Mouse adipose tissue under hypercaloric and isocaloric high-fat diet
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Alexandros Vegiopoulos
PROVIDER: E-MTAB-7755 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of wild-type C57BL-6 mice exposed to a high-fat diet that might have been caused by the oral consumption of the probiotic B. pseudocatenulatum CECT 7765. The aim of this work was to determine whether the daily intake (by oral gavage) of the probiotic (P) B. pseudocatenulatum for seven weeks exerted any modulatory effects, at the level of gene expression, in the liver of C57BL-6 male mice exposed to a high-fat diet (HFD). Male mice were randomly assigned to four experimental groups (n= 5 animals per group) as follows: (1) control group, fed a standard diet (SD); (2) obese group, fed a high-fat diet (HFD); (3) a group that received the SD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (SD+P); and (d) an obese group that was fed the HFD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (HFD+P). At the end of the experimental procedure total RNA was extracted from the liver to compare differential gene expression between the groups. Liver differential gene expression after 7 weeks of supplementation between: 1) the HFD group and the SD group (effects of the high-fat diet); 2) the HFD+P and the HFD (effects of the probiotic on the consumption of a high-fat diet) and 3) the SD+P group and the SD (direct effects of the probiotic on the liver of animals consuming a normal diet).
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Project description:Younger age and obesity increase the incidence and rates of metastasis of triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer. The tissue microenvironment, specifically the extracellular matrix (ECM), is known to promote tumor invasion and metastasis. We sought to characterize the effect of both age and obesity on the ECM of mammary fat pads. We used a diet-induced obesity (DIO) model where 10-week-old female mice were fed a high-fat diet (HFD) for 16 weeks or a control chow diet (CD) where time points were every 4 weeks to monitor age and obesity HFD progression. We isolated the mammary fat pads to characterize the ECM at each time point. Utilizing proteomics, we found that the early stages of obesity were sufficient to induce distinct differences in the ECM composition of mammary fat pads that promote TNBC cell invasion. ECM proteins previously implicated in driving TNBC invasion Collagen IV and Collagen VI, were enriched with weight gain. Together these data implicate ECM changes in the primary tumor microenvironment as mechanisms by which age and obesity contribute to breast cancer progression.
2024-06-06 | PXD050250 | Pride
Project description:Because of the epidemic rise of obesity worldwide, the identification of novel target genes for pharmacological treatment of obesity and related disorders is becoming of high importance. IFRD1 and IFRD2 are members of a novel transcriptional regulators family. Intestinal over-expression of mouse homologue of IFRD1 promoted intestinal triglyceride uptake and induced whole body adiposity in mice. To further elucidate the role of IFRD1 and IFRD2 in vivo, we generated mice lacking both mouse homologues of IFRD1 (TIS7) and IFRD2 (SKMc15) genes. Here, we report that mice deficient in TIS7 and SKMc15 genes, despite normal calorie intake had severely reduced amount of adipose tissue, were resistant to diet-induced obesity and displayed high glucose tolerance. Lower dietary fat entry into the circulation suggested that this phenotype resulted from impaired intestinal lipid transport. We identified down-regulation of CD36, a fatty acid transporter, both on RNA and protein levels. Reporter assays indicated that TIS7 and SKMc15 transcriptionally regulated CD36 expression and CD36 overexpression partially restored fatty acid uptake in vitro. Hence, our study suggested that TIS7 and SKMc15 play an important role in the regulation of the lipid metabolism and might represent a novel strategy for treatment of disorders caused by excess fat intake. To determine whether decreased intestinal lipid absorption might be caused by changes in expression of lipid processing and transport molecules, we performed Affymetrix microarray analyses of total RNA samples isolated from the jejunum of HFD-fed WT type and dKO animals. The moderated t-test was used to calculate p-values for significance of differential gene expression between 3 dKO and 3 wild type mice. These raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate (FDR) and genes with thus adjusted p-values < 0.05 were considered significant. Age-matched (7-10 week old) male wild type and TIS7 (Ifrd1) SKMc15 (Ifrd2) double knock out mice (C57Bl6 background) were caged individually and maintained from 3 weeks up to 8 weeks on a synthetic high saturated fat (HFD) diet (Ssniff). Small intestines (jejunum) were harvested for total RNA isolation. RNAs from 3 WT and 3 dKO mice were subjected to Affymetrix based whole genome gene expression analysis (Mouse 430.2 GeneChip).
2012-07-31 | E-GEOD-27019 | biostudies-arrayexpress
Project description:Overnutrition during pregnancy inM-oM-,M-^Buences the future health of the offspring, with outcomes differing depending on the childM-bM-^@M-^Ys sex. The placenta is involved in the programming of obesity, type 2 diabetes and cardiovascular disease. Sex-specific adaptation of the placenta may be central to the differences in fetal growth and survival. The impact of diet and fetal sex on placental gene expression and epigenetic marks was investigated in mice fed a high-fat (HFD) or a control diet (CD), during the first 15 days of gestation Microarrays analysis revealed that expression was affected by maternal diet and was sexually dimorphic. We analyzed the placentae of 4 mice litters fed with an high-fat diet (HFD) and 4 with a control diet (CD). For each litter, the placenta transcriptome was analysed according to the foetus sex using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.
