{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T06:15:58Z","timestamp":1788156958505,"version":"build-2803163510"},"reference-count":24,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T00:00:00Z","timestamp":1788134400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Nutr."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>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).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Our findings demonstrate that persistent protein restriction spanning both fetal and neonatal periods, followed by post-weaning high-fat intake, constitutes a critical\u201dtwo-hit\u201d 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fnut.2026.1905672","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T05:41:32Z","timestamp":1788154892000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Persistent perinatal protein malnutrition and post-weaning high-fat diet induce metabolic syndrome and hepatic UCP2 overexpression in IUGR offspring"],"prefix":"10.3389","volume":"13","author":[{"given":"Qiong","family":"Zeng","sequence":"first","affiliation":[{"name":"Department of Neurology, The First Affiliated Hospital of Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yixi","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, The First Affiliated Hospital of Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanting","family":"Chen","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Li","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhijian","family":"Deng","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiutong","family":"Chen","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingsa","family":"Wang","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiting","family":"He","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zeming","family":"Ma","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Runjia","family":"Yang","sequence":"additional","affiliation":[{"name":"Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kun","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, The First Affiliated Hospital of Shantou University Medical College","place":["Shantou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,31]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"S869","DOI":"10.1016\/j.ajog.2017.12.012","article-title":"Long-term cardiovascular consequences of fetal growth restriction: biology, clinical implications, and opportunities for prevention of adult disease","volume":"218","author":"Crispi","year":"2018","journal-title":"Am J Obstet Gynecol"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"53","DOI":"10.1016\/S2213-8587(16)30107-3","article-title":"Influence of maternal obesity on the long-term health of 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