| Insulin Sensitivity and β-Cell Function in Adults with Lifetime, Untreated Isolated Growth Hormone Deficiency. | |
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MedLine Citation:
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PMID: 22170707 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Context:GH reduces insulin sensitivity (IS), whereas IGF-I increases it. IGF-I seems to be critical for the development of the β-cells, and impaired IS has been reported in GH deficiency (GHD).Objective:The aim of the study was to assess IS and β-cell function in adult patients with untreated isolated GHD (IGHD) due to a homozygous mutation in the GHRH receptor gene.Design, Setting, and Patients:We conducted a cross-sectional study in 24 GH-naive adult IGHD subjects and 25 controls.Intervention:We performed an oral glucose tolerance test with glucose and insulin measurements at 0, 30, 60, 90, 120, and 180 min.Main Outcome Measure:IS was assessed by homeostasis model assessment index of insulin resistance (IR), quantitative IS check index, oral glucose IS in 2 h (OGIS2) and 3 h (OGIS3). β-Cell function was assayed by homeostasis model assessment index-β, insulinogenic index, and area under the curve of insulin-glucose ratio.Results:During the oral glucose tolerance test, glucose levels were higher in IGHD subjects (P < 0.0001), whereas insulin response presented a trend toward reduction (P = 0.08). The number of individuals with impaired glucose tolerance was higher in the IGHD group (P = 0.001), whereas the frequency of diabetes was similar in the two groups. Homeostasis model assessment index of IR was lower (P = 0.04), and quantitative IS check index and OGIS2 showed a nonsignificant trend toward elevation (P = 0.066 and P = 0.09, respectively) in IGHD. OGIS3 showed no difference between the groups. Homeostasis model assessment index-β, insulinogenic index, and ratio of the areas of the insulin and glucose curves were reduced in the IGDH group (P = 0.015, P < 0.0001, and P = 0.02, respectively).Conclusions:Adult subjects with lifetime congenital untreated IGHD present reduced β-cell function, no evidence of IR, and higher frequency of impaired glucose tolerance. |
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Authors:
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Carla R P Oliveira; Roberto Salvatori; Jose A S Barreto-Filho; Ivina E S Rocha; Andrea Mari; Rossana M C Pereira; Viviane C Campos; Menilsson Menezes; Elenilde Gomes; Rafael A Meneguz-Moreno; Vanessa P Araújo; Natália T F Leite; Adão C Nascimento-Junior; Maria I T Farias; Thaisa A R Viscente; Raquel D C Araújo; Enaldo V Melo; Manuel H Aguiar-Oliveira |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-12-14 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: - ISSN: 1945-7197 ISO Abbreviation: - Publication Date: 2011 Dec |
Date Detail:
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Created Date: 2011-12-15 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Federal University of Sergipe (C.R.P.O., J.A.S.B.-F., I.E.S.R., R.M.C.P., V.C.C., M.M., E.G., R.A.M.-M., V.P.A., N.T.F.L., A.C.N.-J., M.I.T.F., T.A.R.V., R.D.C.A., E.V.M., M.H.A.-O.), Division of Endocrinology, 49060-100 Aracaju, SE, Brazil; The John Hopkins University School of Medicine (R.S.), Division of Endocrinology, Baltimore, Maryland 21287; and National Research Council (A.M.), 35127 Padova, Italy. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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