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      The role of leptin in osteoarthritis

      review-article
      Author(s): , MD a , b , , MD a , b , , MD a , b , , MD a , b , ∗
      Editor(s):
      Publication date (Electronic):
      Journal: Medicine
      Publisher: Wolters Kluwer Health
      Keywords: cartilage, chronic disease, leptin, osteoarthritis, signaling pathway

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          Abstract

          Background:

          The pathogenesis of osteoarthritis (OA) is not clear; leptin may be related to its pathogenesis.

          Methods:

          We reviewed articles on leptin in OA, chondrocytes, and in vitro experiments. It is concluded that leptin may lead to OA via some signaling pathways. At the same time, the concentration of leptin in vitro experiments and OA/rheumatoid arthritis (RA) patients was summarized.

          Results:

          Leptin levels in serum and synovial fluid of OA/RA patients were higher than normal person. In the condition of infection and immunity, serum leptin levels in the peripheral blood significantly increase. Because of the close relationship between obesity, leptin, and OA, it is crucial to study the effects of weight loss and exercise intervention on serum leptin levels to improve the symptoms of OA patients.

          Conclusion:

          Treatment for leptin-increased obesity may be a treatment for OA. The role of leptin in OA cannot be ignored and needs to be further studied.

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          Most cited references61

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          Leptin modulates the T-cell immune response and reverses starvation-induced immunosuppression.

          G. M. Lord, G Matarese, J K Howard … (1998)
          Nutritional deprivation suppresses immune function. The cloning of the obese gene and identification of its protein product leptin has provided fundamental insight into the hypothalamic regulation of body weight. Circulating levels of this adipocyte-derived hormone are proportional to fat mass but maybe lowered rapidly by fasting or increased by inflammatory mediators. The impaired T-cell immunity of mice now known to be defective in leptin (ob/ob) or its receptor (db/db), has never been explained. Impaired cell-mediated immunity and reduced levels of leptin are both features of low body weight in humans. Indeed, malnutrition predisposes to death from infectious diseases. We report here that leptin has a specific effect on T-lymphocyte responses, differentially regulating the proliferation of naive and memory T cells. Leptin increased Th1 and suppressed Th2 cytokine production. Administration of leptin to mice reversed the immunosuppressive effects of acute starvation. Our findings suggest a new role for leptin in linking nutritional status to cognate cellular immune function, and provide a molecular mechanism to account for the immune dysfunction observed in starvation.
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            Abnormal splicing of the leptin receptor in diabetic mice.

            G. Lee, R Proenca, J M Montez … (1996)
            Mutations in the mouse diabetes (db) gene result in obesity and diabetes in a syndrome resembling morbid human obesity. Previous data suggest that the db gene encodes the receptor for the obese (ob) gene product, leptin. A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db. This receptor maps to the same 300-kilobase interval as db, and has at least six alternatively spliced forms. One of these splice variants is expressed at a high level in the hypothalamus, and is abnormally spliced in C57BL/Ks db/db mice. The mutant protein is missing the cytoplasmic region, and is likely to be defective in signal transduction. This suggests that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.
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              Evidence for a key role of leptin in osteoarthritis.

              Hélène Dumond, Nathalie Presle, Bernard Terlain … (2003)
              To evaluate the contribution of leptin (an adipose tissue-derived hormone) to the pathophysiology of osteoarthritis (OA), by determining the level of leptin in both synovial fluid (SF) and cartilage specimens obtained from human joints. We also investigated the effect of leptin on cartilage, using intraarticular injections of leptin in rats. Leptin levels in SF samples obtained from OA patients undergoing either knee replacement surgery or knee arthroscopy were measured by enzyme-linked immunosorbent assay. In addition, histologic sections of articular cartilage and osteophytes obtained during surgery for total knee replacement were graded using the Mankin score, and were immunostained using antibodies to leptin, transforming growth factor beta (TGFbeta), and insulin-like growth factor 1 (IGF-1). For experimental studies, various doses of leptin (10, 30, 100, and 300 microg) were injected into the knee joints of rats. Tibial plateaus were collected and processed for proteoglycan synthesis by radiolabeled sulfate incorporation, and for expression of leptin, its receptor (Ob-Rb), and growth factors by reverse transcriptase-polymerase chain reaction and immunohistochemical analysis. Leptin was observed in SF obtained from human OA-affected joints, and leptin concentrations correlated with the body mass index. Marked expression of the protein was observed in OA cartilage and in osteophytes, while in normal cartilage, few chondrocytes produced leptin. Furthermore, the pattern and level of leptin expression were related to the grade of cartilage destruction and paralleled those of growth factors (IGF-1 and TGFbeta1). Animal studies showed that leptin strongly stimulated anabolic functions of chondrocytes and induced the synthesis of IGF-1 and TGFbeta1 in cartilage at both the messenger RNA and the protein levels. These findings suggest a new peripheral function of leptin as a key regulator of chondrocyte metabolism, and indicate that leptin may play an important role in the pathophysiology of OA.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Wolters Kluwer Health
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: April 2018
                Publication date (Electronic): 06 April 2018
                Volume: 97
                Issue: 14
                Electronic Location Identifier: e0257
                Affiliations
                [a ]Department of Orthopedics, The First Affiliated Hospital of Soochow University
                [b ]Orthopedic Institute, Soochow University, Suzhou, China.
                Author notes
                [∗ ]Correspondence: Ye Sun, Department of Orthopedics, The First Affiliated Hospital of Soochow University, 188 Shi Zi Road, Suzhou 215006, China (e-mail: sunye@ 123456suda.edu.cn ).
                Article
                Publisher ID: MD-D-17-07380 Accession ID: 00257
                DOI: 10.1097/MD.0000000000010257
                PMC ID: 5902277
                PubMed ID: 29620639
                SO-VID: 6e4d525e-d356-400a-9daa-a51ad3b8fc62
                Copyright © Copyright © 2018 the Author(s). Published by Wolters Kluwer Health, Inc.
                License:

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                Date received : 25 November 2017
                Date revision received : 4 March 2018
                Date accepted : 6 March 2018
                Categories
                Subject: 5100
                Subject: Research Article
                Subject: Systematic Review and Meta-Analysis
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: cartilage,chronic disease,leptin,osteoarthritis,signaling pathway
                Data availability:
                Keywords: cartilage, chronic disease, leptin, osteoarthritis, signaling pathway

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