| Analysis of insulin sensitivity in adipose tissue of patients with primary aldosteronism. | |
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MedLine Citation:
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PMID: 20484481 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: The objective of the study was to assess the effect of high aldosterone levels on insulin sensitivity of adipose tissue in humans. METHODS: Visceral adipose tissue (VAT) was obtained from patients with aldosterone-producing adenoma (APA; n=14) and, as controls, nonfunctioning adenoma (NFA; n=14) undergoing laparoscopic adrenalectomy. Homeostasis model assessment index was higher and potassium was lower in APA than NFA (P<0.05). Immunohistochemistry, Western blotting, and real-time PCR were used to detect and quantify mineralocorticoid receptor (MR) expression. Transcript levels of peroxisome proliferative-activated receptor-gamma, insulin receptor, glucose transporter 4, insulin receptor substrate-1 and -2, leptin, adiponectin, IL-6, monocyte chemoattractant protein-1, glucocorticoid receptor (GR)-alpha, 11beta-hydroxysteroid dehydrogenase (HSD11B) type 1, and HSD11B2 were quantified. The effect of increasing aldosterone concentrations on 2-deoxy-[3H]d-glucose uptake was tested in human sc abdominal adipocytes. RESULTS: Expression of MR was demonstrated in VAT, with no difference between APA and NFA as to mRNA levels of MR, GRalpha, HSD11B1, and glucose metabolism and inflammation factors. In cultured adipocytes, basal and insulin-stimulated glucose uptake were unaffected by 1-100 nM (normal/hyperaldosteronism) and impaired only by much higher, up to 10 microM, aldosterone concentrations. The impairment was prevented by RU486 but not by eplerenone. CONCLUSIONS: Gene expression of insulin signaling/inflammatory molecules was similar in VAT of APA and NFA patients, not supporting an effect of aldosterone excess on insulin sensitivity of adipose tissues. Only at pharmacological concentrations and through GR activation, aldosterone reduced glucose uptake in adipocytes. Insulin resistance in primary aldosteronism might occur in compartments other than fat and/or depend on concurrent environmental factors. |
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Authors:
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Riccardo Urbanet; Catia Pilon; Alessandra Calcagno; Alessandro Peschechera; Edwige-Ludiwyne Hubert; Gilberta Giacchetti; Celso Gomez-Sanchez; Paolo Mulatero; Mariacristina Toffanin; Nicoletta Sonino; Maria-Christina Zennaro; Francesco Giorgino; Roberto Vettor; Francesco Fallo |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-19 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 95 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-05 Completed Date: 2010-08-24 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: 4037-42 Citation Subset: AIM; IM |
Affiliation:
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Department of Medical and Surgical Sciences, University of Padova, Via Ospedale 105, 35128 Padova, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adiponectin
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genetics,
metabolism Adrenal Cortex Neoplasms / genetics, metabolism Adrenocortical Adenoma / genetics, metabolism Adrenocorticotropic Hormone / blood Aldosterone / blood Analysis of Variance Blotting, Western Female Humans Hydrocortisone / blood Hyperaldosteronism / metabolism* Immunohistochemistry Insulin / metabolism* Insulin Resistance* Intra-Abdominal Fat / metabolism* Male RNA, Messenger / genetics, metabolism Receptors, Mineralocorticoid / genetics, metabolism Renin / blood Reverse Transcriptase Polymerase Chain Reaction |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin; 0/RNA, Messenger; 0/Receptors, Mineralocorticoid; 11061-68-0/Insulin; 50-23-7/Hydrocortisone; 52-39-1/Aldosterone; 9002-60-2/Adrenocorticotropic Hormone; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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