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Title
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Insulin-like growth factors and pancreas beta cells
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Author
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Abstract
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| Insulin-like growth factors (IGFs) have been implicated in normal growth, and especially foetal pancreas beta-cell development. As low birth weight has been implicated in the development of obesity and type 2 diabetes, much research has evolved into the importance of IGF and their signalling pathways for pancreas beta-cell development, and for type 2 diabetes. Insulin-like growth factor-I signalling has a lot in common with insulin signalling, and is involved in diverse cellular effects such as antiapoptosis, protein synthesis, cell growth and mitogenesis. Insulin-like growth factor-II can be bound by the insulin receptor A subtype and the IGF-1 receptor, which may explain its antiapoptotic effect. Various knock-out model studies indicate that absence of IGF-I or the IGF-1 receptor is critical for foetal and postnatal growth. Similarly, knock-out models of post-receptor molecules (such as IRS-2) point to the physiological role of IGFs for pancreas beta-cell development. A beta-cell-specific IGF-1 receptor knock out model indicates the importance of IGF-I for beta-cell function. The Goto-Kakizaki (GK) rat, a model for diabetes, has insufficient beta-cell development, which may be related to its defective IGF-II synthesis. As normal pancreas beta cells adapt to the prevailing insulin resistance with increasing beta-cell function, it is possible that insulin resistance interacts with IGF signalling in pancreas beta cells. |
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Language
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English
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Source (journal)
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European journal of clinical investigation. - Berlin
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Publication
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Hoboken
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Wiley
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2004
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ISSN
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0014-2972
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DOI
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10.1111/J.1365-2362.2004.01337.X
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Volume/pages
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34
:4
(2004)
, p. 249-255
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ISI
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000220839400002
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Pubmed ID
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15086355
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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