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2 parents", "FASTING GLUCOSE (OGTT)": 99.5, "WAIST HIP RATIO": 0.903, "FASTING INSULIN (IV0INAVG)": 9.8}}, {"GSM624973": {"FASTING GLUCOSE (IV0GAVG)": 94, "BODY MASS INDEX (KG/M2)": 27, "HEMOGLOBIN A1C": 4.9, "GENDER": "male", "2 HOUR GLUCOSE (OGTT)": 117.0, "SI": 6.28, "AGE (YEARS)": 52, "FAMILY HISTORY": "Family history negative", "FASTING GLUCOSE (OGTT)": 91.5, "WAIST HIP RATIO": 0.828, "FASTING INSULIN (IV0INAVG)": 4.2}}, {"GSM624974": {"FASTING GLUCOSE (IV0GAVG)": 94, "BODY MASS INDEX (KG/M2)": 36, "HEMOGLOBIN A1C": 5.3, "GENDER": "female", "2 HOUR GLUCOSE (OGTT)": 99.0, "SI": 6.76, "AGE (YEARS)": 49, "FAMILY HISTORY": "Family history positive - 1 parent", "FASTING GLUCOSE (OGTT)": 88.5, "WAIST HIP RATIO": 0.853, "FASTING INSULIN (IV0INAVG)": 4.5}}], "id": 3873, "ownerprofile_id": "arrayexpress_sid", "platform": 4, "summary_wrapped": "Insulin resistance in skeletal muscle is a key phenotype associated with type 2 diabetes (T2D) and is even present in offspring of...", "geo_gse_id": "E-GEOD-25462", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 11, "sample_count": 50, "tags": ["actin", "actin cytoskeleton", "cytoskeleton", "genome", "glucose", "insulin", "muscle", "serum"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "increased-srf-transcriptional-activity-is-a-novel", "geo_id_plat": "E-GEOD-25462_A-AFFY-44", "name": "Increased SRF Transcriptional Activity is a Novel Signature of Insulin Resistance in Humans and Mice", "created": "Sep.15, 2014", "summary": "Insulin resistance in skeletal muscle is a key phenotype associated with type 2 diabetes (T2D) and is even present in offspring of diabetic parents. However, molecular mediators of insulin resistance remain unclear. We find that the top-ranking gene set in expression analysis of muscle from humans with T2D and normoglycemic insulin resistant subjects with parental family history (FH+) of T2D is increased expression of actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator MKL1. Furthermore, the SRF activator STARS is upregulated in FH+ and T2D and inversely correlated with insulin sensitivity. These patterns are recapitulated in insulin resistant mice, and linked to alterations in two other regulators of this pathway: reduced G-actin and increased nuclear localization of MKL1. Both genetic and pharmacologic manipulation of STARS/MKL1/SRF pathway significantly alter insulin action: 1) Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation; 2) reduced STARS expression increased insulin signalling and glucose uptake, and 3) SRF inhibition by CCG-1423 reduced nuclear MKL1, improved glucose uptake, and improved glucose tolerance in insulin resistant mice in vivo. Thus, SRF pathway alterations are a signature of insulin resistance which may also contribute to T2D pathogenesis and be a novel therapeutic target. Skeletal muscle samples were obtained from 10 subjects with type 2 diabetes, 25 subjects with a family history of type 2 diabetes (one or both parents), and 15 subjects with no family history of type 2 diabetes. In this analysis RNA was isolated for cRNA preparation and hybridized to Affymetrix Human Genome U133 Plus 2.0 microarrays.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-25462", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-25462/samples/"}