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Dlk1 expression relates to visceral fat expansion and insulin resistance in male and female rats with postnatal catch-up growth



Although prenatal and postnatal programming of metabolic diseases in adulthood is well established, the mechanisms underpinning metabolic programming are not. Dlk1, a key regulator of fetal development, inhibits adipocyte differentiation and restricts fetal growth.


Assess DLk1 expression in a Wistar rat model of catch-up growth following intrauterine restriction. Dams fed ad libitum delivered 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 showed catch-up growth (R/C) but those kept on a calorie-restricted diet did not (R/R).


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 < 0.0001). Moreover, in R/C pups the reduced Dlk1 expression in adipose tissue and skeletal muscle correlated with visceral fat (r = −0.820, p < 00001) and HOMA-IR (r = −0.745, p = 0.002).


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 for the early prevention of fetal programming of adult metabolic disorders.

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We would like to thank Dr. Glòria Oliveras Serrat and Ms. Yaiza Martin Gonzalez for the preparation of the tissue histological sections. The study was supported by grant no. PI13/01257 (to A.L.-B.) from the National Institute of Health Carlos III (Fund for Health Research FIS, Spain), project co-financed by FEDER.

Author information

All authors read and approved the final manuscript. G.C.-B., X.R., J.B. and A.L.-B. designed research; G.C.-B. and A.L.-B. wrote the first draft of the manuscript; G.C.-B., X.R. and A.P.-P. conducted research; G.C.-B., S.X.-T. and E.L.-M. analyzed data; and F.d.Z. and L.I. contributed to review the manuscript.

Competing interests

The authors declare no competing interests.

Correspondence to Judit Bassols or Abel López-Bermejo.

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