| The role of insulin-like growth factor (IGF) binding protein-2 in the insulin-mediated decrease in IGF-I bioactivity. | |
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MedLine Citation:
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PMID: 19846739 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Insulin interacts with the GH-IGF system by a reciprocal regulation of IGF-binding proteins (IGFBP) and GH, which in turn regulate insulin sensitivity via bioactive IGF-I. This network is linked to metabolic syndrome and cardiovascular diseases. OBJECTIVE: We evaluated the effect of glucose and insulin on IGFBP-1-4, particularly IGFBP-2, in the regulation of bioactive IGF-I and its relation to insulin resistance. SETTING: The study was conducted at an endocrinology center. RESEARCH DESIGN AND METHODS: Twenty-four healthy subjects (12 men; aged 21-72 yr; body mass index 25.9 +/- 0.9 kg/m(2)) and 19 subjects with impaired glucose tolerance (IGT; eight men; aged 26-71 yr; body mass index 28.9 +/- 1.2 kg/m(2)) were prospectively studied using oral glucose tolerance test and hyperinsulinemic euglycemic clamp. RESULTS: During the clamp, insulin decreased IGF-I bioactivity in both IGT subjects and controls (-16.2 +/- 2.8 and -13.9 +/- 3.3%, respectively; P < 0.01). In addition, insulin increased IGFBP-2 and GH and decreased IGFBP-1 and -4 but did not alter total IGF-I, IGF-II, or IGFBP-3 levels. During the oral glucose tolerance test, GH and IGFBP-1 were markedly suppressed. Subjects with IGT showed more pronounced insulin resistance and lower GH, IGFBP-1, and IGFBP-2 levels (P < 0.05). In multiple regression analysis, IGFBP-2 was an independent predictor of insulin sensitivity (beta = 0.36, P < 0.05) and IGF-I bioactivity (beta = -0.5, P < 0.05). CONCLUSIONS: Our data indicate that insulin acutely decreases IGF-I bioactivity through differential modulation of IGFBPs. Furthermore, IGFBP-2 plays a central role in the insulin-IGF system cross talk and is closely linked to insulin resistance, thereby providing a further explanation for its association with the metabolic syndrome. |
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Authors:
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Ayman M Arafat; Martin O Weickert; Jan Frystyk; Joachim Spranger; Christof Sch??fl; Matthias M??hlig; Andreas F H Pfeiffer |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-10-21 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 94 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-12-04 Completed Date: 2010-01-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 5093-101 Citation Subset: AIM; IM |
Affiliation:
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Department of Endocrinology, Diabetes, and Nutrition, Charit??-University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. ayman.arafat@charite.de |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Animals Biological Markers Blood Glucose / metabolism Body Mass Index Female Glucose Clamp Technique Glucose Tolerance Test Hormones / blood Humans Insulin / physiology* Insulin Resistance / genetics*, physiology* Insulin-Like Growth Factor Binding Protein 2 / physiology* Insulin-Like Growth Factor I / physiology* Lipids / blood Male Metabolic Syndrome X / genetics, physiopathology Mice Middle Aged Obesity / genetics, physiopathology Young Adult |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Blood Glucose; 0/Hormones; 0/Insulin-Like Growth Factor Binding Protein 2; 0/Lipids; 11061-68-0/Insulin; 67763-96-6/Insulin-Like Growth Factor I |
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