| SRR3147430.fastq.gz | Fastqsanger.gz | |||
| SRR3147440.fastq.gz | Fastqsanger.gz | |||
| SRR3147421_1.fastq.gz | Fastqsanger.gz | |||
| SRR3147421_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 34 |
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Project description:Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C epsilon (PKCε), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCε protects against high fat diet-induced hepatic insulin resistance. Here we employ a systems level approach to uncover additional signaling pathways involved in high fat diet-induced hepatic insulin resistance. We used quantitative phosphoproteomics to map global in vivo changes in hepatic protein phosphorylation in chow-fed, high fat-fed, and high fat-fed with PKCε knockdown rats to distinguish the impact of lipid- and PKCε-induced protein phosphorylation.
2018-08-30 | PXD010209 | Pride
Project description:Insulin resistance in high fat diet mouse (adipose)
| PRJNA347988 | ENA
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
Project description:We demonstrate that the ketogenic diet a low carbohydrate diet can induce fibrosis and NASH regardless of body weight loss compared to high-fat diet (HFD) fed mice. KD-fed mice develop severe hepatic injury, inflammation, and steatosis. In addition, KD increases IL-6-JNK signaling and aggravates diet induced-glucose intolerance and hepatic insulin resistance compared to HFD. Notably, pharmacological inhibition of IL-6 and JNK reverses KD‐induced glucose intolerance and restores insulin sensitivity.
2023-01-31 | GSE218025 | GEO
Project description:The aim of this study was to compare the effects of cocoa butter and safflower oil on hepatic transcript profiles, lipid metabolism and insulin sensitivity in healthy rats. Cocoa butter-based high-fat feeding for three days did not affect plasma total triglyceride (TG) levels or TG-rich VLDL particles or hepatic insulin sensitivity, but changes in hepatic gene expression were induced that might lead to increased lipid synthesis, lipotoxicity, inflammation and insulin resistance if maintained. Safflower oil increased hepatic β-oxidation, was beneficial in terms of circulating TG-rich VLDL particles, but led to reduced hepatic insulin sensitivity. The effects of safflower oil on hepatic gene expression were partly overlapping with those exerted by cocoa butter, but fewer transcripts from anabolic pathways were altered. Increased hepatic cholesterol levels and increased expression of hepatic CYP7A1 and ABCG5 mRNA, important gene products in bile acid production and cholesterol excretion, were specific effects elicited by safflower oil only. Common effects on gene expression included increased levels of p8, DIG-1 IGFBP-1 and FGF21, and reduced levels of SCD-1 and SCD-2. This indicates that a lipid-induced program for hepatic lipid disposal and cell survival was induced by three days of high-fat feeding, independent on the lipid source. Based on the results, we speculate that hepatic TG infiltration leads to reduced expression of SCD-1, which might mediate either neutral, beneficial or unfavourable effects on hepatic metabolism upon high-fat feeding, depending on which fatty acids were provided by the diet. Keywords: Hepatic gene expression Two-condition experiment. Biological replicates: 4 male rat livers from rats on a standard diet, 4 male rat livers from rats on a cocoa butter diet, 4 male rat livers from rats on a high-fat (safflower oil) diet. One replicate per array.
2010-05-18 | E-GEOD-13936 | biostudies-arrayexpress
Project description:We previously demonstrated that antisense oligonucleotide (ASO)-mediated knockdown of Mboat7, the gene encoding Membrane Bound O-Acyltransferase 7, in the liver and adipose tissue of mice promoted high fat diet-induced hepatic steatosis, hyperinsulinemia, and systemic insulin resistance. Thereafter, other groups showed that hepatocyte-specific genetic deletion of Mboat7 promoted striking fatty liver and NAFLD progression in mice but does not alter insulin sensitivity, suggesting the potential for cell autonomous roles. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. We generated floxed Mboat7 mice and created hepatocyte- and adipocyte-specific knockout mice using Cre-recombinase mice under the control of the albumin and adiponectin promoter, respectively. After chow and high fat diet feeding (60% kCal fat), mice were subjected to metabolic phenotyping and tissues to molecular workup and analysis. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. The expression of Mboat7 in white adipose tissue closely correlates with diet-induced obesity across a panel of ~100 inbred strains of mice fed a high fat/high sucrose diet. Moreover, we found that adipocyte-specific genetic deletion of Mboat7 is sufficient to promote hyperinsulinemia, systemic insulin resistance, and mild fatty liver. Unlike in the liver, where Mboat7 plays a relatively minor role in maintaining arachidonic acid (AA)-containing PI pools, Mboat7 is the major source of AA-containing PI pools in adipose tissue. Our data demonstrate that MBOAT7 is a critical regulator of adipose tissue PI homeostasis, and adipocyte MBOAT7-driven PI biosynthesis is closely linked to hyperinsulinemia and insulin resistance in mice.
2023-05-10 | PXD039894 | Pride
Project description:High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice
| PRJNA210832 | ENA
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
Project description:The impact of high fat diet on secreted milk small RNA transcriptome was studied by isolating total RNA from milk fat fraction collected on lactation day 10 from control diet fed (C; n=5; 10% fat; 7% sucrose; Research Diets #D12450J, Brunswick, NJ) and high fat diet fed (HF; n=4; Research Diets #D12492, 60% of total kcal energy is fat and match 7% of total kcal is sucrose; Brunswick, NJ) mice.
2018-02-08 | GSE99280 | GEO