0
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Glucocorticoid Effects on the Diurnal Rhythm of Circulating Leptin Levels

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          It is known that circulating leptin shows diurnal variation with a nocturnal rise; however, the mechanisms generating this rhythm have not been fully elucidated. Glucocorticoids are a potent stimulator of leptin secretion, and there is a reciprocal relationship between circulating leptin and glucocorticoid levels. We hypothesized that glucocorticoids could modulate the diurnal rhythm of circulating leptin. We therefore explored the diurnal variation of leptin under situations in which subjects showed no or some shift of glucocorticoid diurnal rhythm, such as prednisolone-administered humans, and adrenalectomized and corticosterone-replaced (ADX+B) rats. The peak level of plasma cortisol immunoreactivity was shifted from early morning to noon by prednisolone administration. The nocturnal increment of plasma leptin in prednisolone-administered patients (71.2 ± 14.2% from 08:00 h value) was significantly greater than that in normal volunteers (12.2 ± 7.5% from 08:00 h value), but the timing of nadir and the peak of plasma leptin was not shifted. In normal rats, the plasma concentration of leptin showed the diurnal rhythm with the bottom at 16:00 h and the top between midnight and early morning. The amplitude of leptin diurnal rhythm was significantly reduced in ADX+B rats (08:00 h: 3.0 ± 0.2, 16:00 h: 2.7 ± 0.2, 00:00 h; 3.7 ± 0.2 ng/ml) compared with sham operated rats (08:00 h: 3.0 ± 0.2, 16:00 h 2.2 ± 0.2, 00:00 h: 4.7 ± 0.4 ng/ml); but ADX+B rats still retained similar timing of nadir and the peak of plasma leptin as observed in sham rats. These results indicate that glucocorticoids enhance the amplitude of leptin diurnal rhythm, and are consistent with previous findings showing that glucocorticoids increase leptin secretion. Glucocorticoids appear to play modulatory, but not essential roles in generating leptin diurnal rhythm.

          Related collections

          Most cited references 5

          • Record: found
          • Abstract: found
          • Article: not found

          Induction of ob gene expression by corticosteroids is accompanied by body weight loss and reduced food intake.

          Genetic studies in mice have identified the ob gene product as a potential signaling factor regulating body weight homeostasis and energy balance. It is suggested that modulation of ob gene expression results in changes in body weight and food intake. Glucocorticoids are shown to have important metabolic effects and to modulate food intake and body weight. In order to test the hypothesis that these metabolic effects of glucocorticoids are linked to changes in the expression of the ob gene, ob mRNA levels were evaluated in rats treated with different glucocorticosteroids at catabolic doses and correlated to the kinetics of changes in body weight gain and food intake. Results from time course experiments demonstrate that adipose tissue ob gene expression is rapidly induced by glucocorticosteroids. This induction is followed by a concordant decrease in body weight gain and food consumption. These data suggest that the catabolic effects of corticosteroids on body weight mass and food intake might be mediated by changes in ob expression. Modulation of ob expression may therefore constitute a mechanism through which hormonal, pharmacological, or other factors control body weight homeostasis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Dexamethasone regulates obese expression in isolated rat adipocytes.

             K Shima,  M Iida,  T. Murakami (1995)
            An obese (ob) gene product, expressed specifically in adipose tissues, regulates energy balance. Here we report adipocytes in adipose tissue actually express ob mRNA and that a synthetic glucocorticoid (dexamethasone) regulates expression of the ob gene. Addition of 100 nM dexamethasone to isolated rat adipocytes rapidly induced a 4-8 fold increase in ob mRNA. This increase in ob mRNA level was apparent within 1 h, and reached a maximum at about 7 h after stimulation. The dexamethasone-stimulated increase of ob mRNA was only partially blocked by protein synthesis inhibitors cycloheximide (20 micrograms/ml) or anisomycin (200 microM). This suggests that new protein synthesis is not necessarily required for the observed dexamethasone-stimulated increase in ob mRNA.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Regulation of Expression ofobmRNA and Protein by Glucocorticoids and cAMP

                Bookmark

                Author and article information

                Journal
                HRE
                Horm Res Paediatr
                10.1159/issn.1663-2818
                Hormone Research in Paediatrics
                S. Karger AG
                1663-2818
                1663-2826
                2000
                2000
                09 March 2001
                : 54
                : 2
                : 69-73
                Affiliations
                aSecond Department of Internal Medicine, Kochi Medical School, Kohasu, Nankoku, Kochi and bFukuyama Yuuai Hospital, Fukuyama, Hiroshima, Japan
                Article
                53234 Horm Res 2000;54:69–73
                10.1159/000053234
                11251369
                © 2001 S. Karger AG, Basel

                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.

                Page count
                Figures: 3, Tables: 2, References: 28, Pages: 5
                Categories
                Original Paper

                Comments

                Comment on this article