Role of IGFBP-3 in the regulation of beta-cell mass during obesity: adipose tissue/beta-cell cross talk.

Authors: Palau, N  Rebuffat, SA  Altirriba, J  Piquer, S  Hanzu, FA  Gomis, R  Barbera, A 
Citation: Palau N, etal., Endocrinology. 2012 Jan;153(1):177-87. doi: 10.1210/en.2011-0181. Epub 2011 Nov 8.
Pubmed: (View Article at PubMed) PMID:22067319
DOI: Full-text: DOI:10.1210/en.2011-0181

In obesity an increase in beta-cell mass occurs to cope with the rise in insulin demand. This beta-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 beta-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 beta-cell proliferation rate, probably through an IGF-I-dependent mechanism. This cross talk between the visceral-pancreatic adipose tissue and beta-cells is a novel mechanism that participates in the control of beta-cell plasticity.

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CRRD Object Information
CRRD ID: 10402755
Created: 2015-10-28
Species: All species
Last Modified: 2015-10-28
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.