ArticleFrontiers in nutrition2026
Persistent perinatal protein malnutrition and post-weaning high-fat diet induce metabolic syndrome and hepatic UCP2 overexpression in IUGR offspring.
Article in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Adults born with intrauterine growth restriction (IUGR) are at a significantly increased risk of developing metabolic syndrome. Postnatal nutritional patterns are critical modifiers of this risk. This study investigated the effects of different perinatal nutritional interventions on glucose/lipid metabolism and hepatic steatosis in IUGR offspring, and explored the role of hepatic uncoupling protein 2 (UCP2). Methods: An IUGR rat model was established via maternal low-protein (LP) diet during pregnancy. Male offspring were divided into five groups with distinct diets during gestation (G), lactation (L, 0-3w), and post-weaning (PW, 4-12w): ND+ND (Normal/ Normal/ Normal), ND+HFD (Normal/ High-fat/ High-fat), IUGR+ND (LP/ Normal/ Normal), IUGR+HFD (LP/ High-fat/ High-fat), and IUGR+LPD+HFD (LP/ LP/ High-fat). Results: At 12 weeks, only the IUGR+LPD+HFD group, exposed to persistent perinatal malnutrition followed by a high-fat diet, developed pronounced central obesity, glucose intolerance, insulin resistance, severe dyslipidemia (highest TG, lowest HDL-C), and marked hepatic steatosis. Notably, hepatic UCP2 protein expression was significantly upregulated specifically in the IUGR+LPD+HFD and ND+HFD groups, whereas UCP2 mRNA levels were unchanged across groups. In contrast, IUGR offspring receiving adequate postnatal nutrition (IUGR+ND, IUGR+HFD) were largely protected from these metabolic disturbances. Discussion: Our findings demonstrate that persistent protein restriction spanning both fetal and neonatal periods, followed by post-weaning high-fat intake, constitutes a critical"two-hit" model leading to full metabolic syndrome in IUGR offspring, which is closely associated with post-transcriptional upregulation of hepatic UCP2. This highlights the importance of early nutritional rehabilitation and suggests UCP2 as a potential mediator and biomarker of metabolically programmed risk.
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