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Series GSE36935 Query DataSets for GSE36935
Status Public on Mar 30, 2012
Title Role of IGFBP-3 in the Regulation of β-Cell Mass during Obesity: Adipose Tissue/ β-Cell Cross Talk
Organism Rattus norvegicus
Experiment type Expression profiling by array
Summary 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)
 
Overall design 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).
 
Contributor(s) Palau N, Rebuffat SA, Altirriba J, Piquer S, Hanzu FA, Gomis R, Barbera A
Citation(s) 22067319
Submission date Mar 29, 2012
Last update date Jul 31, 2017
Contact name Jordi Altirriba
E-mail(s) altirriba@hotmail.com
Organization name Centre Médical Universitaire de Genève
Department Dpts de Médecine Interne et de Physiologie cellulaire et Métabolisme
Lab Laboratoire du Métabolisme
Street address Rue Michel-Servet 1
City Genève
ZIP/Postal code 1211
Country Switzerland
 
Platforms (1)
GPL1355 [Rat230_2] Affymetrix Rat Genome 230 2.0 Array
Samples (5)
GSM906555 Cafeteria diet 1
GSM906556 Cafeteria diet 2
GSM906557 Standard diet 1
Relations
BioProject PRJNA157313

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Supplementary file Size Download File type/resource
GSE36935_RAW.tar 20.8 Mb (http)(custom) TAR (of CEL)
Processed data included within Sample table

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