Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

11 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse adipocytes and white adipose tissue of mice maintained on normal chow or high fat diet

ABSTRACT: We studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions; We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a high fat diet. Experiment Overall Design: Primary cultures of mouse adipocytes,harvested from visceral adipose tissue, were exposed to forskolin (10uM) or vehicle control (DMSO) for 2 hours. White adipose tissue (epididymal fat pads) were collected from mice maintained on a 60% high fat diet for 12 weeks and from control mice on normal chow.

ORGANISM(S): Mus musculus

SUBMITTER: Marc Montminy

PROVIDER: E-GEOD-14363 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from adipocytes and white adipose tissue of mice maintained on normal chow or high fat diet

Project description:We studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a high fat diet. Keywords: signaling study

2009-03-03 | GSE14363 | GEO

Expression data from browning inguinal white adipose tissue in UCP1/ApoE-DKO mice

Project description:Differentiation of brown adipocytes is a crucial process for adaptive thermogenesis, which is stimulated by various factors. We found robust browning of inguinal white adipose tissue in UCP1/ApoE-DKO mice, but not in ApoE-KO mice, under high-fat diet condition. We used microarray to determine the genes specifically regulated in the browning white adipose tissue in UCP1/ApoE-DKO mice.

2018-10-01 | GSE95273 | GEO

scRNA of preadipocytes and mature adipocytes from mice exposed to a mouse model of early life stress

Project description:Background: Adipose tissue homeostasis is a complex process influenced by many mechanisms that become dysregulated with obesity. We have previously shown that Maternal Separation and Early Weaning (MSEW), a mouse model of early life stress, exacerbates high-fat diet (HF)-induced fat deposition in female mice, but not male mice. In addition, we have shown that this exacerbated adiposity is due to an increase in visceral adipose tissue, and fat depot known to be linked with cardio-metabolic dysfunction. Purpose: The aim of this study was to determine differential gene expression patterns in gonadal white adipose tissue (gWAT), a visceral fat, in female mice exposed to MSEW compared to controls. Adipose tissue is composed of many different stromal cell types including preadipocytes, mature adipocytes, and immune cells. Preadipocytes are the precursor stem cells that differentiate into mature adipocytes that can uptake and store lipids and have a more predominte endocrine function. Methods: Control and MSEW mice were weaned onto either a low-fat diet (LF) or a high-fat diet (HF) for 20 weeks. Fresh gonadal white adipose tissue was harvested after euthanasia and subjected to collagenase digestion. Tissue was centrifuged and filtered to separate the mature fraction from the stromal vascular fraction. Magnetic Activated Cell Sorting (MACs) was used to further isolate adipocytes from other cell types. Pre-and mature adipocytes were collected and saved in Purezol at -80oC for later RNA extraction using the Promega ReliaPrep RNA miniprep systems. Total RNA was sent to Novogene for scRNAseq analysis.

2021-12-31 | GSE168751 | GEO

MBOAT7-Driven Lysophosphatidylinositol Acylation in Adipocytes Contributes to Systemic Glucose Homeostasis

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

EPAC1 enhances energy expenditure by selectively inducing brown and beige adipose tissue growth

Project description:Brown adipose tissue (BAT) is a central thermogenic organ that enhances energy expenditure (EE) and cardiometabolic health. However, regulators that specifically increase the number of thermogenic adipocytes are still an unmet need. Here, we show by phosphoproteomics that cAMP activates distinct signaling pathways in brown progenitors, with the cAMP-EPAC1 axis enhancing proliferation and differentiation of thermogenic but not white adipocytes. Further analysis revealed that a specific subpopulation of preadipocytes that are PDGFRα-positive express EPAC1. In vivo, pharmacological activation of EPAC1 enhances BAT growth and browning of white fat, leading to increased EE and reduced diet-induced adiposity. In contrast, mice lacking EPAC1 in PDGFRα-positive preadipocytes show the opposite phenotype. Importantly, EPAC1 activation enhances proliferation and differentiation of human brown adipocytes and human brown fat organoids. Interestingly, a coding variant in EPAC1 that positively correlates with BMI abolishes norepinephrine-induced proliferation of brown adipocytes. Thus, EPAC1 might be an attractive target to enhance thermogenic adipocyte number and EE to combat metabolic diseases.

