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Relationship between IGF-1 and body weight in inflammatory bowel diseases: Cellular and molecular mechanisms involved
Authors
Ana M. Gómez-Lahoz
Borja Hernández-Breijo
+29 more
Carlos Taxonera
David Cano-Martínez
Fernando Gomollón
Francisco Mesonero
Ignacio Marín-Jiménez
Irene D. Román
Isabel Vera
Iván Guerra
Javier P. Gisbert
Joaquín Hinojosa
José Luis Cabriada
Laura Sebastián Monasor
Laura Sempere
Lidia Ruiz-Llorente
Luis Bujanda
Luis G. Guijarro
M.Val Toledo-Lobo
Manuel Barreiro-de Acosta
Marisa Iborra
María Chaparro
María del Carmen Boyano-Adánez
María Dolores Martín-Arranz
Melchor Alvarez-Mon
Miguel A. Ortega
on behalf of the PREDICROHN study group from GETECCU
Patricia Sanmartín Salinas
Rosa Rodríguez-Torres
Sofía Zoullas
Valle García-Sánchez
Publication date
1 January 2021
Publisher
'Elsevier BV'
Doi
Cite
Abstract
Inflammatory bowel diseases (IBD), represented by ulcerative colitis (UC) and Crohn''s disease (CD), are characterized by chronic inflammation of the gastrointestinal tract, what leads to diarrhea, malnutrition, and weight loss. Depression of the growth hormone-insulin-like growth factor-1 axis (GH-IGF-1 axis) could be responsible of these symptoms. We demonstrate that long-term treatment (54 weeks) of adult CD patients with adalimumab (ADA) results in a decrease in serum IGF-1 without changes in serum IGF-1 binding protein (IGF1BP4). These results prompted us to conduct a preclinical study to test the efficiency of IGF-1 in the medication for experimental colitis. IGF-1 treatment of rats with DSS-induced colitis has a beneficial effect on the following circulating biochemical parameters: glucose, albumin, and total protein levels. In this experimental group we also observed healthy maintenance of colon size, body weight, and lean mass in comparison with the DSS-only group. Histological analysis revealed restoration of the mucosal barrier with the IGF-1 treatment, which was characterized by healthy quantities of mucin production, structural maintenance of adherers junctions (AJs), recuperation of E-cadherin and ß-catenin levels and decrease in infiltrating immune cells and in metalloproteinase-2 levels. The experimentally induced colitis caused activation of apoptosis markers, including cleaved caspase 3, caspase 8, and PARP and decreases cell-cycle checkpoint activators including phosphorylated Rb, cyclin E, and E2F1. The IGF-1 treatment inhibited cyclin E depletion and partially protects PARP levels. The beneficial effects of IGF-1 in experimental colitis could be explained by a re-sensitization of the IGF-1/IRS-1/AKT cascade to exogenous IGF-1. Given these results, we postulate that IGF-1 treatment of IBD patients could prove to be successful in reducing disease pathology. © 2021 The Author
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Repositorio Universidad de Zaragoza
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