Background and aims. Intrauterine growth restriction (IUGR) is a risk factor for long-term metabolic dysfunctions such as insulin resistance, dyslipidemia, glucose intolerance, type 2 diabetes and nonalcoholic fatty liver disease (NAFLD). The liver, involved in lipid/glucose homeostasis, is particularly vulnerable to nutritional programming during the perinatal period. Oxidative stress (OS) associated with stress-induced premature senescence (SIPS) have been involved in metabolic and liver dysfunctions and to the onset/maintenance of glucose intolerance and insulin resistance. This study aims to investigate in a rat model, whether IUGR can lead at adulthood to metabolic and hepatic disorders associated with OS and SIPS and, whether transient postnatal overfeeding (OF), inducing a catch-up growth, could amplify these dysfunctions.
Methods. Pregnant rats were randomly allocated to a control diet (23% casein, CTRL) or to a low-protein diet (9% casein, LPD) to induce IUGR. At birth, litter size was adjusted to 10 or reduced to 4 pups (2 males and 2 females) to induce OF during lactation period. Body fat distribution (computed tomography), glucose tolerance test (IPGTT), liver histology (steatosis, fibrosis, OS, SIPS), plasma analyses (lipids profile) were performed in males at 6 months of life.​
Results. In IUGR vs. CTRL males,  higher visceral fat content, glucose intolerance, increased transaminase levels, hepatic steatosis and fibrosis, liver OS and SIPS were observed and amplified by OF condition. 
Conclusion. IUGR in rats leads at adulthood to metabolic disorders and NALFD amplified by transient postnatal OF. These alterations are associated with liver OS and SIPS.

STRESS INDUCED PREMATURE SENESCENCE IS ASSOCIATED WITH METABOLIC AND HEPATIC DISORDERS IN INTRAUTERINE GROWTH RESTRICTION RAT MODEL AMPLIFIED BY TRANSIENT POSTNATAL OVERFEEDING