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Insulin-like growth factor binding protein-3 induces insulin resistance in adipocytes in vitro and in rats in vivo

Title
Insulin-like growth factor binding protein-3 induces insulin resistance in adipocytes in vitro and in rats in vivo
Authors
Kim H.S.Ali O.Shim M.Lee K.-W.Vuguin P.Muzumdar R.Barzilai N.Cohen P.
Ewha Authors
김혜순
SCOPUS Author ID
김혜순scopus
Issue Date
2007
Journal Title
Pediatric Research
ISSN
0031-3998JCR Link
Citation
vol. 61, no. 2, pp. 159 - 164
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Insulin-like growth factor binding protein (IGFBP)-3 binds to IGF and modulates their actions and also possesses intrinsic activities. We investigated its effects on insulin action and found that when IGFBP-3 was added to fully differentiated 3T3-L1 adipocytes in culture, insulin-stimulated glucose transport was significantly inhibited to 60% of control in a time- and dose-dependent manner. Tumor necrosis factor (TNF)-α treatment also inhibited glucose transport to the same degree as IGFBP-3 and, in addition, increased IGFBP-3 levels 3-fold. Co-treatment with TNF-α and IGFBP-3 antisense partially prevented the inhibitory effect of TNF-α on glucose transport, indicating a role for IGFBP-3 in cytokine-induced insulin resistance. Insulin-stimulated phosphorylation of the insulin receptor was markedly decreased by IGFBP-3 treatment. IGFBP-3 treatment suppressed adiponectin expression in 3T3-L1 adipocytes. Infusion of IGFBP-3 to Sprague-Dawley rats for 3 h decreased peripheral glucose uptake by 15% compared with controls as well as inhibiting glycogen synthesis. Systemic administration of IGFBP-3 to rats for 7 d resulted in a dramatic 40% decrease in peripheral glucose utilization and glycogen synthesis. These in vitro and in vivo findings demonstrate that IGFBP-3 has potent insulin-antagonizing capability and suggest a role for IGFBP-3 in cytokine-induced insulin resistance and other mechanisms involved in the development of type-2 diabetes. © International Pediatrics Research Foundation, Inc. 2007. All Rights Reserved.
DOI
10.1203/pdr.0b013e31802d8a30
Appears in Collections:
의과대학 > 의학과 > Journal papers
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