Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

74 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse skeletal muscle in streptozotocin diabetes with or without insulin treatment

ABSTRACT: Metabolic abnormalities underlying diabetes are primarily the result of the lack of adequate insulin action and the associated changes in protein phosphorylation and gene expression. Affymetrix oligonucleotide microarrays were used to study the changes in the transcriptional program of mouse skeletal muscle in insulin-deficient diabetes. Mice which were made diabetic by streptozotocin treatment were compared to controls. Also, the reversibility of these changes was ascertained by treating a subset of the diabetic mice with insulin.

INSTRUMENT(S): Affymetrix Fluidics Station 400

ORGANISM(S): Mus musculus

SUBMITTER: Ronald Kahn

PROVIDER: E-CBIL-25 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Coordinated patterns of gene expression for substrate and energy metabolism in skeletal muscle of diabetic mice.

Yechoor Vijay K VK Patti Mary-Elizabeth ME Saccone Robert R Kahn C Ronald CR

Proceedings of the National Academy of Sciences of the United States of America 20020729 16

Metabolic abnormalities underlying diabetes are primarily the result of the lack of adequate insulin action and the associated changes in protein phosphorylation and gene expression. To define the full set of alterations in gene expression in skeletal muscle caused by diabetes and the loss of insulin action, we have used Affymetrix oligonucleotide microarrays and streptozotocin-diabetic mice. Of the genes studied, 235 were identified as changed in diabetes, with 129 genes up-regulated and 106 do ...[more]

PMID: 12149437

Similar Datasets

Transcription profiling of skeletal muscle from diabetic or non-diabetic Mexican Americans with or without a family history of diabetes

Project description:Type 2 diabetes mellitus (DM) is characterized by insulin resistance and pancreatic beta-cell dysfunction. In high-risk subjects, the earliest detectable abnormality is insulin resistance in skeletal muscle. Impaired insulin-mediated signaling, gene expression, and glycogen synthesis, and accumulation of intramyocellular triglycerides have all been linked with insulin resistance, but no specific defect responsible for insulin resistance and DM has been identified in humans. To identify genes potentially important in the pathogenesis of DM, we analyzed gene expression in skeletal muscle from healthy metabolically characterized nondiabetic (family history negative and positive for DM) and diabetic Mexican-American subjects. We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function. While NRF-1 expression is decreased only in diabetic subjects, expression of both PPARg coactivator 1-alpha and -beta (PGC1-a/PPARGC1, and PGC1-b/PERC), coactivators of NRF-1 and PPARg-dependent transcription, is decreased in both diabetic subjects and family history positive nondiabetic subjects. Decreased PGC1 expression may be responsible for decreased expression of NRFdependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM.

2007-06-28 | E-CBIL-28 | biostudies-arrayexpress

Transcription profiling of liver from B6 and 129 mice fed on low and high fat diets

Project description:Both environmental and genetic factors play important roles in the development of the metabolic syndrome. To elucidate how these factors interact under normal conditions, C57Bl/6 (B6) and 129S6/SvEvTac (129) mice were placed on a low-fat or high-fat diet. Liver samples were extracted and hybridized to Affymetrix Genome U74 (version 2) arrays.

2007-04-06 | E-CBIL-24 | biostudies-arrayexpress

Transcription profiling of human skeletal muscle from males with type 2 diabetes to identify genes involved in oxidative phosphorylation

Project description:DNA microarrays can be used to discover gene expression changes characteristic of human disease. This is challenging, however, when relevant differences are subtle at the level of individual genes. We introduce an analytical strategy, Gene Set Enrichment Analysis, designed to detect modest but coordinate changes in the expression of groups of functionally related genes. Using this approach, we identify a set of genes involved in oxidative phosphorylation whose expression is coordinately decreased in human diabetic muscle. Expression of these genes is high at sites of insulin-mediated glucose disposal, activated by PGC-1a, and correlated with total-body aerobic capacity. Our results associate this gene set with clinically important variation in human metabolism, and illustrate the value of pathway relationships in the analysis of genomic profiling experiments.

2007-07-17 | E-CBIL-30 | biostudies-arrayexpress

Transcription profiling of rat insulinoma-beta (INS-1E) cells exposed to the cytokines IL-1-beta and IFN-gamma for six different lengths of time and with or without the inducible NO synthase blocker NMA

Project description:Locally released cytokines contribute to beta cell dysfunction and apoptosis in Type 1 diabetes. In vitro exposure of insulin producing INS-1E cells to the cytokines interleukin (IL)-1beta + interferon (IFN) gamma leads to a significant increase in apoptosis. To characterize the genetic networks implicated in beta cell dysfunction and apoptosis and its dependence on nitric oxide (NO) production, we performed a time course analysis using the Affymetrix RG U34A microarry. INS-1E cells were exposed in duplicate to IL-1beta + IFN-gamma for six different time points (1, 2, 4, 8, 12, and 24 h) with or without the inducible NO synthase blocker.

