Frontiers in nutrition · 2026
Persistent perinatal protein malnutrition and post-weaning high-fat diet induce metabolic syndrome and hepatic UCP2 overexpression in IUGR offspring.
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Zeng Qiong, Wu Yixi, Chen Yanting, Li Qing, Deng Zhijian, Chen Xiutong, Wang Jingsa, He Yiting, Ma Zeming, Yang Runjia, Lin Kun
Аннотация
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.
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.