For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
11
views
68
references
 Top references
cited by
82
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      658
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Leptin resistance: underlying mechanisms and diagnosis

      review-article

      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 and its receptors have been identified as key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity and metabolic disorders, such as insulin resistance and dyslipidemia. Mechanisms underlying the development of leptin resistance include mutations in the genes encoding leptin and its receptors, as well as proteins involved in self-regulation of leptin synthesis and blood–brain barrier permeability. Leptin resistance encompasses a complex pathophysiological phenomenon with a number of potential research lines. In this review, we analyze the existing data on the methods used to diagnose leptin resistance.

          Related collections

          Most cited references68

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

          Identification and expression cloning of a leptin receptor, OB-R.

          Louis A Tartaglia, Marlene Dembski, Xun Weng … (1995)
          The ob gene product, leptin, is an important circulating signal for the regulation of body weight. To identify high affinity leptin-binding sites, we generated a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin. After a binding survey of cell lines and tissues, we identified leptin-binding sites in the mouse choroid plexus. A cDNA expression library was prepared from mouse choroid plexus and screened with a leptin-AP fusion protein to identify a leptin receptor (OB-R). OB-R is a single membrane-spanning receptor most related to the gp130 signal-transducing component of the IL-6 receptor, the G-CSF receptor, and the LIF receptor. OB-R mRNA is expressed not only in choroid plexus, but also in several other tissues, including hypothalamus. Genetic mapping of the gene encoding OB-R shows that it is within the 5.1 cM interval of mouse chromosome 4 that contains the db locus.
          Article 0 comments Cited 469 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.

            P Ducy, M Amling, S. Takeda … (2000)
            Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.
            Article 0 comments Cited 258 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The weight of leptin in immunity.

              Antonio La Cava, Giuseppe Matarese (2004)
              Leptin is an adipocyte-derived hormone/cytokine that links nutritional status with neuroendocrine and immune functions. As a hormone, leptin regulates food intake and basal metabolism, and is sexually dimorphic - that is, its serum concentration is higher in females than in males with a similar body fat mass. As a cytokine, leptin can affect thymic homeostasis and the secretion of acute-phase reactants such as interleukin-1 and tumour-necrosis factor. Similar to other pro-inflammatory cytokines, leptin promotes T helper 1 (TH1)-cell differentiation and can modulate the onset and progression of autoimmune responses in several animal models of disease. Here, we review the advances and controversy for a role of leptin in the pathophysiology of immune responses.
              Article 0 comments Cited 215 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Metab Syndr Obes
                Journal ID (iso-abbrev): Diabetes Metab Syndr Obes
                Journal ID (publisher-id): Diabetes, Metabolic Syndrome and Obesity
                Title: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1178-7007
                Publication date Collection: 2019
                Publication date (Electronic): 25 January 2019
                Volume: 12
                Pages: 191-198
                Affiliations
                [1 ]Federal State Budgetary Institution, Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russian Federation, evg.uchasova@ 123456yandex.ru
                [2 ]Federal State Budget Educational Institution of Higher Education, Kemerovo State Medical University of the Ministry of Healthcare of the Russian Federation, Kemerovo, Russian Federation
                [3 ]Autonomous Public Healthcare Institution of the Kemrovo Region, Kemerovo Regional Clinical Hospital Named After S.V. Beliyaev, Regional Center for Diabetes, Kemerovo, Russian Federation
                Author notes
                Correspondence: Evgenya Uchasova, Federal State Budgetary Institution, Research Institute for Complex Issues of Cardiovascular Diseases, Laboratory of Research Homeostasis, 6 Sosnovy Boulevard, Kemerovo 650002, Russian Federation, Tel +7 3842 640 553, Email evg.uchasova@ 123456yandex.ru
                Article
                Publisher ID: dmso-12-191
                DOI: 10.2147/DMSO.S182406
                PMC ID: 6354688
                PubMed ID: 30774404
                SO-VID: 5d88d091-f354-476b-a886-d22496087c82
                Copyright © © 2019 Gruzdeva et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: leptin,leptin resistance,soluble leptin receptor
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: leptin, leptin resistance, soluble leptin receptor

                Comments

                Comment on this article

                scite_

                Similar content658

                See all similar

                Cited by80

                See all cited by

                Most referenced authors1,049

                See all reference authors