U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 17

1.
Full record GDS4845

Streptozotocin induced type 1 diabetes: liver

Analysis of liver from C57BL/6N males treated with streptozotocin (STZ) to induce type 1 diabetes (T1D). Liver mitochondria of STZ males showed increased oxygen consumption. Results provide insight into molecular mechanisms underlying the enhanced performance of T1D STZ liver mitochondria.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 agent sets
Platform:
GPL6246
Series:
GSE39752
13 Samples
Download data: CEL
DataSet
Accession:
GDS4845
ID:
4845
2.

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

(Submitter supplied) Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
5 Samples
Download data: CEL
Series
Accession:
GSE79008
ID:
200079008
3.

Liver adapts mitochondrial function to insulin-resistant and diabetic states in mice

(Submitter supplied) Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4845
Platform:
GPL6246
13 Samples
Download data: CEL
Series
Accession:
GSE39752
ID:
200039752
4.

Bezafibrate reduces the elevated hepatic fumarate in insulin-deficient mice.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
35 Samples
Download data: CEL
Series
Accession:
GSE179719
ID:
200179719
5.

Bezafibrate reduces the elevated hepatic fumarate level in insulin-deficient streptozotocin mice [skeletal muscle tissue]

(Submitter supplied) In addition to high intracellular glucose level, the diabetic state is also characterized by altered metabolites, which are pivotal regulators of glucotoxic pathways. In this study we analyzed Bezafibrate (BEZ) treated Streptozotocin (STZ) mice, which showed improved glucose metabolism compared to untreated STZ controls. In order to identify the key molecules and pathways, which participate in the beneficial effects of BEZ, we analyzed the skeletal muscle, white adipose tissue (WAT) and liver samples of BEZ-treated mice using non-targeted metabolomics (NMR spectroscopy), targeted metabolomics (mass spectrometry), microarrays and enzyme activity measurements with a particular focus on the liver. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
17 Samples
Download data: CEL
Series
Accession:
GSE179718
ID:
200179718
6.

Bezafibrate reduces the elevated hepatic fumarate level in insulin-deficient streptozotocin mice [visceral adipose tissue]

(Submitter supplied) In addition to high intracellular glucose level, the diabetic state is also characterized by altered metabolites, which are pivotal regulators of glucotoxic pathways. In this study we analyzed Bezafibrate (BEZ) treated Streptozotocin (STZ) mice, which showed improved glucose metabolism compared to untreated STZ controls. In order to identify the key molecules and pathways, which participate in the beneficial effects of BEZ, we analyzed the skeletal muscle, white adipose tissue (WAT) and liver samples of BEZ-treated mice using non-targeted metabolomics (NMR spectroscopy), targeted metabolomics (mass spectrometry), microarrays and enzyme activity measurements with a particular focus on the liver. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
18 Samples
Download data: CEL
Series
Accession:
GSE179717
ID:
200179717
7.

JNK activation of BIM promotes hepatic oxidative stress, steatosis and insulin resistance in obesity

(Submitter supplied) The BCL-2 family are crucial regulators of the mitochondrial pathway of apoptosis in normal physiology and disease. Besides their role in cell death, BCL-2 proteins have been implicated in the regulation of mitochondrial oxidative phosphorylation and cellular metabolism. However, it remains unclear whether these proteins have a physiological role in glucose homeostasis and metabolism in vivo. Here we report that fat accumulation in the liver increases JNK-dependent BIM expression in hepatocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: GTF
Series
Accession:
GSE102982
ID:
200102982
8.

Mouse HFD Liver Skeletal Muscle SLC16A13 Knock-Out

(Submitter supplied) Genome-wide association identified SLC16A13 as novel type 2 diabetes gene locus. The SLC16A13 gene encodes for SLC16A13/MCT13, member of the solute carrier 16 family of monocarboxylate transporters. This transporter family recently raised interest in metabolic research with the identification of SLC16A11 polymorphisms associated with type 2 diabetes; and human as well as mouse data suggest causal relationship between SLC16A11/MCT11 transporter dysfunction and type 2 diabetes development. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
44 Samples
Download data: TXT
Series
Accession:
GSE152937
ID:
200152937
9.

Gene expression analysis of directly converted brown adipocytes (dBAs).

