The increased ratio of 11β-hydroxysteroid dehydrogenase type 1 versus 11β-hydroxysteroid dehydrogenase type 2 in chronic periodontitis irrespective of obesity

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Abstract

11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive cortisone to active cortisol, has been reported to play an important role in metabolic diseases as well as chronic inflammatory diseases. The involvement of 11β-HSD1 in chronic periodontitis was investigated in the present study. The relationship between the levels of 11β-HSD1, chronic periodontitis, and body mass index (BMI) was analyzed. The expression of 11β-HSD1 mRNA was significantly higher in the chronic periodontitis group than in the control group. Since the expression of 11β-HSD2, which converts active cortisol to inactive cortisone, was slightly lower in the chronic periodontitis group than in the controls, the ratio of 11β-HSD1 versus 11β-HSD2 was significantly higher in the chronic periodontitis group than in the controls. A correlation was not observed between BMI and the level of 11β-HSD1 or between BMI and the ratio of 11β-HSD1 versus 11β-HSD2. These results suggested that an increase in the ratio of 11β-HSD1 versus 11β-HSD2 was associated with chronic periodontitis irrespective of obesity.

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Most cited references 34

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11beta-hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress.

Y Kotelevtsev, M. Holmes, A Burchell … (1997)

Glucocorticoid hormones, acting via nuclear receptors, regulate many metabolic processes, including hepatic gluconeogenesis. It recently has been recognized that intracellular glucocorticoid concentrations are determined not only by plasma hormone levels, but also by intracellular 11beta-hydroxysteroid dehydrogenases (11beta-HSDs), which interconvert active corticosterone (cortisol in humans) and inert 11-dehydrocorticosterone (cortisone in humans). 11beta-HSD type 2, a dehydrogenase, thus excludes glucocorticoids from otherwise nonselective mineralocorticoid receptors in the kidney. Recent data suggest the type 1 isozyme (11beta-HSD-1) may function as an 11beta-reductase, regenerating active glucocorticoids from circulating inert 11-keto forms in specific tissues, notably the liver. To examine the importance of this enzyme isoform in vivo, mice were produced with targeted disruption of the 11beta-HSD-1 gene. These mice were unable to convert inert 11-dehydrocorticosterone to corticosterone in vivo. Despite compensatory adrenal hyperplasia and increased adrenal secretion of corticosterone, on starvation homozygous mutants had attenuated activation of the key hepatic gluconeogenic enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, presumably, because of relative intrahepatic glucocorticoid deficiency. The 11beta-HSD-1 -/- mice were found to resist hyperglycamia provoked by obesity or stress. Attenuation of hepatic 11beta-HSD-1 may provide a novel approach to the regulation of gluconeogenesis.

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Does central obesity reflect "Cushing's disease of the omentum"?

I J Bujalska, S Kumar, P M Stewart (1997)

Central obesity results in a cluster of metabolic abnormalities contributing to premature death. Glucocorticoids regulate adipose-tissue differentiation, function, and distribution, and in excess, cause central obesity. Glucocorticoid hormone action is, in part, controlled by two isoforms of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) which interconverts hormonally active cortisol to inactive cortisone. We studied cortisol metabolism within different adipose tissue depots. We analysed expression and activity of the two isoforms (1 and 2) of 11 beta-HSD in cultured omental and subcutaneous adipose stromal cells from 16 patients undergoing elective abdominal surgery. Only the type 1 isoform (11 beta-HSD1) was expressed in adipose stromal cells. The predominant activity was oxo-reductase (conversion of cortisone to cortisol greater than cortisol to cortisone) and was higher in omental than subcutaneous fat (cortisone to cortisol, median 57.6 pmol mg-1 h-1 [95% CI 25.8-112.9] vs 0 pmol mg-1 h-1 [0-0.6], p < 0.001). 11 beta-HSD1 oxo-reductase activity was further increased (127.5 pmol mg-1 h-1 [82.1-209], p < 0.05) when omental adipose stromal cells were treated with cortisol and insulin. Adipose stromal cells from omental fat, but not subcutaneous fat, can generate active cortisol from inactive cortisone through the expression of 11 beta-HSD1. The expression of this enzyme is increased further after exposure to cortisol and insulin. In vivo, such a mechanism would ensure a constant exposure of glucocorticoid specifically to omental adipose tissue, suggesting that central obesity may reflect "Cushing's disease of the omentum".

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Association of the metabolic syndrome with severe periodontitis in a large U.S. population-based survey.

