Abstract
Resistin is a potential link between obesity and insulin resistance or type 2 diabetes. In rodents, resistin is primarily expressed in and secreted from mature adipocytes, with some expression in pancreatic islets and portions of the pituitary and hypothalamus. Its secretion can be up-regulated by several factors, including insulin and glucose. The exposure of rodents, or their cells, to resistin results in decreased response to insulin. This is likely in part due to an upregulation of suppressor of cytokine signaling (SOCS)-3, which interferes with the activation of insulin receptor substrate (IRS)-1. However, in humans resistin is expressed primarily by macrophages and seems to be involved in the recruitment of other immune cells and the secretion of pro-inflammatory factors, including tumor necrosis factor (TNF)α. Human resistin may interfere with insulin signaling by stimulating the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which dephosphorylates 3-phosphorylated phosphoinositide (PIP3). Resistin also seems to be involved in the development of atherosclerosis in humans by promoting the formation of foam cells and the proliferation and migration of vascular endothelial and smooth muscle cells. Many of the inflammatory related functions of human resistin appear to be regulated by activation of the nuclear factor (NF)κB transcription factor. The divergent roles of resistin in humans and rodents are evident by the data presented in this review but they will not be able to be fully understood until the resistin receptor is identified.
Keywords: Resistin, insulin sensitivity, glucose, mice, rats, humans, adipose tissue, macrophages
Current Protein & Peptide Science
Title: Role of Resistin in Insulin Sensitivity in Rodents and Humans
Volume: 10 Issue: 1
Author(s): K. M. Barnes and J. L. Miner
Affiliation:
Keywords: Resistin, insulin sensitivity, glucose, mice, rats, humans, adipose tissue, macrophages
Abstract: Resistin is a potential link between obesity and insulin resistance or type 2 diabetes. In rodents, resistin is primarily expressed in and secreted from mature adipocytes, with some expression in pancreatic islets and portions of the pituitary and hypothalamus. Its secretion can be up-regulated by several factors, including insulin and glucose. The exposure of rodents, or their cells, to resistin results in decreased response to insulin. This is likely in part due to an upregulation of suppressor of cytokine signaling (SOCS)-3, which interferes with the activation of insulin receptor substrate (IRS)-1. However, in humans resistin is expressed primarily by macrophages and seems to be involved in the recruitment of other immune cells and the secretion of pro-inflammatory factors, including tumor necrosis factor (TNF)α. Human resistin may interfere with insulin signaling by stimulating the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which dephosphorylates 3-phosphorylated phosphoinositide (PIP3). Resistin also seems to be involved in the development of atherosclerosis in humans by promoting the formation of foam cells and the proliferation and migration of vascular endothelial and smooth muscle cells. Many of the inflammatory related functions of human resistin appear to be regulated by activation of the nuclear factor (NF)κB transcription factor. The divergent roles of resistin in humans and rodents are evident by the data presented in this review but they will not be able to be fully understood until the resistin receptor is identified.
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Cite this article as:
Barnes M. K. and Miner L. J., Role of Resistin in Insulin Sensitivity in Rodents and Humans, Current Protein & Peptide Science 2009; 10 (1) . https://dx.doi.org/10.2174/138920309787315239
DOI https://dx.doi.org/10.2174/138920309787315239 |
Print ISSN 1389-2037 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5550 |
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