2023-11-11 | PXD046709 | Pride

Effect of sesaminol on C2C12 cells on myogenesis pathway

Project description:Adipocytes are key players in maintaining energy homeostasis and are classified into two different categories: white and brown adipocyte. While white adipocytes store energy as triacylglycerols in lipid droplets, brown adipocytes combust excess chemical energy and release in the form of heat through uncoupled respiration. This characteristic phenomenon of brown fat attracts researchers and pharmacological industries to view brown fat as one of the potential therapeutic targets for obesity and associated metabolic disease. In the current study, we investigated the effect of a small molecule, sesaminol (SML) on brown fat activity and found that SML induces thermogenic program in primary white adipocytes as well as chow diet fed mice. In particular, SML treatment to mice elevated mitochondrial complex proteins and the rate oxygen consumption in brown and white fat. Administration of SML to high fat diet (HFD) challenged mice decreased weight gain, adiposity and cholesterol levels along with an increase of brown fat gene program in brown and white fat. Mechanistically, SML repressed the myogenic gene program in C2C12 myoblasts and increased all mitochondrial marker genes as appeared in brown adipose cells. Together, our results demonstrate that SML stimulates brown adipose function and protects mice against diet induced weight gain.

2020-03-27 | GSE147599 | GEO

Post-natal development of brown adipocytes in white fat: Phases independent and dependent of the ambient temperature

Project description:Decreased ambient temperature, from birth to weaning, significantly reduced fat mass (FM) and adiposity in developing mice. Changes in FM content in 10 day-old mice raised at 17°C were not accompanied by precocious induction of brown adipocytes in inguinal white adipose tissue (WAT). Brown phenotype was induced in 21 day-old mice independently of ambient temperature (17°C or 29°C) however the expression of Ucp1 and other brown fat biomarker genes was greater in animals raised at 17°C suggesting increased adaptive thermogenesis. Accordingly, we predict that the induction of brown adipocytes in WAT follows a strict developmental program and the number of potential brown adipocytes in WAT is determined genetically. Microarray analysis of gene expression was performed on inguinal white adipose tissue dissected from 10 and 21 day-old mice kept at different temperature conditions, that is, in mice maintained at 17°C or 29oC during early post-natal development.

2015-05-03 | E-GEOD-62350 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from adipocytes and white adipose tissue of mice maintained on normal chow or high fat diet

| PRJNA111399 | ENA

Transgenic expression of BEN, a member of TFII-I family, in various murine adipose tissues

Project description:The white adipose organ is composed of both subcutaneous and several intra-abdominal depots. Excess abdominal adiposity is a major risk factor for metabolic disease in rodents and humans, while expansion of subcutaneous fat does not carry the same risks. Brown adipose produces heat as a defense against hypothermia and obesity, and the appearance of brown-like adipocytes within white adipose tissue depots is associated with improved metabolic phenotypes. Thus, understanding the differences in cell biology and function of these different adipose cell types and depots may be critical to the development of new therapies for metabolic disease. Here, we found that BEN, a determination factor of brown fat function. BEN transgenic mice displayed increased energy expenditure, limited weight gain, and improved glucose tolerance in response to a high-fat diet. These results demonstrate that BEN is a cell-autonomous determinant of a brown fat function and thermogenesis.

2018-01-10 | E-MTAB-4163 | biostudies-arrayexpress

RNA sequencing of white adipose tissue of lean and obese mice

Project description:We report differential expressed genes in white adipose tissue of mice fed with a low-fat diet or a high-fat diet.

2018-04-23 | GSE112999 | GEO