Carreras Badosa, GemmaRemesar Betlloch, XavierPrats Puig, AnnaXargay i Torrent, SílviaLizarraga Mollinedo, EstherZegher, Francis deIbáñez, LourdesBassols, JuditLópez Bermejo, Abel2020-04-302020-04-302019-05-150031-3998https://hdl.handle.net/2445/158153Background: Although prenatal and postnatal programming of metabolic diseases in adulthood is well established, the mechanims underpinning metabolic programming are not. DLK1, a key regulator of fetal development, inhibits adipocyte differentiation and restricts fetal growth. Methods: Assess Dlk1 expression in Wistar rat model of catch-up growth following intrauterine restriction. Dams fed ad libitum deliverd control pups (C) and dams on a 50% calorie-restricted diet delivered pups with low birth weight (R). Restricted offspring fed a standard rat chow showd catch-up growth (R/C) but those kept on a calorie-restricted diet did not (R/R). Results: Decreased Dlk1 expression was observed in adipose tissue and skeletal muscle of R/C pups along with excessive visceral fat accumulation, decreased circulating adiponectin, increased triglycerides and HOMA-IR (from p<0.05 to p<0.001). Moreover, in R/C pups, the reduced Dlk1 expression in adipose tissue and skeletal muscle correlated with visceral fat (r= -0.820; p<0.0001) and HOMA-IR (r= -0.745; p=0.002). Conclusions: Decreased Dlk1 expression relates to visceral fat expansion and insulin resistance in a rat model of catch-up growth following prenatal growth restriction. Modulation of Dlk1 expression could be among the targets of the early prevention of fetal preogramming of adult metabolic disorders.7 p.application/pdfeng(c) International Pediatric Research Foundation, 2019Medicina prenatalTrastorns del metabolismeRates (Animals de laboratori)Prenatal medicineDisorders of metabolismRats as laboratory animalsinfo:eu-repo/semantics/article6900732020-04-30info:eu-repo/semantics/openAccess31091532