Expression data from murine adipose tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE38445 | GEO | 2015/06/03
SECONDARY ACCESSION(S): PRJNA167972
REPOSITORIES: GEO
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Project description:Our previous studies have linked Trans-fat and monosodium glutamate (MSG) to the development of Nonalcoholic Fatty Liver Disease (NAFLD). We have also shown that MSG can interact with another commonly consumed food additive, aspartame, to impair glucose homeostasis, which is also disrupted in NAFLD. This most recent nutrigenomic study shows how aspartame, MSG and Trans-fat can unfavorably alter hepatic and adipose tissue gene expression. We used microarray analysis to examine changes in liver gene transcription in response to TFA MSG and/or ASP feeding in male C57Bl/6J mice.
2015-06-03 | GSE38444 | GEO
Project description:Gender dimorphism exists in the physiological response to diet and other environmental factors. Trans-hydrogenated fatty acid (TFA) intake is associated with an increase in coronary heart disease (CHD), and gender differences in the incidence of CHD are well documented. Neonatal administration of Monosodium Glutamate (MSG) causes stunted heart growth and hypoplasticity; and gender dimorphism at the growth hormone axis has been demonstrated in MSG-treated rodents. The identification of gender dimorphism in cardiac nutrigenomics may provide the basis for gender-specific medicine in the future. We used microarray analysis to examine changes in cardiac gene transcription in response to TFA and/or MSG feeding in male and female C57Bl/6J mice. Our study animals were bred from female C57Bl/6J mice fed a standard chow diet until 6 weeks of age whereupon they were placed on one of 4 different dietary regimens for a period of 3 weeks prior to mating. The four dietary regimens used in this study were: [1] Standard Chow (Control diet) with ad lib drinking water. [2] Standard Chow, with ad lib drinking water containing 0.64 g/L Monosodium Glutamate (MSG diet). [3] Trans fat diet of 20% (w/w) Partially Hydrogenated Vegetable Shortening containing 8.68% w/w Trans fatty acids(TFA diet). [4] Trans fat Diet #5C4M together with ad lib drinking water containing 0.64 g/L Monosodium Glutamate (TFA+MSG diet). Following mating, the 4 groups of dams were maintained on their respective diets throughout the gestation and nursing period. Male and female offspring used in the following experiments were weighed, weaned onto the same diets and maintained on their respective dietary regimens until they reached 32 weeks of age.Cardiac tissues (8 per diet group) were used at 32 weeks for RNA extraction and hybridization on Affymetrix microarrays.
2011-12-31 | E-GEOD-22881 | biostudies-arrayexpress
Project description:Gender dimorphism exists in the physiological response to diet and other environmental factors. Trans-hydrogenated fatty acid (TFA) intake is associated with an increase in coronary heart disease (CHD), and gender differences in the incidence of CHD are well documented. Neonatal administration of Monosodium Glutamate (MSG) causes stunted heart growth and hypoplasticity; and gender dimorphism at the growth hormone axis has been demonstrated in MSG-treated rodents. The identification of gender dimorphism in cardiac nutrigenomics may provide the basis for gender-specific medicine in the future. We used microarray analysis to examine changes in cardiac gene transcription in response to TFA and/or MSG feeding in male and female C57Bl/6J mice.
2011-12-31 | GSE22881 | GEO
Project description:This study looks at the effect of dietary manipulation on the development of hepatic steatosis and changes in hepatic gene expression in a feline model. We used microarray analysis to examine changes in hepatic gene transcription in response to Trans fat, High Fructose Corn Syrup (HFCS) and/or Monosodium Glutamate (MSG) in the domestic cat. The use of human Affymetrix arrays for the study of feline gene expression has previously been validated by Dowling and Bienzle, 2005, Journal of General Virology. 86(Pt 8), 2239-48 (PMID 16033971). Our study animals were bred from female Felis catus previously placed on one of 4 different dietary regimens for a period of 3 weeks prior to mating. The four dietary regimens used in this study were: [1] Standard Chow Control feline diet (Test Diet Purina catalog #5003); [2] MSG diet consisting of Control diet with 1.125% added Monosodium Glutamate (Diet A: Test Diet Purina catalog #5C1J); [3] Trans-fat/HFCS diet, containing 8.6% Trans fat and 24% HFCS (Diet B: Test Diet Purina catalog #5B4K); and [4] Trans-fat/HFCS and MSG diet, containing 8.6% Trans fat, 24% HFCS and 1.125% MSG (Diet C: Test Diet Purina catalog #5C1H). Following mating, the 4 groups of dams were maintained on their respective diets throughout the gestation and nursing period. Male offspring used in the following experiments were weaned onto the same diets and maintained on their respective dietary regimens until they reached 9 months of age. Hepatic tissues (4-5 per diet group) were used for RNA extraction and hybridization on Affymetrix microarrays.
