| Glucose metabolism after normalization of markers of iron overload by venesection in subjects with hereditary hemochromatosis. | |
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MedLine Citation:
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PMID: 20673928 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hereditary hemochromatosis (HH) is associated with abnormal glucose metabolism (AGM). We investigated the effect on glucose metabolism of normalization of the markers of iron overload by phlebotomy in subjects with HH. We prospectively studied 11 newly diagnosed subjects with HH and AGM using a standard 75-g oral glucose tolerance test. Basal quantitative insulin sensitivity check index (QUICKI) and stimulated oral glucose insulin sensitivity index (OGIS) insulin sensitivity was calculated from glucose and insulin data, whereas β-cell function was assessed using C-peptide concentration after adjusting for ambient insulin sensitivity. After normalization of ferritin and transferrin saturations by venesection for 12 (range, 8-16) months, subjects were studied again using the same methods. From 11 subjects with AGM at the time that HH was diagnosed, 7 had impaired glucose tolerance (IGT) and 4 had type 2 diabetes mellitus (T2DM). Normalization of the iron stores (ferritin and transferrin) improved the glucose tolerance status of 4 patients with IGT (to normal glucose tolerance), whereas 2 of those with IGT progressed to T2DM. In 5 patients, glucose tolerance status did not change (4 T2DM and 1 IGT). The area under the insulin and the C-peptide curve during the oral glucose tolerance test and the hepatic insulin extraction increased (P = .05), whereas no statistically significant changes occurred in insulin sensitivity. However, the disposition index, a measure of the ability of insulin release to compensate for insulin resistance, improved significantly (P = .02). Normalization of ferritin and transferrin saturation by venesection in subjects with HH and AGM led to improvements in some, but not all, measures of insulin secretion and action. Most patients with AGM had an improvement in glucose tolerance status, probably due to the augmented action of insulin in peripheral tissues. |
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Authors:
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Mensud Hatunic; Francis M Finucane; Suzanne Norris; Giovanni Pacini; John J Nolan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-01 |
Journal Detail:
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Title: Metabolism: clinical and experimental Volume: 59 ISSN: 1532-8600 ISO Abbreviation: Metab. Clin. Exp. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-24 Completed Date: 2010-12-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375267 Medline TA: Metabolism Country: United States |
Other Details:
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Languages: eng Pagination: 1811-5 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Metabolic Research Unit, St James's Hospital, Trinity College, Dublin, Ireland. mensudhatunic@gmail.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Glucose / metabolism* Glucose Tolerance Test Hemochromatosis / genetics, metabolism* Humans Insulin Resistance Iron Overload / metabolism* Middle Aged |
| Chemical | |
Reg. No./Substance:
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50-99-7/Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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