Gopalakrishnan Netuveli, John Deanfield, Francesco D’Aiuto … (2008)

Metabolic syndrome and periodontitis both have an increasing prevalence worldwide; however, limited information is available on their association. The objective of the study was to assess the association between periodontitis and the metabolic syndrome in a cross-sectional survey of a nationally representative sample of the noninstitutionalized civilians in the United States. Data analysis from the Third National Health and Nutrition Examination Survey on 13,994 men and women aged 17 yr or older who received periodontal examination were studied. Association of diagnosis and extent of periodontitis (gingival bleeding, probing pocket depths) with the metabolic syndrome and its individual component conditions (central obesity, hypertriglyceridemia, low high-density lipoprotein-cholesterol, hypertension, and insulin resistance) were measured. Adjustment for age, sex, years of education, poverty to income ratio, ethnicity, general conditions, and smoking were considered. The prevalence of the metabolic syndrome was 18% [95% confidence interval (CI) 16-19], 34% (95% CI 29-38), and 37% (95% CI 28-48) among individuals with no-mild, moderate, and severe periodontitis, respectively. After adjusting for confounders, participants aged older than 45 yr suffering from severe periodontitis were 2.31 times (95% CI 1.13-4.73) more likely to have the metabolic syndrome than unaffected individuals. Diagnosis of metabolic syndrome increased by 1.12 times (95% CI 1.07-1.18) per 10% increase in gingival bleeding and 1.13 times (95% CI 1.03-1.24) per 10% increase in the proportion of periodontal pockets. Severe periodontitis is associated with metabolic syndrome in middle-aged individuals. Further studies are required to test whether improvements in oral health lead to reductions in cardiometabolic traits and the risk of metabolic syndrome or vice versa.

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Author and article information

Contributors

Takaya Nakata: nakata-t@cc.osaka-dent.ac.jp

Atsuko Fujita: fujita-a@cc.osaka-dent.ac.jp

Makoto Umeda: umeda-m@cc.osaka-dent.ac.jp

Hiroaki Yoshida: hiro-y@cc.osaka-dent.ac.jp

Kaoru Inami: inami@cc.osaka-dent.ac.jp

Hiroaki Masuzaki: hiroaki@med.u-ryukyu.ac.jp

Hirofumi Sawai: sawai@cc.osaka-dent.ac.jp

Journal

Journal ID (nlm-ta): Springerplus

Journal ID (iso-abbrev): Springerplus

Title: SpringerPlus

Publisher: Springer International Publishing (Cham )

ISSN (Electronic): 2193-1801

Publication date (Electronic): 16 January 2016

Publication date PMC-release: 16 January 2016

Publication date Collection: 2016

Volume: 5

Electronic Location Identifier: 40

Affiliations

[ ]Department of Periodontology, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Osaka 573-1121 Japan

[ ]First Department of Oral and Maxillofacial Surgery, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Osaka 573-1121 Japan

[ ]Department of Orthodontics, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Osaka 573-1121 Japan

[ ]Division of Endocrinology, Diabetes and Metabolism, Hematology, Rheumatology (Second Department of Internal Medicine), Graduate School of Medicine, University of the Ryukyus, 1 Senbaru, Nishiharacho, Nakagamigun, Okinawa 903-0213 Japan

[ ]Department of Internal Medicine, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Osaka 573-1121 Japan

Article

Publisher ID: 1679

DOI: 10.1186/s40064-016-1679-6

PMC ID: 4715141

PubMed ID: 26835222

SO-VID: 5a557277-55f1-4bc5-a8d5-144df6a23145

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 2 November 2015

Date accepted : 6 January 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001691, Japan Society for the Promotion of Science;

Award ID: Grants-in-Aid for Scientific Research (C) (#22592105)

Award ID: Grants-in-Aid for Scientific Research (C) (#25462941)

Award Recipient : Hirofumi Sawai

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ScienceOpen disciplines: Uncategorized

Keywords: 11β-hydroxysteroid dehydrogenase type 1,11β-hydroxysteroid dehydrogenase type 2,chronic periodontitis,cortisol,obesity

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ScienceOpen disciplines: Uncategorized

Keywords: 11β-hydroxysteroid dehydrogenase type 1, 11β-hydroxysteroid dehydrogenase type 2, chronic periodontitis, cortisol, obesity

The increased ratio of 11β-hydroxysteroid dehydrogenase type 1 versus 11β-hydroxysteroid dehydrogenase type 2 in chronic periodontitis irrespective of obesity

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Most cited references 34

11beta-hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress.

Does central obesity reflect "Cushing's disease of the omentum"?

Association of the metabolic syndrome with severe periodontitis in a large U.S. population-based survey.

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