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      Influence of CYP11B2 Gene Polymorphism on the Prevalence of Hypertension and the Blood Pressure in Japanese Men: Interaction with Dietary Salt Intake

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          Abstract

          Aims: CYP11B2 gene encodes a key enzyme for the production of aldosterone. Our aim is to investigate the association of –344T/C polymorphism with hypertension in Japanese men. The interaction between genotypes and dietary salt intake was also considered. Methods: Three hundred and ten Japanese male workers participated in this study. Daily salt intake was calculated from a food frequency questionnaire. Melting curve analysis was used to determine CYP11B2 genotypes. Results:There was a significant association between the CT + TT genotype and higher prevalence of hypertension (odds ratio: 3.03; p = 0.014). The association presented in a recessive manner and was strongest in the high-salt intake group (odds ratio: 9.44; p = 0.049). Only in the high-intake group, systolic blood pressure (SBP) was significantly higher in the CT + TT group than in the CC group (p = 0.038). The SBP had a positive correlation with salt intake in the CT + TT group (p for linear trend = 0.021), but not in the CC group (p for interaction = 0.011). Conclusions: CYP11B2 gene –344C/T polymorphism affects the risk of hypertension in Japanese men and high-salt intake levels strengthen this association. This gene-diet interaction warrants further study to elucidate the efficacy of salt restriction as an antihypertensive therapy in different genotypes.

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          Plasma aldosterone is independently associated with the metabolic syndrome.

          Murielle Bochud, Jürg Nussberger, Conrad Shamlaye … (2006)
          The aim of this study was to analyze the associations of plasma aldosterone and plasma renin activity with the metabolic syndrome and each of its components. We analyzed data from a family based study in the Seychelles made up of 356 participants (160 men and 196 women) from 69 families of African descent. In multivariable models, plasma aldosterone was associated positively (P < 0.05) with blood pressure in older individuals (interaction with age, P < 0.05) and with waist circumference in men (interaction with sex, P < 0.05) and negatively with high-density lipoprotein cholesterol, in particular in individuals with elevated urinary potassium excretion (interaction with urinary potassium, P < 0.05); plasma renin activity was significantly associated with triglycerides and fasting blood glucose. Plasma aldosterone, but not plasma renin activity, was associated with the metabolic syndrome per se, independently of the association with its separate components. The observation that plasma renin activity was associated with some components of the metabolic syndrome, whereas plasma aldosterone was associated with other components of the metabolic syndrome, suggests different underlying mechanisms. These findings reinforce previous observations suggesting that aldosterone is associated with several cardiovascular risk factors and also suggest that aldosterone might contribute to the increased cardiovascular disease risk in individuals of African descent with the metabolic syndrome.
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            The product of the CYP11B2 gene is required for aldosterone biosynthesis in the human adrenal cortex.

            R Natarajan, J. Nadler, T Luna … (1991)
            The steroid 11 beta-hydroxylase (P450c11) enzyme is responsible for the conversion of 11-deoxycortisol to cortisol in the zona fasciculata of the adrenal cortex. Animal studies have suggested that this enzyme or a closely related isozyme is also responsible for the successive 11 beta- and 18-hydroxylation and 18-oxidation of deoxycorticosterone required for aldosterone synthesis in the zona glomerulosa. There are two distinct 11 beta-hydroxylase genes in man, CYP11B1 and CYP11B2, which are predicted to encode proteins with 93% amino acid identity. We used a sensitive assay based on the polymerase chain reaction to analyze the expression of the CYP11B1 and B2 genes. Transcripts of CYP11B1 were detected at high levels in surgical specimens of normal adrenals and also in an aldosterone-secreting adrenal tumor. Transcripts of CYP11B2 were found at low levels in normal adrenals, but at a much higher level in the aldosterone-secreting tumor. CYP11B2 mRNA levels were increased in cultured zona glomerulosa cells by physiological levels of angiotensin-II. The entire coding regions of both CYP11B1 and B2 cDNAs were cloned from the tumor mRNA. Expression of these cDNAs in cultured COS-1 cells demonstrated that the CYP11B1 product could only 11 beta-hydroxylate 11-deoxycortisol or deoxycorticosterone, whereas the CYP11B2 product could also 18-hydroxylate cortisol or corticosterone. A small amount of aldosterone was synthesized from deoxycorticosterone only in cells expressing CYP11B2 cDNA. These data demonstrate that the product of CYP11B2 is required for the final steps in the synthesis of aldosterone.
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              Glucocorticoid-suppressible hyperaldosteronism results from hybrid genes created by unequal crossovers between CYP11B1 and CYP11B2.

              Aaron P White, Barry J. Connell, L. Pascoe … (1992)
              Glucocorticoid-suppressible hyperaldosteronism (GSH) is an autosomal dominant form of familial hypertension. The biochemical abnormalities seen in this disorder may be remedied by administration of dexamethasone, implying that aldosterone synthesis is being abnormally regulated by corticotropin. The final three steps of aldosterone synthesis, 11 beta- and 18-hydroxylation and 18-oxidation, are mediated by a cytochrome P450 in the zona glomerulosa of the adrenal cortex termed CYP11B2. A related isozyme in the zona fasciculata, CYP11B1, is required for cortisol synthesis; this isozyme, which is normally expressed at much higher levels than CYP11B2, only has 11 beta-hydroxylase activity. These isozymes are encoded by genes on human chromosome 8q22. We have now studied four unrelated patients with GSH. We found that each patient has one chromosome that carries three CYP11B genes instead of two. This has presumably been generated by unequal meiotic crossing-over. The extra gene is a hybrid with 5' regulatory and coding regions corresponding to CYP11B1 and 3' coding regions from CYP11B2. The breakpoint is in intron 2 in two cases, intron 3 in one, and exon 4 in one. Cells transfected with hybrid cDNAs containing up to the first three exons of CYP11B1 synthesized aldosterone at levels near that of cells carrying normal CYP11B2, but cells transfected with hybrids containing the first five or more exons of CYP11B1 could not synthesize detectable amounts of aldosterone. These data demonstrate that GSH is caused by expression of a gene that is regulated like CYP11B1 but that encodes a protein able to synthesize aldosterone.
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                Author and article information

                Journal
                Journal ID (publisher-id): JNN
                Journal ID (nlm-ta): Lifestyle Genomics
                Journal ID (doi): 10.1159/issn.2504-3188
                Title: Lifestyle Genomics
                Publisher: S. Karger AG
                ISSN (Print): 2504-3161
                ISSN (Electronic): 2504-3188
                Publication date Subscription-year: 2008
                Publication date (Print): August 2008
                Publication date (Electronic): 06 August 2008
                Volume: 1
                Issue: 5
                Pages: 252-258
                Affiliations
                aDepartment of Molecular Epidemiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, and bDepartment of Health Informatics, Kyoto University School of Public Health, Kyoto, Japan
                Article
                Publisher ID: 150006 Other ID: J Nutrigenet Nutrigenomics 2008;1:252–258
                DOI: 10.1159/000150006
                PubMed ID: 19776632
                SO-VID: aca3d718-a377-4581-9df7-f11ace46eb96
                Copyright © © 2008 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 17 December 2007
                Date accepted : 22 May 2008
                Page count
                Figures: 2, Tables: 2, References: 35, Pages: 7
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Nutrition & Dietetics,Health & Social care,Public health
                Keywords: Salt intake,Hypertension,Blood pressure,CYP11B2 polymorphism
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics, Health & Social care, Public health
                Keywords: Salt intake, Hypertension, Blood pressure, CYP11B2 polymorphism

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