Wolverhampton Intellectual Repository and E-Theses >
Research Institutes >
Research Institute in Healthcare Science >
Diabetes, Physiology and Molecular Medicine Research Group >
Visfatin regulates insulin secretion, insulin receptor signalling and mRNA expression of diabetes-related genes in mouse pancreatic beta-cells.
this identifier to cite or link
to this item:
|Title: ||Visfatin regulates insulin secretion, insulin receptor signalling and mRNA expression of diabetes-related genes in mouse pancreatic beta-cells.|
|Citation: ||Journal of molecular endocrinology, 44 (3):171-178|
|Publisher: ||Society for Endocinology|
|Journal: ||Journal of molecular endocrinology|
|Issue Date: ||2010 |
|PubMed ID: ||19906834|
|Abstract: ||The role of the adipocyte-derived factor visfatin in metabolism remains controversial, although some pancreatic beta-cell-specific effects have been reported. This study investigated the effects of visfatin upon insulin secretion, insulin receptor activation and mRNA expression of key diabetes-related genes in clonal mouse pancreatic beta-cells. beta-TC6 cells were cultured in RPMI 1640 and were subsequently treated with recombinant visfatin. One-hour static insulin secretion was measured by ELISA. Phospho-specific ELISA and western blotting were used to detect insulin receptor activation. Real-time SYBR Green PCR array technology was used to measure the expression of 84 diabetes-related genes in both treatment and control cells. Incubation with visfatin caused significant changes in the mRNA expression of several key diabetes-related genes, including marked up-regulation of insulin (9-fold increase), hepatocyte nuclear factor (HNF)1beta (32-fold increase), HNF4alpha (16-fold increase) and nuclear factor kappaB (40-fold increase). Significant down-regulation was seen in angiotensin-converting enzyme (-3.73-fold) and UCP2 (-1.3-fold). Visfatin also caused a significant 46% increase in insulin secretion compared to control (P<0.003) at low glucose, and this increase was blocked by co-incubation with the specific nicotinamide phosphoribosyltransferase inhibitor FK866. Both visfatin and nicotinamide mononucleotide induced activation of both insulin receptor and extracellular signal-regulated kinase (ERK)1/2, with visfatin-induced insulin receptor/ERK1/2 activation being inhibited by FK866. We conclude that visfatin can significantly regulate insulin secretion, insulin receptor phosphorylation and intracellular signalling and the expression of a number of beta-cell function-associated genes in mouse beta-cells.|
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Polymerase Chain Reaction
|Appears in Collections: ||Diabetes, Physiology and Molecular Medicine Research Group|
|Files in This Item:|
There are no files associated with this item.
All Items in WIRE are protected by copyright, with all rights reserved, unless otherwise indicated.