For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
25
views
50
references
 Top references
cited by
62
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      473
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Leptin signaling

      review-article
      Author(s): 1 , 2 ,
      Publication date (Electronic):
      Journal: F1000Prime Reports
      Publisher: Faculty of 1000 Ltd

      Read this article at

      ScienceOpenPublisherPMC
      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

          Leptin is secreted by adipose tissue and regulates energy homeostasis, glucose and lipid metabolism, immune function, and other systems. The binding of leptin to its specific receptor activates various intracellular signaling pathways, including Janus kinase 2 (JAK2)/ signal transducer and activator of transcription 3 (STAT3), insulin receptor substrate (IRS)/phosphatidylinositol 3 kinase (PI3K), SH2-containing protein tyrosine phosphatase 2 (SHP2)/mitogen-activated protein kinase (MAPK), and 5' adenosine monophosphate-activated protein kinase (AMPK)/ acetyl-CoA carboxylase (ACC), in the central nervous system and peripheral tissues. Understanding of leptin signaling provides insights into its roles in health and disease.

          Related collections

          Most cited references50

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

          A key role of leptin in the control of regulatory T cell proliferation.

          Veronica De Rosa, Claudio Procaccini, Gaetano Calì … (2007)
          We report here that leptin can act as a negative signal for the proliferation of human naturally occurring Foxp3(+)CD4(+)CD25(+) regulatory T (T(reg)) cells. Freshly isolated T(reg) cells produced leptin and expressed high amounts of leptin receptor (ObR). In vitro neutralization with leptin monoclonal antibody (mAb), during anti-CD3 and anti-CD28 stimulation, resulted in T(reg) cell proliferation, which was interleukin-2 (IL-2) dependent. T(reg) cells that proliferated in the presence of leptin mAb had increased expression of Foxp3 and remained suppressive. The phenomena appeared secondary to leptin signaling via ObR and, importantly, leptin neutralization reversed the anergic state of the T(reg) cells, as indicated by downmodulation of the cyclin-dependent kinase inhibitor p27 (p27(kip1)) and the phosphorylation of the extracellular-related kinases 1 (ERK1) and ERK2. Together with the finding of enhanced proliferation of T(reg) cells observed in leptin- and ObR-deficient mice, these results suggest a potential for therapeutic interventions in immune and autoimmune diseases.
          Article 0 comments Cited 180 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Leptin and Inflammation.

            Noriko Iikuni, Queenie Lam, Liwei Lu … (2008)
            The past few years of research on leptin have provided important information on the link between metabolism and immune homeostasis. Adipocytes influence not only the endocrine system but also the immune response through several cytokine-like mediators known as adipokines, which include leptin. It is widely accepted that leptin can directly link nutritional status and pro-inflammatory T helper 1 immune responses, and that a decrease of leptin plasma concentration during food deprivation can lead to an impaired immune function. Additionally, several studies have implicated leptin in the pathogenesis of chronic inflammation, and the elevated circulating leptin levels in obesity appear to contribute to the low-grade inflammatory background which makes obese individuals more susceptible to increased risk of developing cardiovascular diseases, type II diabetes, or degenerative disease including autoimmunity and cancer. Conversely, reduced levels of leptin such as those found in malnourished individuals have been linked to increased risk of infection and reduced cell-mediated immune responses. We discuss here the functional influences of leptin in the physiopathology of inflammation, and the effects of leptin in the modulation of such responses.
            Article 0 comments Cited 125 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The hypothalamic arcuate nucleus: a key site for mediating leptin's effects on glucose homeostasis and locomotor activity.

              Jae K. Lee, Min Liu, Robert A McGovern … (2004)
              Leptin is required for normal energy and glucose homeostasis. The hypothalamic arcuate nucleus (ARH) has been proposed as an important site of leptin action. To assess the physiological significance of leptin signaling in the ARH, we used mice homozygous for a FLPe-reactivatable, leptin receptor null allele (Lepr(neo/neo) mice). Similar to Lepr(db/db) mice, these mice are obese, hyperglycemic, hyperinsulinemic, infertile, and hypoactive. To selectively restore leptin signaling in the ARH, we generated an adeno-associated virus expressing FLPe-recombinase, which was delivered unilaterally into the hypothalamus using stereotaxic injections. We found that unilateral restoration of leptin signaling in the ARH of Lepr(neo/neo) mice leads to a modest decrease in body weight and food intake. In contrast, unilateral reactivation markedly improved hyperinsulinemia and normalized blood glucose levels and locomotor activity. These data demonstrate that leptin signaling in the ARH is sufficient for mediating leptin's effects on glucose homeostasis and locomotor activity.
              Article 0 comments Cited 119 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): F1000Prime Rep
                Journal ID (iso-abbrev): F1000Prime Rep
                Title: F1000Prime Reports
                Publisher: Faculty of 1000 Ltd
                ISSN (Electronic): 2051-7599
                Publication date (Electronic): 04 September 2014
                Publication date Collection: 2014
                Volume: 6
                Electronic Location Identifier: 73
                Affiliations
                [1 ]Department of Internal Medicine, Soonchunhyang University College of Medicine 22, Daesagwan-gil (657 Hannam-dong), Yongsan-gu, SeoulKorea
                [2 ]Division of Endocrinology, Diabetes and Metabolism, and the Institute for Diabetes, Obesity and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania 12-104 Smilow Center for Translational Research, 3400 Civic Center Boulevard, Building 421, Philadelphia, Pennsylvania 19104USA
                Article
                Publisher ID: 73
                DOI: 10.12703/P6-73
                PMC ID: 4166933
                PubMed ID: 25343030
                SO-VID: c3245164-5b09-467b-9ca9-0f442a0339f3
                Copyright © © 2014 Faculty of 1000 Ltd
                License:

                All F1000Prime Reports articles are distributed under the terms of the Creative Commons Attribution-Non Commercial License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Review Article

                Data availability:

                Comments

                Comment on this article

                scite_

                Similar content473

                See all similar

                Cited by57

                See all cited by

                Most referenced authors857

                See all reference authors