2006-06-14 | E-CBIL-10 | biostudies-arrayexpress

Microarray analysis of in vitro differentiation of adult human pancreatic progenitor cells

Project description:We have developed an in vitro culture system that allows us to expand progenitor cells from human islet preparations and differentiate them into insulin-producing cells. We noticed however, that cultures from individual islet preparations had very heterogeneous outcomes, from good differentiation to almost none. We therefore speculated that our progenitor cell cultures contained different kinds of cells and that the true endocrine progenitor cells are present in the successful cultures, but not in the unsuccessful ones. To address this issue and to begin to identify markers for the true endocrine progenitor cells we compared global gene expression between a very successful culture (final insulin-expression 10% of islets) and an unsuccessful one (final insulin-expression 0%). We also included RNA from freshly isolated islets for control purposes. The cultures from donor A yielded substantial differentiation, while the cultures from donor B showed no successful differentiation.

2014-10-31 | E-MTAB-3050 | biostudies-arrayexpress

Transcription profiling of pancreatic islets in wild type and Tcf-1 knock-out mice to identify target genes Tcf-1 that may be responsible of mediating beta cell growth

Project description:Mutations in several transcription factors lead to a subtype of type 2 diabetes called maturity-onset diabetes of the young (MODY), which are characterized by autosomal dominant inheritance, an early age of disease onset, and development of marked hyperglycemia with a progressive impairment in insulin secretion (Shih and Stoffel, 2002). The most frequent form of MODY is caused by mutations in the gene encoding hepatocyte nuclear factor-1a (HNF-1a, TCF1). Mutant mice with loss of Tcf1 function as well as transgenic mice expressing a naturally occurring dominant-negative form of human TCF1(P291fsinsC) in pancreatic beta cells develop progressive hyperglycemia due to impaired glucose-stimulated insulin secretion (Hagenfeldt-Johansson et al., 2001; Yamagata et al., 2002). Importantly, these mice exhibit a progressive reduction in beta cell number, proliferation rate, and pancreatic insulin content. These data indicate that Tcf-1 target genes are also required for maintenance of normal beta cell mass. In this study we sought to identify target genes of Tcf-1 that may be responsible of mediating beta cell growth by comparing gene expression profiles of Tcf-1 knock-out and wild-type littermates in isolated pancreatic islets.

2007-02-27 | E-CBIL-21 | biostudies-arrayexpress

Expression profiles of novel pancreatic cell lines

Project description:We studied the expression profiles of two different cell lines that were generated in our laboratory from tumors found in mice expressing the SV40 T antigen under the control of the upstream glucokinase promoter. The first cell line, called GKP2 cells, was derived from an insulinoma and expresses insulin and pdx1 along with other markers of beta cells. The second cell line, named GKP4 cells, was derived from periductal tumors that did not express insulin or pdx1 but expressed genes of the endocrine lineage, such as Isl1 and Nkx2.2. Interstingly, a small fraction of the GKP4 cells can spontaneously turn on the expression of insulin and pdx1, indicating that they could be islet cell progenitors. The aim of our project was to identify the genes expressed specifically in GKP4 cells. To do so, we compared the gene expression profiles of GKP4 cells with GKP2 cells using DNA microarray.

2014-07-22 | E-MTAB-2773 | biostudies-arrayexpress

Transcription profiling of fat and normal adipocytes from insulin receptor knockout mice sorted into small and large cells

Project description:Mice with fat-specific disruption of the insulin receptor gene (FIRKO mice) have low fat mass, and are protected against obesity and obesity-related glucose intolerance. FIRKO mice also exhibit polarization of adipocytes into populations of large and small cells. Other PubMed identifiers for this study: 15131120,12110165,15131119

2007-04-06 | E-CBIL-23 | biostudies-arrayexpress

Transcription profiling of muscle insulin receptor knock-out mice treated with streptozotocin to induce diabetes

Project description:The targeted muscle insulin receptor knockout (MIRKO) model was used, in which there is a complete absence of the insulin-receptor signaling in skeletal muscle but normal insulin and glucose levels. By comparing skeletal muscle gene-expression profiles from MIRKO mice and their controls (lox/lox) under three different metabolic conditions (namely, in the basal state, after streptozotocin (STZ)-induced diabetes, and after STZ-induced diabetes rendered euglycemic with insulin treatment), we can address the following three important questions. (i) What is the direct effect of the loss of insulin signaling on gene expression in skeletal muscle? (ii) What is the contribution of the metabolic and other changes that accompany diabetes to induce indirect changes in gene expression? (iii) How are these pathways regulated and implicated in the pathophysiology of diabetes?

2006-11-24 | E-CBIL-19 | biostudies-arrayexpress

Panc-1 Cell Differentiation

Project description:This study (Experiment) consists of 16 arrays.The purpose of our microarray experiment was to assess changes in gene expression during this differentiation program. The basic experiment was to compare gene expression in control cells cultured in SCM and in cells that had been cultured in SFM for 24 hours. Three biological replicates were prepared for each condition and one of the biological replicates was analyzed by microarray in triplicate, for a total of 5 array hybridizations for each time point. Duplicate biological samples were also prepared from cells that had been exposed to SFM for 8 hours, 3 days, and 8 days.

2014-09-22 | E-MTAB-2935 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data