2014-06-11 | E-GEOD-30040 | biostudies-arrayexpress
Project description:This study looks at the effect of dietary manipulation on the development of hepatic steatosis and changes in hepatic gene expression in a feline model. We used microarray analysis to examine changes in hepatic gene transcription in response to Trans fat, High Fructose Corn Syrup (HFCS) and/or Monosodium Glutamate (MSG) in the domestic cat. The use of human Affymetrix arrays for the study of feline gene expression has previously been validated by Dowling and Bienzle, 2005, Journal of General Virology. 86(Pt 8), 2239-48 (PMID 16033971).
2014-06-11 | GSE30040 | GEO
Project description:C57BL/6J mice were from The Jackson Laboratory (Maine, USA) and were housed/caged and fed a standard chow diet until 6 weeks of age whereupon they were placed in one of 4 different dietary regimens for a period of 3 weeks prior to mating. Mice were housed under pathogen-free conditions of 21± 1°C, 40 to 60% humidity, and a 12 h-12 h light/dark cycle. The 4 diet regimens used in this study were: [1] ad lib Standard Chow (Control diet) with ad lib drinking water. [2] Ad lib Standard Chow, with ad lib drinking water containing 0.64 mg/ml (97 mg/Kg body weight) monosodium glutamate (MSG diet). [3] Ad lib Test Diet Purina 5001 with 20% 55-HFCS (5B4K, Purina, USA), and ad lib drinking water (HFCS diet). [4] Ad lib Purina 5001 with 20% 55-HFCS, and ad lib drinking water containing 0.64 mg/ml (97 mg/K body weight) monosodium glutamate (HFCS+MSG diet). See Table 1 for diet composition. Following mating, the 4 groups of dams were maintained on their respective diets throughout the gestation and nursing period. Male offspring used in these experiments were weighed, then weaned onto the same diets and maintained in this regimen until they reached either 16 or 32 weeks of age. Total RNA was prepared from the liver and visceral white adipose tissue (WAT) taken from 16-week-old mice in the 4 different diet groups using Qiagen RNeasy Kit (Qiagen USA) according to the manufacturers instructions and stored at -80 o C.<br>
2009-10-01 | E-MEXP-1909 | biostudies-arrayexpress
Project description:Objective: Nonalcoholic fatty liver disease (NAFLD) is linked to obesity and diabetes, suggesting an important role of adipose tissue in the pathogenesis of NAFLD. Here we aim to investigate the interaction between adipose tissue and liver in NAFLD, and identify potential early plasma markers that predict NASH. Research Design and Methods: C57Bl/6 mice were chronically fed a high fat diet to induce NAFLD and compared with mice fed low fat diet. Extensive histological and phenotypical analyses coupled with a time-course study of plasma proteins using multiplex assay was performed. Results: Mice exhibited pronounced heterogeneity in liver histological scoring, leading to classification into 4 subgroups: LF-low (LFL) responders displaying normal liver morphology, LF-high (LFH) responders showing benign hepatic steatosis, HF-low (HFL) responders displaying pre-NASH with macrovesicular lipid droplets, and HF-high (HFH) responders exhibiting overt NASH characterized by ballooning of hepatocytes, presence of Mallory bodies, and activated inflammatory cells. Compared to HFL responders, HFH mice gained weight more rapidly and exhibited adipose tissue dysfunction characterized by decreased final fat mass, enhanced macrophage infiltration and inflammation, and adipose tissue remodelling. Plasma haptoglobin, IL-1β, TIMP-1, adiponectin and leptin were significantly changed in HFH mice. Multivariate analysis indicated that in addition to leptin, plasma CRP, haptoglobin, eotaxin and MIP-1α early in the intervention were positively associated with liver triglycerides. Intermediate prognostic markers of liver triglycerides included IL-18, IL-1β, MIP-1γ and MIP-2, whereas insulin, TIMP-1, GCP-2 and MPO emerged as late markers. Conclusions: Our data support the existence of a tight relationship between adipose tissue dysfunction and NASH pathogenesis and point to several novel potential predictive biomarkers for NASH. Keywords: Expression profiling by array Male wildtype C57Bl/6 mice were fed LFD or HFD for 21 weeks. Mice were divided into 4 groups based on liver histology.
