Resistin down-regulates insulin receptor expression, and modulates cell viability in rodent pancreatic beta-cells

James E.P. Brown, David J. Onyango, Simon J. Dunmore

Research output: Contribution to journalArticle

Abstract

The adipokine resistin is known to induce insulin resistance in rodent tissues. Increases in adipose tissue mass are known to have a negative effect on pancreatic beta-cell function, although the mechanisms are poorly understood. This study investigated the effects of resistin on insulin secretion, insulin receptor expression and cell viability in pancreatic beta-cells. BTC-6 or BRIN-BD11 cells were treated for 24h with resistin, and insulin receptor expression, insulin secretion and cell viability were measured. Incubation with 40ng/ml resistin caused significant decreases in insulin receptor mRNA and protein expression, but did not affect insulin secretion. At low concentrations, resistin caused significant increases in cell viability. These data implicate resistin as a factor that may regulate beta-cell function/viability, and suggests a potential mechanism by which increased adiposity causes beta-cell dysfunction.
Original languageEnglish
Pages (from-to)3273-3276
Number of pages4
JournalFEBS Letters
Volume581
Issue number17
Early online date21 Jun 2007
DOIs
Publication statusPublished - 10 Jul 2007

Fingerprint

Resistin
Insulin Receptor
Insulin-Secreting Cells
Rodentia
Cell Survival
Down-Regulation
Cells
Insulin
Tissue
Adipokines
Adiposity
Insulin Resistance
Adipose Tissue
Messenger RNA
Proteins

Keywords

  • adipokine
  • beta-cell
  • cell viability
  • insulin receptor
  • resistin

Cite this

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abstract = "The adipokine resistin is known to induce insulin resistance in rodent tissues. Increases in adipose tissue mass are known to have a negative effect on pancreatic beta-cell function, although the mechanisms are poorly understood. This study investigated the effects of resistin on insulin secretion, insulin receptor expression and cell viability in pancreatic beta-cells. BTC-6 or BRIN-BD11 cells were treated for 24h with resistin, and insulin receptor expression, insulin secretion and cell viability were measured. Incubation with 40ng/ml resistin caused significant decreases in insulin receptor mRNA and protein expression, but did not affect insulin secretion. At low concentrations, resistin caused significant increases in cell viability. These data implicate resistin as a factor that may regulate beta-cell function/viability, and suggests a potential mechanism by which increased adiposity causes beta-cell dysfunction.",
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Resistin down-regulates insulin receptor expression, and modulates cell viability in rodent pancreatic beta-cells. / Brown, James E.P.; Onyango, David J.; Dunmore, Simon J.

In: FEBS Letters, Vol. 581, No. 17, 10.07.2007, p. 3273-3276.

Research output: Contribution to journalArticle

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