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      Adiponectin and Leptin Adipocytokines in Metabolic Syndrome: What Is Its Importance?

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          Abstract

          The global obesity epidemic has motivated a large number of investigations related to adipose tissue. Within the advances in this area, a variety of factors secreted by adipose tissue and with regulatory activity on caloric intake, energy expenditure, reproduction, locomotor activity, glycidic and lipid metabolism, immune response, and bone physiology have been described. Among these adipocyte hormones, collectively called “adipokines” or “adipocytokines,” leptin (LEP) and adiponectin are addressed in this review. The regulation of adipocytokines is altered in diseases such as obesity, atherosclerosis, type 2 diabetes mellitus, and metabolic syndrome (MS) due to the increase in the mass of white adipose tissue. LEP and adiponectin have a broad spectrum of functions in regulating metabolism and are an important link between obesity and MS. Because these adipocytokines have opposite effects on subclinical inflammation and insulin resistance, it has been suggested that the combined use of these 2 adipocytokines may work as a better biomarker in the diagnosis of MS than using them individually. In this review, we address the characteristics and main functions of adipocytokines derived from adipose tissue such as adiponectin and LEP, which in the Colombian context could give good guidance for the management of MS, especially in populations of children and adolescents.

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          Most cited references 106

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          Cloning of adiponectin receptors that mediate antidiabetic metabolic effects.

          Adiponectin (also known as 30-kDa adipocyte complement-related protein; Acrp30) is a hormone secreted by adipocytes that acts as an antidiabetic and anti-atherogenic adipokine. Levels of adiponectin in the blood are decreased under conditions of obesity, insulin resistance and type 2 diabetes. Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice. Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes. This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through activation of AMP kinase and PPAR-alpha. Here we report the cloning of complementary DNAs encoding adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) by expression cloning. AdipoR1 is abundantly expressed in skeletal muscle, whereas AdipoR2 is predominantly expressed in the liver. These two adiponectin receptors are predicted to contain seven transmembrane domains, but to be structurally and functionally distinct from G-protein-coupled receptors. Expression of AdipoR1/R2 or suppression of AdipoR1/R2 expression by small-interfering RNA supports our conclusion that they serve as receptors for globular and full-length adiponectin, and that they mediate increased AMP kinase and PPAR-alpha ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectin.
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            Identification and expression cloning of a leptin receptor, OB-R.

            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.
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              Visfatin: a protein secreted by visceral fat that mimics the effects of insulin.

              Fat tissue produces a variety of secreted proteins (adipocytokines) with important roles in metabolism. We isolated a newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Further study of visfatin's physiological role may lead to new insights into glucose homeostasis and/or new therapies for metabolic disorders such as diabetes.
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                Author and article information

                Journal
                DDE
                10.1159/issn.2673-1738
                International Journal of Diabetes and Metabolism
                S. Karger AG
                2673-1797
                2673-1738
                2020
                December 2020
                17 September 2020
                : 26
                : 3
                : 93-102
                Affiliations
                aProject Bank Team, Public Health Research Division, National Institute of Health, Bogotá, Colombia
                bNutrition Group, Public Health Research Division, National Institute of Health, Bogotá, Colombia
                Author notes
                *María Luz Gunturiz Albarracin, Project Bank Team, Public Health Research Division, National Institute of Health, Avenue Street 26 No. 51-20 CAN, Bogotá D.C. (Colombia), mgunturiz@ins.gov.co
                Article
                510521 Dubai Diabetes Endocrinol J 2020;26:93–102
                10.1159/000510521
                © 2020 The Author(s) Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. 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: 2, Tables: 1, Pages: 10
                Categories
                Review Article

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