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Project description:Type 2 diabetes (T2D) has become an epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD+ biosynthesis, and the NAD+-dependent protein deacetylase SIRT1. Here we show that NAMPT-mediated NAD+ biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD+ intermediate, ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD+ and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a novel intervention against diet- and age-induced T2D. 4 regular chow fed mice (RC1-4) vs 4 high-fat diet fed (HFD) (HFD1a-4a) mice were analyzed on one chip (Chip-A). 4 HFD mice (HFD1b-4b) vs 4 HFD-NMN treated mice (NMN1-4) were examined on the other chip (Chip-B).
2011-12-05 | E-GEOD-31647 | biostudies-arrayexpress
Project description:Maternal obesity can program metabolic syndrome in offspring but the mechanisms are not well characterized. Moreover, the consequences of maternal overnutrition in the absence of frank obesity remain poorly understood. This study aimed to determine the effects of maternal consumption of a high fat-sucrose diet on the skeletal muscle metabolic and transcriptional profiles of adult offspring. Female Sprague Dawley rats were fed either a diet rich in saturated fat and sucrose (HFD, 23.5% fat, 20% sucrose wt/wt) or a standard chow diet (NFD, 7% fat, 10% sucrose w/w) for the 3 weeks prior to mating and throughout pregnancy and lactation. Although maternal weights were not different between groups at conception or weaning, HFD dams were ~22% heavier than chow fed dams from mid-pregnancy until 4 days post-partum. Adult male offspring of HFD dams were not heavier than controls but demonstrated features of insulin resistance including elevated plasma insulin concentration (+40%, P<0.05). Next Generation mRNA Sequencing was used to identify differentially expressed genes in the soleus muscle of offspring, and Gene Set Enrichment Analysis (GSEA) to detect coordinated changes that are characteristic of a biological function. GSEA identified 15 pathways enriched for up-regulated genes, including cytokine signaling (P<0.005), starch and sucrose metabolism (P<0.017), and inflammatory response (P<0.024). A further 8 pathways were significantly enriched for down-regulated genes including oxidative phosphorylation (P<0.004) and electron transport (P<0.022). Western blots confirmed a ~60% reduction in the phosphorylation of the insulin signaling protein Akt (P<0.05) and ~70% reduction in mitochondrial complexes II (P<0.05) and V expression (P<0.05). On a normal diet, offspring of HFD dams developed an insulin resistant phenotype, with transcriptional evidence of muscle cytokine activation, inflammation and mitochondrial dysfunction. These data indicate that maternal overnutrition, even in the absence of pre-pregnancy obesity can promote metabolic dysregulation and predispose offspring to type 2 diabetes. Messenger RNA profile of skeletal muscle of male offspring from female Sprague Dawley rats fed either a diet rich in saturated fat and sucrose (HFD, 23.5% fat, 20% sucrose wt/wt) or a standard chow diet (NFD, 7% fat, 10% sucrose w/w) for the 3 weeks prior to mating and throughout pregnancy and lactation. There were 5 HFD samples compared to 6 NFD control samples.
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Project description:The present study aimed to examine the effect of high-fat diet prior to pregnancy on the liver of mouse offspring. Female C57BL/6J mice were fed a normal chow (15.2% fat by energy) (CTR and CTR-PP groups) or a high-fat chow (31.2% fat by energy) (HFD and HFD-PP groups) for 3−4 weeks and then mated with male C57BL/6J mice fed normal chow. Some mothers continued on the same diet until pups reached 21 days of age (CTR and HFD), and others were fed the different chows from gestational day 0 (CTR-PP and HFD-PP) to determine the effects of a high-fat diet during the pre-pregnancy period in HFD-PP/CTR and HFD/CTR-PP comparisons. RNA sample was taken from liver of 3-week-old mouse prenatally received high-fat diet prior to pregnancy, during pregnancy and lactation, or through prior to and during pregnancy and lactation, while control RNA was taken from control counterpart prenatally received normal diet alone. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
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Project description:A number of studies have proposed that excess food intake, particularly of high fat diets arise due dysregulation of homeostatic mechanisms regulating neuroendocrine control of appetite and energy balance. Current dogma suggests high fat diets invoke hypothalamic inflammation which reduces hypothalamic sensitivity to metabolic and hormonal cues of conveying peripheral status of energy balance, such as leptin and insulin. A hypothesis for the mechanism leading to hypothalamic inflammation is based on high fat diet mediated changes in gut microbiota which are then proposed to increase circulating levels of lipopolysaccharide (LPS). This in turn activates a hypothalamic inflammatory response via the toll-like receptor (TLR4) and CD14. The aim of this study was to determine hypothalamic gene expression in response to long term feeding of a high fat diet, taking into account the importance of using a control diet with a similar composition and balanced for sucrose content.
2018-10-23 | E-MTAB-6929 | biostudies-arrayexpress
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
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