Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157313 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity. Adipose tissue from control lean and obese rats were obtained. RNA was extracted and processed for further hybridization on Affymetrix microarrays (GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA)).
2014-02-15 | E-GEOD-44372 | biostudies-arrayexpress
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue (pWAT) due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity.
2014-02-15 | GSE44373 | GEO
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity.
2014-02-15 | GSE44372 | GEO
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue (pWAT) due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity. Pancreatic islets from control lean and cafeteria diet fed obese rats were obtained. RNA was extracted and processed for further hybridization on Affymetrix microarrays (GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA)).
2014-02-15 | E-GEOD-44373 | biostudies-arrayexpress
Project description:In obesity an increase in β-cell mass occurs to cope with the rise in insulin demand. This β -cell plasticity is essential to avoid the onset of hyperglycemia, although the molecular mechanisms that regulate this process remain unclear. This study analyzed the role of adipose tissue in the control of β -cell replication. Using a diet-induced model of obesity, we obtained conditioned media from three different white adipose tissue depots. Only in the adipose tissue depot surrounding the pancreas did the diet induce changes that led to an increase in INS1E cells and the islet replication rate. To identify the factors responsible for this proliferative effect, adipose tissue gene expression analysis was conducted by microarrays and quantitative RT-PCR. Of all the differentially expressed proteins, only the secreted ones were studied. IGF binding protein 3 (Igfbp3) was identified as the candidate for this effect. Furthermore, in the conditioned media, although the blockage of IGFBP3 led to an increase in the proliferation rate, the blockage of IGF-I receptor decreased it. Taken together, these data show that obesity induces specific changes in the expression profile of the adipose tissue depot surrounding the pancreas, leading to a decrease in IGFBP3 secretion. This decrease acts in a paracrine manner, stimulating the β -cell proliferation rate, probably through an IGF-I-dependent mechanism. This cross talk between the visceral-pancreatic adipose tissue and β -cells is a novel mechanism that participates in the control of β -cell plasticity. (Endocrinology 153: 177–187, 2012)
2012-03-30 | GSE36935 | GEO
Project description:COUP-TFII Controls Mouse Postnatal Pancreatic β-Cell Mass through GLP-1 β-Catenin
| PRJNA143305 | ENA
Project description:In obesity an increase in β-cell mass occurs to cope with the rise in insulin demand. This β -cell plasticity is essential to avoid the onset of hyperglycemia, although the molecular mechanisms that regulate this process remain unclear. This study analyzed the role of adipose tissue in the control of β -cell replication. Using a diet-induced model of obesity, we obtained conditioned media from three different white adipose tissue depots. Only in the adipose tissue depot surrounding the pancreas did the diet induce changes that led to an increase in INS1E cells and the islet replication rate. To identify the factors responsible for this proliferative effect, adipose tissue gene expression analysis was conducted by microarrays and quantitative RT-PCR. Of all the differentially expressed proteins, only the secreted ones were studied. IGF binding protein 3 (Igfbp3) was identified as the candidate for this effect. Furthermore, in the conditioned media, although the blockage of IGFBP3 led to an increase in the proliferation rate, the blockage of IGF-I receptor decreased it. Taken together, these data show that obesity induces specific changes in the expression profile of the adipose tissue depot surrounding the pancreas, leading to a decrease in IGFBP3 secretion. This decrease acts in a paracrine manner, stimulating the β -cell proliferation rate, probably through an IGF-I-dependent mechanism. This cross talk between the visceral-pancreatic adipose tissue and β -cells is a novel mechanism that participates in the control of β -cell plasticity. (Endocrinology 153: 177–187, 2012) Adult male Wistar rats (Charles River Laboratories, Wilmington, MA), 7 wk old (weighing 225–250 g), were caged individually in a 12-h light, 12-h dark cycle in a temperature- and humidity-controlled environment. Animals were divided into two dietary sets for 30 days. One group was fed with standard chow diet (supplying 8% of calories as fat; type AO4 from Panlab, Barcelona, Spain). The second group was fed with a cafeteria diet (66% of calories as fat), as previously described (Endocrinology 146:4362–4369, 2005). Adipose tissue from the mesenteric surrounding the pancreas (pMES), was excised, weighed, cut, and rapidly frozen in liquid nitrogen for RNA isolation. Ten micrograms of total RNA from pMES adipose tissue were converted into cRNA, biotinylated, fragmented, and hybridized to GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA). Five microarrays were hybridized, three with independent samples coming from rats fed with standard chow (lean group) and two with independent samples coming from rats fed with the cafeteria diet (obese group).
2012-03-29 | E-GEOD-36935 | biostudies-arrayexpress
Project description:Role of microRNAs in compensatory b-cell mass expansion associated with pregnancy and obesity
| PRJNA151823 | ENA
Project description:Gene expression profile of tungstate-induced beta cell mass increase in STZ rats
| PRJNA91183 | ENA
Project description:Secreted Frizzled-Related Protein 5 is Downregulated in Obesity and Promotes β-Cell Proliferation [10 days]
| PRJNA188421 | ENA