{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T10:02:18Z","timestamp":1753869738896,"version":"3.41.2"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,12,15]],"date-time":"2019-12-15T00:00:00Z","timestamp":1576368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","award":["HRC 15\/510"],"award-info":[{"award-number":["HRC 15\/510"]}],"id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Nutrition Food Res"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:sec><jats:title>Scope<\/jats:title><jats:p>Glucose intolerance during pregnancy is associated with short\u2010 and long\u2010term maternal and offspring health consequences. In young male mice, knockout of the major pro\u2010inflammatory mediator interleukin\u20101\u2010receptor\u20101 (IL1R1) protects against high\u2010fat diet (HFD)\u2010induced glucose intolerance and metabolic dysfunction. This phenotype has not been examined during pregnancy. The hypothesis that IL1R1 depletion will protect females against HFD\u2010induced glucose intolerance and metabolic dysfunction before, during, and post pregnancy is tested.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>C57BL\/6J control and IL1R1 knockout (IL1R1<jats:sup>\u2212\/\u2212<\/jats:sup>) mice are randomized to either a control diet (10%\u00a0kcal from fat) or HFD (45%\u00a0kcal from fat), and three distinct cohorts are established: nulliparous, pregnant, and postpartum females. Contrary to the authors\u2019 hypothesis, it is found that IL1R1<jats:sup>\u2212\/\u2212<\/jats:sup> does not protect against glucose intolerance in nulliparous or pregnant females, and while control HFD animals see a resolution of glucose tolerance postpartum, IL\u20101R1<jats:sup>\u2212\/\u2212<\/jats:sup> mice remain impaired. These effects are accompanied by adipocyte hypertrophy, hyperleptinemia, and increased adipose tissue inflammatory gene expression. Maternal genotype differentially affects fetal growth in male and female fetuses, demonstrating sexual dimorphism in this genotype prior to birth.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings suggest that IL1R1 signaling is important for normal metabolic functioning in females, during and outside of pregnancy.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201900770","type":"journal-article","created":{"date-parts":[[2019,11,18]],"date-time":"2019-11-18T05:10:19Z","timestamp":1574053819000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Interleukin\u20101 Receptor\u20101 Deficiency Impairs Metabolic Function in Pregnant and Non\u2010Pregnant Female Mice"],"prefix":"10.1002","volume":"65","author":[{"given":"Jasmine F","family":"Plows","sequence":"first","affiliation":[{"name":"The Liggins Institute University of Auckland  85 Park Road Grafton 1023 Auckland New 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