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Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin
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Brown, James E. P., Conner, Alex C., Digby, Janet E., Ward, Kenya L., Ramanjaneya, Manjunath, Randeva, Harpal S. and Dunmore, Simon J. (2010) Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin. Peptides, Vol.31 (No.5). pp. 944-949. doi:10.1016/j.peptides.2010.02.004 ISSN 0196-9781.
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Official URL: http://dx.doi.org/10.1016/j.peptides.2010.02.004
Abstract
Obesity is an established risk factor for type 2 diabetes. Activation of the adiponectin receptors has a clear role in improving insulin resistance although conflicting evidence exists for its effects on pancreatic beta-cells. Previous reports have identified both adiponectin receptors (ADR-1 and ADR-2) in the beta-cell. Recent evidence has suggested that two distinct regions of the adiponectin molecule, the globular domain and a small N-terminal region, have agonist properties. This study investigates the effects of two agonist regions of adiponectin on insulin secretion, gene expression, cell viability and cell signalling in the rat beta-cell line BRIN-BD11, as well as investigating the expression levels of adiponectin receptors (ADRs) in these cells. Cells were treated with globular adiponectin and adiponectin (15-36) +/- leptin to investigate cell viability, expression of key beta-cell genes and ERK1/2 activation. Both globular adiponectin and adiponectin (15-36) caused significant ERK1/2 dependent increases in cell viability. Leptin co-incubation attenuated adiponectin (15-36) but not globular adiponectin induced cell viability. Globular adiponectin, but not adiponectin (15-36), caused a significant 450% increase in PDX-1 expression and a 45% decrease in LPL expression. ADR-1 was expressed at a higher level than ADR-2, and ADR mRNA levels were differentially regulated by non-esterified fatty acids and peroxisome-proliferator-activated receptor agonists. These data provide evidence of roles for two distinct adiponectin agonist domains in the beta-cell and confirm the potentially important role of adiponectin receptor agonism in maintaining beta-cell mass. (C) 2010 Elsevier Inc. All rights reserved.
| Item Type: | Journal Article | ||||
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| Subjects: | Q Science > QD Chemistry R Medicine > RS Pharmacy and materia medica |
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| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016) Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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| Journal or Publication Title: | Peptides | ||||
| Publisher: | Elsevier Inc | ||||
| ISSN: | 0196-9781 | ||||
| Official Date: | May 2010 | ||||
| Dates: |
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| Volume: | Vol.31 | ||||
| Number: | No.5 | ||||
| Number of Pages: | 6 | ||||
| Page Range: | pp. 944-949 | ||||
| DOI: | 10.1016/j.peptides.2010.02.004 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access |
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