Mus musculus
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ABSTRACT:
PROVIDER: PRJNA92427 | ENA |
REPOSITORIES: ENA
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Project description:5 arrays from obese insulin-resistant and lean insulin-sensitive females adipose tissue at fasting and after 3h hyperinsulinemia 5 arrays from obese insulin-resistant and lean insulin-sensitive females adipose tissue at fasting and after 3h hyperinsulinemia FIR x 5, FIS x 5, HIR x 5, HIS x 5 F=fasting, H=hyperinsulinemia, IR=Insulin-resistant, IS=Insulin-sensitive (FIR, FIS, HIR, HIS)
2012-02-21 | E-GEOD-26637 | biostudies-arrayexpress
Project description:5 arrays from obese insulin-resistant and lean insulin-sensitive females adipose tissue at fasting and after 3h hyperinsulinemia
2012-02-21 | GSE26637 | GEO
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days. Adipose tissue (epididymal), skeletal muscle (gastrocnemius), and liver were harvested from lean (LC) and insulin resistant, obese Zucker rats untreated (FC) or treated with one of four PPARγ ligands (pioglitazone [Pio], rosiglitazone [Rosi], troglitazone [Tro], and AG035029 [AG]).
2011-02-11 | E-GEOD-21329 | biostudies-arrayexpress
Project description:High blood levels of free fatty acids link obesity with type-2 diabetes, but this connection remains poorly understood. We have investigated lipolysis and glucose homeostasis in recently diagnosed obese type-2 diabetics; in obese insulin resistant non-diabetic subjects (obese-IR) matched for age, sex, body composition and fasting insulin levels; and in healthy lean individuals. Our results show that obese-IR dissociate lipolysis from glycemic control, revealing that the action of compensatory hyperinsulinemia on blood glucose is not mediated by reduced lipolysis. In the obese adipose tissue free fatty acids and glycerol levels were elevated in spite of high local levels of insulin or lactate; correlated with adipocyte size and metabolic inflammation, with reduced adipose tissue mRNA levels of genes implicated in beta-adrenergic signaling, de-novo lipogenesis, and increased expression of genes implicated in adipose tissue hyperplasia. These results shed light on the nature of the interaction between lipolysis and glucose homeostasis and indicate an possible adaptive response to fatness.
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Project description:Microarray analysis comparing gene expression profiles of primary cultured preadipocytes from non-diabetic lean vs non-diabetic obese Pima Indian subjects (a subset of the subjects from the adipocyte genechip project, GSE2508). Primary cultured abdominal subcutaneous preadipocytes from 14 lean (7 Males / 7 Females) and 14 obese (7M/7F) subjects were hybridized individually to Affymetrix oligonucleotide arrays HG-U133A and B. Keywords = Obesity Keywords = inflammation Keywords = microarray Keywords = gene expression Keywords = preadipocyte Keywords = stromal-vascular cells Keywords = adipose tissue Keywords: other
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Project description:In mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice. We used expression microarrays to generate transcription profiles of perigonadal ATMs from lean (C57BL/6J Lep +/+) and obese (C57BL/6J Lep ob/ob) mice. Profiling purified FBs and FBCs, we identified 521 transcripts whose expression was differentially (nominal p-value < 0.01) expressed between FBs from lean and obese mice and 1509 genes whose expression was differentially (nominal p-value <0.01) expressed between FBC from lean and obese mice
2013-12-18 | GSE53403 | GEO
Project description:In mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice. We used expression microarrays to generate transcription profiles of perigonadal ATMs from lean (C57BL/6J Lep +/+) and obese (C57BL/6J Lep ob/ob) mice. Profiling purified FBs and FBCs, we identified 521 transcripts whose expression was differentially (nominal p-value < 0.01) expressed between FBs from lean and obese mice and 1509 genes whose expression was differentially (nominal p-value <0.01) expressed between FBC from lean and obese mice RNA was isolated from sorted FBC (F4/80+, CD11b+, CD11c+) cells and FB ( F4/80+, CD11b+, CD11c-) cells and using RNeasy micro-kits (Qiagen), using a PicoPure RNA isolation kit then amplified two-rounds. Labeled cRNA Mouse Genome 430 2.0 arrays (purified FB and FBC adipose tissue macrophages. There was a total of sixteen samples. FB and FBC populations were isolated from 4 lean and 4 obese mice.
2013-12-18 | E-GEOD-53403 | biostudies-arrayexpress
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days.
2011-02-11 | GSE21329 | GEO