Source:http://linkedlifedata.com/resource/pubmed/id/17785698
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2007-9-5
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pubmed:abstractText |
Severe insulin resistance resulting from known or putative genetic defects affecting the insulin receptor or post-insulin receptor signalling represents a clinical spectrum ranging from Donohue's and Rabson-Mendenhall syndrome, where the genetic defect is identified, through to the milder phenotype of type A insulin resistance, where a genetic defect can only be detected in around 10% of cases. Paradoxically, subjects with these conditions may present with hypoglycaemia due to mismatch of post-prandial glucose excursion and compensatory hyperinsulinaemia. Ultimately, treatment with insulin and insulin sensitisers will be unsuccessful and subjects may succumb to diabetes or its complications. Recombinant human IGF-I alone or combined with its binding protein (IGFBP-3) provides an alternative therapy as IGF-I receptor shares structural and functional homology with the insulin receptor and recombinant human insulin-like growth factor I (rhIGF-I) therapy could improve glucose disposal by signalling through the IGF-I receptor, whilst reducing the adverse effects of high insulin concentrations. There are also data which indicate that IGF-I signalling through the IGF-I receptor on the pancreatic beta-cell may be important in maintaining insulin secretion. Pilot studies confirmed that rhIGF-I could reduce glucose and insulin levels in subjects with type A insulin resistance and those with Rabson-Mendenhall syndrome with sustained beneficial effects on HbA1c. Continued study has confirmed efficacy of rhIGF-I when combined with IGFBP-3 in the treatment of Donohue's and type A insulin resistance subjects. Observations that IGF-I treatment can improve C-peptide levels in these subjects may indicate that it might be more valuable as a first line intervention to preserve beta-cell function, rather than its current use as a medication of last resort in subjects where all other therapies have failed.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0804-4643
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
157 Suppl 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S51-6
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17785698-Drug Therapy, Combination,
pubmed-meshheading:17785698-Humans,
pubmed-meshheading:17785698-Insulin Resistance,
pubmed-meshheading:17785698-Insulin-Like Growth Factor Binding Protein 3,
pubmed-meshheading:17785698-Insulin-Like Growth Factor I,
pubmed-meshheading:17785698-Receptor, Insulin,
pubmed-meshheading:17785698-Recombinant Proteins,
pubmed-meshheading:17785698-Severity of Illness Index,
pubmed-meshheading:17785698-Signal Transduction
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pubmed:year |
2007
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pubmed:articleTitle |
IGF-I treatment of insulin resistance.
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pubmed:affiliation |
University of Cambridge, Department of Paediatrics, Box 116, Addenbrookes Hospital, Hills Road, Cambridge, CB2 2QQ, UK.
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pubmed:publicationType |
Journal Article,
Review
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