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Links from GEO DataSets

Items: 9

1.

Gene expression profiling in skeletal muscle of PCOS after pioglitazone therapy

(Submitter supplied) Insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes. Studies have shown that thiazolidinediones (TZD) improve metabolic disturbances in PCOS patients. We hypothesized that the effect of TZD in PCOS is in part mediated by changes in the transcriptional profile of muscle favoring insulin sensitivity. Using Affymetrix microarrays, we examined the effect of pioglitazone (30 mg/day for 16 weeks) on gene expression in skeletal muscle of 10 obese women with PCOS metabolically characterized by a euglycemic-hyperinsulinemic clamp. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS4132 GDS4133
Platform:
GPL570
43 Samples
Download data: CEL
Series
Accession:
GSE8157
ID:
200008157
2.
Full record GDS4133

Obese women with polycystic ovary syndrome and obese, healthy women: skeletal muscle

Analysis of skeletal muscle from obese women with polycystic ovary syndrome (PCOS) and obese, healthy women. Results provide insight into whether pioglitazone ameliorates preexisting abnormalities in PCOS patients.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state sets
Platform:
GPL570
Series:
GSE8157
23 Samples
Download data: CEL
3.
Full record GDS4132

PPAR-γ agonist pioglitazone effect on obese women with polycystic ovary syndrome: skeletal muscle

Analysis of skeletal muscle from obese women with polycystic ovary syndrome (PCOS) before and after thiazolidinedione (TZD) pioglitazone treatment. TZDs improve metabolic disturbances in PCOS patients. Results provide insight into the molecular mechanisms underlying the effect of TZD in PCOS.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent sets
Platform:
GPL570
Series:
GSE8157
20 Samples
Download data: CEL
4.

Reduced expression of mitochondrial oxidative metabolism genes in skeletal muscle of women with PCOS

(Submitter supplied) Recently, abnormalities in mitochondrial oxidative phosphorylation (OXPHOS) have been implicated in the pathogenesis of skeletal muscle insulin resistance in type 2 diabetes. In the present study, we hypothesized that decreased expression of OXPHOS genes could be of similar importance for insulin resistance in the polycystic ovary syndrome (PCOS). Using the HG-U133 Plus 2.0 expression array from Affymetrix, we analyzed gene expression in skeletal muscle from obese women with PCOS (n=16) and age- and body mass index-matched control women (n=13) metabolically characterized by euglycemic-hyperinsulinemic clamp and indirect calorimetry. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3104
Platform:
GPL570
29 Samples
Download data: CEL
Series
Accession:
GSE6798
ID:
200006798
5.
Full record GDS3104

Insulin-resistant polycystic ovary syndrome: muscle

Analysis of vastus lateralis muscles from women with insulin-resistant polycystic ovary syndrome (PCOS). Insulin resistance in skeletal muscles is a risk factor for the development of type 2 diabetes in women with PCOS. Results provide insight into the pathogenesis of insulin resistance in PCOS.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state sets
Platform:
GPL570
Series:
GSE6798
29 Samples
Download data: CEL
DataSet
Accession:
GDS3104
ID:
3104
6.

Non-cell Autonomous Mechanisms Control Mitochondrial Gene Dysregulation in Polycystic Ovary Syndrome

(Submitter supplied) The aim of this study was to gain further insight into the mechanisms leading to metabolic dysfunction in skeletal muscle in PCOS, and to determine whether primary myotubes retain the gene expression signature of PCOS in vivo. We investigated the transcriptomic profile of skeletal muscle tissue and primary myotube cultures from insulin resistant women with PCOS compared to healthy controls.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
24 Samples
Download data: TSV, XLSX
7.

Transcription profiling of myotubes from patients with type 2 diabetes

(Submitter supplied) Microarray-based studies of skeletal muscle from patients with type 2 diabetes and high-risk individuals have demonstrated that insulin resistance and reduced mitochondrial biogenesis co-exist early in the pathogenesis of type 2 diabetes independent of hyperglycaemia and obesity. It is unknown whether reduced mitochondrial biogenesis or other transcriptional alterations co-exist with impaired insulin-responsiveness in primary human muscle cells from patients with type 2 diabetes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3681
Platform:
GPL8300
20 Samples
Download data: CEL
Series
Accession:
GSE12643
ID:
200012643
8.
Full record GDS3681

Type 2 diabetes: myotube

Analysis of myotube cell lines established from type 2 diabetes (T2D) subjects. Insulin resistance and reduced mitochondrial biogenesis coexist early in T2D pathogenesis independent of hyperglycemia and obesity. Results provide insight into the effect of T2D on developing skeletal muscle cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 disease state sets
Platform:
GPL8300
Series:
GSE12643
20 Samples
Download data: CEL
DataSet
Accession:
GDS3681
ID:
3681
9.

Pioglitazone treatment of Lethal Yellow mice

(Submitter supplied) Goal of the experiment: To examine differential gene expression in the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice treated with vehicle or pioglitazone. Brief description of the experiment: The objective of this study was to use whole mouse genome DNA microarrays (Codelink) to examine gene expression the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice. Women with polycystic ovary syndrome (PCOS) treated with thiazolidinediones (TZD), such as pioglitazone, show reduced androgen levels and improved ovulatory function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL2897
8 Samples
Download data
Series
Accession:
GSE8806
ID:
200008806
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