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6246 GPL6244
9 Samples
Download data: CEL
Series
Accession:
GSE56635
ID:
200056635
10.

Gene expression analysis of directly converted brown adipocytes (dBAs). [mouse]

(Submitter supplied) Comparasion of each cell mRNA expression pattern Mouse fibroblasts were directly converted into brown adipocytes (dBAs) by transducing some transcription factors. To characterize the dBAs more in detail, RNA extracted from the mouse brown adipose tissue, mouse dBAs, and mouse iPS-derived brown adipocytes (iBAs) were subjected to DNA microarray analysis, and global gene expression profiles of the cells were compared.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
3 Samples
Download data: CEL
Series
Accession:
GSE56634
ID:
200056634
11.

Gene expression analysis of directly converted brown adipocytes (dBAs). [human]

(Submitter supplied) Comparasion of each cell mRNA expression pattern Human fibroblasts were directly converted into brown adipocytes (dBAs) by transducing some transcription factors. To characterize the dBAs more in detail, RNA extracted from the human WAs, human dBAs, and human iPS-derived brown adipocytes (iBAs) were subjected to DNA microarray analysis, and global gene expression profiles of the cells were compared.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
6 Samples
Download data: CEL
Series
Accession:
GSE56633
ID:
200056633
12.

Altered gene expression profiles in the hippocampus and prefrontal cortex of type 2 diabetic rats

(Submitter supplied) There has been an incresing body of epidemiologic and biochemical evidence implying the role of cerebral insulin resistance in Alzheimer-type dementia. For a better understanding of the insulin effect on the central nervous system we performed microarray-based gene expression profiling in the hippocampus, striatum and prefrontal cortex of streptozotocin-induced and spontaneously diabetic Goto-Kakizaki rats as model animals for type 1 and type 2 diabetes, respectively. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL15011
27 Samples
Download data: TXT
Series
Accession:
GSE34451
ID:
200034451
13.

Uncovering the hepatic gene expression variations and sex-differences as response to high-fat diet consumption in the highly genetically diversity of the Collaborative Cross mouse model

(Submitter supplied) Hepatic gene expression variations and sex-differences due to high-fat diet consumption using the Collaborative Cross mouse model
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
84 Samples
Download data: FPKM_TRACKING
Series
Accession:
GSE126490
ID:
200126490
14.

Effect of aging on mitochondrial gene expression using C57BL/6N liver mitochondria

(Submitter supplied) To investigate the effect of aging on mitochondrial gene expression we isolated liver mitochondria from 4 12-week and 4 65-week C57BL/6N WT mice. We then isolated RNA and prepared the barcoded library using PCR-cDNA Barcoding Kit SQK-PCB109 and ran it on MinIOn R9.4.1 Flow cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24973
8 Samples
Download data: TSV
Series
Accession:
GSE208177
ID:
200208177
15.

Genetic regulator of mitochondrial metabolism and insulin resistance

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL24247
18 Samples
Download data: TXT, WIG
Series
Accession:
GSE162021
ID:
200162021
16.

Genetic regulator of mitochondrial metabolism and insulin resistance [RNA-Seq]

(Submitter supplied) Mitochondrial energy metabolism and function are key processes underlying the pathophysiology of insulin resistance and predisposition to type 2 diabetes. This is because mitochondria produce most of the energy required by the cell. Impaired energy production, use of energy stores and mitochondrial dysfunction are major features in metabolic diseases. Nevertheless, it remains uncertain how mitochondrial dysfunction can cause, contribute to, or result in insulin resistance and metabolic diseases. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: WIG
Series
Accession:
GSE162020
ID:
200162020
17.

Genetic regulator of mitochondrial metabolism and insulin resistance [ncRNA-Seq]

(Submitter supplied) Mitochondrial energy metabolism and function are key processes underlying the pathophysiology of insulin resistance and predisposition to type 2 diabetes. This is because mitochondria produce most of the energy required by the cell. Impaired energy production, use of energy stores and mitochondrial dysfunction are major features in metabolic diseases. Nevertheless, it remains uncertain how mitochondrial dysfunction can cause, contribute to, or result in insulin resistance and metabolic diseases. more...
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: CSV, TXT
Series
Accession:
GSE161978
ID:
200161978
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=5|qty=4|blobid=MCID_6737c23ebea12f4e7c7db064|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center