High-fat diet decreases expression of genes controlling lipid metabolism, mitochondrial function and skeletal system development in adipose tissue, along with increased expression of extracellular matrix remodeling- and inflammation-related genes
ABSTRACT: We identified differentially expressed genes in epididymal white adipose tissue of high fat diet(HFD)-fed mice compared to low fat diet-fed mice using microarray analysis. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation-reduction, insulin sensitivity, and skeletal system development were downregulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodeling, and inflammation were upregulated. The top 10 up- or downregulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1, and Gpnmb, whose roles in obesity-associated adipose tissue deterioration are poorly understood. Total RNA of epididymal white adipose tissue was obtained from low fat diet (10 kcal% fat)- and high fat diet(45 kcal% fat)-fed mice and mRNA expression was measured using microarray analysis.
Project description:Time-course analysis of adipocyte gene expression profiles response to high fat diet. The hypothesis tested in the present study was that in diet-induced obesity, early activation of TLR-mediated inflammatory signaling cascades by CD antigen genes, leads to increased expression of pro-inflammatory cytokines and chemokines, resulting in chronic low-grade inflammation. Early changes in collagen genes may trigger the accumulation of ECM components, promoting fibrosis in the later stages of diet-induced obesity. New therapeutic approaches targeting visceral adipose tissue genes altered early by HFD feeding may help ameliorate the deleterious effects of a diet-induced obesity. Total RNA obtained from isolated epididymal and mesenteric adipose tissue of C57BL/6J mice fed normal diet or high fat diet for 2, 4, 8, 20 and 24weeks
Project description:Analysis of epididymal AT transcriptome between Kit-deficient mast cell-deficient mice and Kit Wild-type mast cell deficient mice after 16 weeks of HFD feeding Overall design: Total RNA was isolated from epididymal AT WBB6F1.KitW/Wv mice, WBB6F1.Cpa3Cre/+ and WBB6F1.Cpa3+/+ mice that were fed a HFD (60% kcal from fat) or chow diet (6% fat) for 12 weeks
Project description:The effects of the administration of maple syrup extract (MSX) on hepatic gene expression were investigated in mice fed high-fat diet. Male C57BL/6J mice aged 3 weeks were purchased from Charles River Japan (Kanagawa, Japan) and housed in a room maintained at 23 ± 1°C and 49 ± 16% humidity with a 12-h light/dark cycle (light 08:00–20:00; dark 20:00–08:00). For 1 week acclimation period after purchase, all the mice were fed a low-fat diet (10 kcal% fat). Then, they were randomly divided into three different dietary groups: the first group with the food containing fat at 10 kcal% as low-fat diet, the second group with 45 kcal% as high-fat diet, and the third with HFD plus 0.06% MSX. The mice were fed ad libitum for 8 weeks.
Project description:Dietary administration of n-3 polyunsaturated fatty acids (PUFA) is often associated with altered adipose tissue (AT) morphology and/or function in obese mice. However, it is unclear whether these observations are an indirect consequence of reduced weight gain or result from direct actions of n-3 PUFA. Here we studied the AT of fat-1 transgenic mice that convert endogenous n-6 to n-3 PUFA. These mice display equivalent weight gain and fat accretion to their wild-type (WT) counterparts. We performed Affymetrix microarray in epididymal AT of male hemizygous fat-1(+/-) transgenic mice and their wild type littermates that had been fed high fat diets from 6 weeks of age (diet-93075, 55% Kcal from fat, Harlan Teklad). Mice were sacrificed after 8 weeks on the HF diet. At sacrifice epididymal adipose tissues excised for the microarray study (n=3 per group) were rapidly homogenized in QIAZOL (QIAGEN) and snap frozen in liquid nitrogen.
Project description:We used transcriptome microarrays to identify gene expression changes in macrophages isolated from adipose tissue of lean and obese mice. Overall design: F4/80+ adipose tissue macrophages were isolated from epididymal fat of mice fed normal chow diet (NCD, lean mice) or 60% high-fat diet (HFD, obese mice) for 16 weeks.
