Stella Bernardi1, Bruno Fabris2, Merlin Thomas3, Barbara Toffoli4, Christos Tikellis5, Riccardo Candido6, Cristiana Catena7, Paolo Mulatero8, Fabio Barbone9, Oriano Radillo10, Giorgio Zauli11, Paola Secchiero12. 1. Department of Morphology, Surgery and Experimental Medicine, LTTA Centre, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara, Italy; Baker IDI, Heart and Diabetes Research Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia. Electronic address: stella.bernardi@aots.sanita.fvg.it. 2. Department of Medical, Surgical and Health Sciences, University of Trieste, Ospedale di Cattinara, Strada di Fiume 447, 34149 Trieste, Italy. Electronic address: b.fabris@fmc.units.it. 3. Baker IDI, Heart and Diabetes Research Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia. Electronic address: merlin.thomas@bakeridi.edu.au. 4. Institute for Maternal and Child Health, IRCCS Burlo Garofolo, 34100 Trieste, Italy. Electronic address: tffbbr@unife.it. 5. Baker IDI, Heart and Diabetes Research Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia. Electronic address: chris.tikellis@bakeridi.edu.au. 6. Diabetological Centre, via Puccini 48/50, 34148 Trieste, Italy. Electronic address: riccardocandido@yahoo.it. 7. Department of Medical and Biological Sciences, University of Udine, Ospedale Santa Maria della Misericordia, Udine, Italy. Electronic address: nocciocat@hotmail.com. 8. Division of Internal Medicine and Hypertension, University of Torino, Ospedale San Giovanni Battista, 10126 Torino, Italy. Electronic address: paolo.mulatero@libero.it. 9. Department of Medical, Experimental and Clinical Sciences, University of Udine, Ospedale Santa Maria della Misericordia, Udine, Italy. Electronic address: fabio.barbone@uniud.it. 10. Institute for Maternal and Child Health, IRCCS Burlo Garofolo, 34100 Trieste, Italy. Electronic address: radillo@burlo.trieste.it. 11. Institute for Maternal and Child Health, IRCCS Burlo Garofolo, 34100 Trieste, Italy. Electronic address: zla.grg@unife.it. 12. Department of Morphology, Surgery and Experimental Medicine, LTTA Centre, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara, Italy. Electronic address: paola.secchiero@unife.it.
Abstract
BACKGROUND: Inflammation is believed to link obesity to insulin resistance, as in the setting of metabolic syndrome (MetS). Osteoprotegerin (OPG) is a soluble protein that seems to exert proatherogenic and prodiabetogenic effects. This study aims at determining OPG levels in MetS and whether OPG might contribute to MetS development and progression. METHODOLOGY/PRINCIPAL FINDINGS: Circulating OPG was measured in 46 patients with MetS and 63 controls, and was found significantly elevated in those with MetS. In addition, circulating and tissue OPG was significantly increased in high-fat diet (HFD) fed C57BL6 mice, which is one of the animal models for the study of MetS. To evaluate the consequences of OPG elevation, we delivered this protein to C57BL6 mice, finding that it promoted systemic and adipose tissue proinflammatory changes in association with metabolic abnormalities. CONCLUSIONS/SIGNIFICANCE: These data suggest that OPG may trigger adipose tissue proinflammatory changes in MetS/HFD-induced obesity.
BACKGROUND: Inflammation is believed to link obesity to insulin resistance, as in the setting of metabolic syndrome (MetS). Osteoprotegerin (OPG) is a soluble protein that seems to exert proatherogenic and prodiabetogenic effects. This study aims at determining OPG levels in MetS and whether OPG might contribute to MetS development and progression. METHODOLOGY/PRINCIPAL FINDINGS: Circulating OPG was measured in 46 patients with MetS and 63 controls, and was found significantly elevated in those with MetS. In addition, circulating and tissue OPG was significantly increased in high-fat diet (HFD) fed C57BL6 mice, which is one of the animal models for the study of MetS. To evaluate the consequences of OPG elevation, we delivered this protein to C57BL6 mice, finding that it promoted systemic and adipose tissue proinflammatory changes in association with metabolic abnormalities. CONCLUSIONS/SIGNIFICANCE: These data suggest that OPG may trigger adipose tissue proinflammatory changes in MetS/HFD-induced obesity.
Authors: Diana Moldovan; Crina Rusu; Alina Potra; Ioan Moldovan; Ioan Mihai Patiu; Mirela Gherman-Caprioara; Ina Maria Kacso Journal: Int Urol Nephrol Date: 2017-02-04 Impact factor: 2.370
Authors: Carmen Gómez-Vaquero; Irene Martín; Estibaliz Loza; Loreto Carmona; José Ivorra; José Antonio Narváez; Javier Hernández-Gañán; Pedro Alía; Javier Narváez Journal: PLoS One Date: 2016-12-02 Impact factor: 3.240