Resistin down-regulates insulin receptor expression, and modulates cell viability in rodent pancreatic beta-cells.
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.
Brown
James E P
JE
Diabetes and Metabolic Disorders Research Group, Research Institute in Healthcare Sciences, University of Wolverhampton, Wolverhampton, UK. jepbrown@hotmail.com
Onyango
David J
DJ
Dunmore
Simon J
SJ
D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D051381:Rats; D011972:Receptor, Insulin / Q000235:genetics* / Q000378:metabolism; D052243:Resistin / Q000494:pharmacology*
D007328:Insulin; D052243:Resistin; D011972:Receptor, Insulin