2010-09-09 | E-GEOD-24031 | biostudies-arrayexpress
Project description:Adipose tissue dysfunction is closely associated with the development and progression of nonalcoholic fatty liver disease (NAFLD). Recent studies have implied an important role of prohibitin-1 (PHB1) in adipose tissue function. In the current study, we aimed to explore the function of adipocyte PHB1 in the development and progression of NAFLD. The PHB1 protein levels in adipose tissues were markedly decreased in mice fed a high-fat diet (HFD) compared to those fed a chow diet. To explore the function of adipocyte PHB1 in the progression of NAFLD, mice with adipocyte-specific (adipo) deletion of Phb1 (Phb1adipo-/- mice) were generated. Notably, Phb1adipo-/- mice did not develop obesity but displayed severe liver steatosis under HFD feeding. Compared to HFD-fed wild-type (WT) mice, HFD-fed Phb1adipo-/- mice displayed dramatically lower fat mass with significantly decreased levels of total adipose tissue inflammation, including macrophage and neutrophil number as well as the expression of inflammatory mediators. To our surprise, although liver steatosis in Phb1adipo-/- mice was much more severe, liver inflammation and fibrosis were similar to WT mice after HFD feeding. RNA sequencing analyses revealed that the interferon pathway was markedly suppressed while the bone morphogenetic protein 2 pathway was significantly up-regulated in the liver of HFD-fed Phb1adipo-/- mice compared with HFD-fed WT mice. Conclusion: HFD-fed Phb1adipo-/- mice display a subtype of the lean NAFLD phenotype with severe hepatic steatosis despite low adipose mass. This subtype of the lean NAFLD phenotype has similar inflammation and fibrosis as obese NAFLD in HFD-fed WT mice; this is partially due to reduced total adipose tissue inflammation and the hepatic interferon pathway.
2022-09-17 | GSE213355 | GEO
Project description:Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of liver disease affecting 20-30% of the population in developed countries. NAFLD is strongly associated with abdominal obesity and is recognized as the hepatic manifestation of the metabolic syndrome. In a subgroup of patients with NAFLD inflammation and fibrosis develops, this so-called Non-Alcoholic Steatohepatitis (NASH) may progress to cirrhosis and hepatocellular carcinoma. A multi-hit hypothesis has been proposed in which during the first “hit” fat accumulation occurs in hepatocytes from excessive delivery of fatty acids from adipose tissue, in addition there is an imbalance in lipid synthesis and export. However, the reason why fat accumulation is subsequently followed by inflammation and fibrosis in some patients is poorly understood. We studied the role of gene expression at the transcriptional level using microarray in bariatric patients from whom the liver histology was available. Patients scheduled for bariatric surgery were recruited in Pretoria/South-Africa. At the time of the procedure, tissue samples of the visceral and subcutaneous fat were taken for molecular analysis as well as liver tissue for histology, also full biochemical data was collected. Patients were grouped according histology: group I (<5% steatosis), group II (NAFLD, 30-50% steatosis) and group III (NASH). The 15 samples were used for microarray (nr patients respectively for stages I-II-III: 6-4-5).This dataset is part of the TransQST collection.
2015-07-02 | E-GEOD-59045 | biostudies-arrayexpress
Project description:Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of liver disease affecting 20-30% of the population in developed countries. NAFLD is strongly associated with abdominal obesity and is recognized as the hepatic manifestation of the metabolic syndrome. In a subgroup of patients with NAFLD inflammation and fibrosis develops, this so-called Non-Alcoholic Steatohepatitis (NASH) may progress to cirrhosis and hepatocellular carcinoma. A multi-hit hypothesis has been proposed in which during the first “hit” fat accumulation occurs in hepatocytes from excessive delivery of fatty acids from adipose tissue, in addition there is an imbalance in lipid synthesis and export. However, the reason why fat accumulation is subsequently followed by inflammation and fibrosis in some patients is poorly understood. We studied the role of inflammatory processes in visceral and subcutaneous fat at the transcriptional level using microarray in bariatric patients from whom the liver histology was available. Patients scheduled for bariatric surgery were recruited in two centers (Pretoria/South-Africa and Antwerpen/Belgium). At the time of the procedure, tissue samples of the visceral and subcutaneous fat were taken for molecular analysis as well as liver tissue for histology, also full biochemical data was collected. Patients were grouped according histology: group I (<5% steatosis), group II (NAFLD, 30-50% steatosis), group III (NASH) and group IV (NASH + fibrosis F2-F3). The following samples were used for microarray (number of 'patients' respectively for stages I-II-III-IV): visceral fat (9-7-7-5), subcutaneous fat (6-6-6-5). Microarrays were run in two batches (15xxx versus 17xxx CEL file samples; indicated in the description field). Samples from two patients (FN61; FN76) were put twice on array (15078+17881; 15064+17877) to verify and exclude batch effects. Please note that, due to technical repeats with two patient samples, the number of 'visceral fat samples' for stages I-II-III-IV is 10-7-8-5.
2015-08-04 | E-GEOD-58979 | biostudies-arrayexpress