{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T01:50:31Z","timestamp":1791510631119,"version":"4.3.4"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,12,13]],"date-time":"2013-12-13T00:00:00Z","timestamp":1386892800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>Metabolic programming via components of the maternal diet during gestation may play a role in the development of different aspects of the metabolic syndrome. Using a mouse model, we aimed to characterize the role of maternal western\u2010type diet in the development of non\u2010alcoholic fatty liver disease (<jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>) in the offspring.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Female mice were fed either a western (W) or low\u2010fat control (L) semisynthetic diet before and during gestation and lactation. At weaning, male offspring were assigned either the W or the L diet, generating four experimental groups: <jats:styled-content style=\"fixed-case\">WW<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> WL<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> LW<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">LL<\/jats:styled-content> offspring. Biochemical, histological and epigenetic indicators were investigated at 29\u00a0weeks of age.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Male offspring exposed to prenatal and post\u2010weaning western\u2010style diet (<jats:styled-content style=\"fixed-case\">WW<\/jats:styled-content>) showed hepatomegaly combined with accumulation of hepatic cholesterol and triglycerides. This accumulation was associated with up\u2010regulation of de novo lipid synthesis, inflammation and dysregulation of lipid storage. Elevated hepatic transaminases and increased expression of <jats:italic>Tnfa, Cd11, Mcp1<\/jats:italic> and <jats:italic>Tgfb<\/jats:italic> underpin the severity of liver injury. Histopathological analysis revealed the presence of advanced steatohepatitis in <jats:styled-content style=\"fixed-case\">WW<\/jats:styled-content> offspring. In addition, alterations in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> methylation in key metabolic genes (<jats:italic>Ppara<\/jats:italic>,<jats:italic> Insig<\/jats:italic>,<jats:italic> and Fasn<\/jats:italic>) were detected.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Maternal dietary fat intake during early development programmes susceptibility to liver disease in male offspring, mediated by disturbances in lipid metabolism and inflammatory response. Long\u2010lasting epigenetic changes may underlie this dysregulation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12197","type":"journal-article","created":{"date-parts":[[2013,11,14]],"date-time":"2013-11-14T06:27:21Z","timestamp":1384410441000},"page":"215-227","source":"Crossref","is-referenced-by-count":86,"title":["Maternal western diet primes non\u2010alcoholic fatty liver disease in adult mouse offspring"],"prefix":"10.1111","volume":"210","author":[{"given":"M. G. 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