Project description:We investigated phenotypic differences underpinning obesity susceptibility or resistance based on metabolic and transcriptional profiling in C57BL/6J mice fed a high-fat diet (HFD) Overall design: Total RNA of epididymal adipose tissues and liver was obtained from normal diet, high-fat diet-fed mice and mRNA expression-associated with lipid, and glucose metabolism was measured.
Project description:We used MeDIP-Seq to screen for genes that may be regulated by DNA methylation in macrophages isolated from adipose tissue of lean and obese mice. Overall design: F4/80+ adipose tissue macrophages were isolated from epididymal fat of mice fed a 10% low fat diet, (LFD, lean mice) or 60% high-fat diet (HFD, obese mice) for 16 weeks.
Project description:To assess whether changes in islet gene expression contribute to differences in phenotypes in response to high fat diet or tretament with pioglitazone, Agilent Whole Mouse Genome Oligo Microarrays were performed on RNA isolated from islets of 4 mice per each treatment group for discovery analysis of gene expression. Male 8 week-old BL6 and BLKS mice were fed normal chow (18% kcal from fat), HFD (42% kcal from fat), or HFD supplemented with the PPAR-γ agonist pioglitazone (PIO) (140 mg PIO/kg diet) for 16 weeks.
Project description:Obesity is tightly associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms of obesity-induced fatty liver remain largely unknown.In order to identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, we performed a clustering analysis of Affymetrix arrays,which revealed that a number of mRNAs were dys-regulated in the livers of mice fed a high-fat diet (HFD), compared with mice fed a normal chow diet (ND). To identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, male C57BL/6 mice aged 8 weeks were fed a normal diet (ND) or high-fat-diet (HFD) containing 60 Kcal% of fat for 12 weeks. Then mice were sacrificed and total RNAs were isoloated from hepatic tissues. Affymetrix array hybridisation and scanning were performed using Mouse Genome 430 2.0 chips.Total RNA samples obtained from six mice per group (ND and HFD) and pooled by each of the two were used for microarray analysis.
Project description:To profile the expression of circulating miRNAs in a mouse model of diet-induced obesity (DIO) with subsequent weight-reduction with low-fat diet (LFD), eighteen C57BL/6 male mice were grouped into three subgroups as: (1) Control: the mice fed with the standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice fed with 58 kcal% high-fat diet for 12 wks; (3) DIO+LFD: the mice fed with high-fat diet for 8 wks to induce obesity, then changed to 10.5 kcal% low-fat diet for subsequent 4 wks. C57BL/6 mice were purchased from BioLasco (Taipei, Taiwan). All housing conditions were maintained, and surgical procedures, including analgesia, were performed in an Association for Assessment and Accreditation of Laboratory Animal Care International (AAALAC)-accredited SPF facility according to national and institutional guidelines. In this experiment, eighteen C57BL/6 wild type male mice were randomly grouped into three subgroups (n=6 in each group): (1) Control: the control mice were fed ad libitum a standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice were fed ad libitum a 58 kcal% HFD (D12331; Research Diets Inc., New Brunswick, NJ) for 12 wks to induce obesity; (3) DIO+LFD: the mice fed ad libitum a 58 kcal% HFD (D12331) for 8 wks to induce obesity, then continued the feeding of 10.5 kcal% LFD (D 12329; Research Diets Inc.) for additional 4 wks. Weight measurements were performed on a weekly basis to for these three groups of mice. Evaluation of blood glucose levels was performed at the beginning and in the end of the experiment to confirm that the HFD-fed mice developed an obese and insulin resistant phenotype. After the end of experiment at 12w, all mice were killed. The abdominal WAT of each mice was removed and weighted. Paraffin-embedded abdominal WAT was sectioned at 5 μm and stained with hematoxylin and eosin to measure mean adipocyte area. A volume of 1 mL of whole blood was collected into a plain tube and allowed to clot for 1 hour. The sera samples were aliquoted after centrifugation at 3,000 × g for 10 minutes and stored at −80°C until further analysis.