Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin.

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Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin. / Brown, JE; Conner, Alex; Digby, JE; Ward, KL; Ramanjaneya, M; Randeva, HS; Dunmore, SJ.

In: Peptides, Vol. 31, No. 5, 01.05.2010, p. 944-9.

Research output: Contribution to journalArticle

Harvard

Brown, JE, Conner, A, Digby, JE, Ward, KL, Ramanjaneya, M, Randeva, HS & Dunmore, SJ 2010, 'Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin.', Peptides, vol. 31, no. 5, pp. 944-9. https://doi.org/10.1016/j.peptides.2010.02.004

APA

Vancouver

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Brown, JE ; Conner, Alex ; Digby, JE ; Ward, KL ; Ramanjaneya, M ; Randeva, HS ; Dunmore, SJ. / Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin. In: Peptides. 2010 ; Vol. 31, No. 5. pp. 944-9.

Bibtex

@article{59efd5c7702349b785142175d484665b,
title = "Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin.",
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.",
author = "JE Brown and Alex Conner and JE Digby and KL Ward and M Ramanjaneya and HS Randeva and SJ Dunmore",
year = "2010",
month = may
day = "1",
doi = "10.1016/j.peptides.2010.02.004",
language = "English",
volume = "31",
pages = "944--9",
journal = "Peptides",
issn = "0196-9781",
publisher = "Elsevier",
number = "5",

}

RIS

TY - JOUR

T1 - Regulation of beta-cell viability and gene expression by distinct agonist fragments of adiponectin.

AU - Brown, JE

AU - Conner, Alex

AU - Digby, JE

AU - Ward, KL

AU - Ramanjaneya, M

AU - Randeva, HS

AU - Dunmore, SJ

PY - 2010/5/1

Y1 - 2010/5/1

N2 - 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.

AB - 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.

U2 - 10.1016/j.peptides.2010.02.004

DO - 10.1016/j.peptides.2010.02.004

M3 - Article

C2 - 20156502

VL - 31

SP - 944

EP - 949

JO - Peptides

JF - Peptides

SN - 0196-9781

IS - 5

ER -