{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:12:33Z","timestamp":1785420753383,"version":"3.56.0"},"posted":{"date-parts":[[2026,6,11]]},"group-title":"Physiology","reference-count":84,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T00:00:00Z","timestamp":1781136000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"award":["T32HD117733-01"],"award-info":[{"award-number":["T32HD117733-01"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>Early-life exposures during critical periods of development significantly impact lifelong metabolic risk and likely contribute to the rising rates of obesity, type 2 diabetes, and metabolic dysfunction\u2013associated steatotic liver disease (MASLD) in children. Here, we evaluated the safety and metabolic effects of semaglutide, a GLP-1 receptor agonist (GLP-1 RA), administered from preconception through lactation in dams fed a high-fat diet (HFD) or standard diet, and assessed metabolic outcomes in dams and their offspring. Offspring were weaned to a standard diet. We found that semaglutide improved body composition and glucose metabolism in HFD-fed dams during pregnancy. These maternal changes persisted 10 weeks after weaning despite discontinuation of semaglutide treatment. HFD exposure impaired glucose homeostasis and promoted hepatic steatosis in offspring at 18 weeks. These effects were ameliorated by maternal semaglutide treatment. Importantly, metabolic improvements in dams and offspring occurred without adverse effects on conception rate or fetal viability. These findings suggest that GLP-1 RA during the perinatal period can improve maternal and offspring metabolic health in a mouse model of obesity and support further investigation of GLP-1\u2013based therapies to mitigate maternal metabolic dysfunction and improve metabolic risk in children.<\/jats:p>\n                <jats:sec>\n                  <jats:title>ARTICLE HIGHLIGHTS<\/jats:title>\n                  <jats:p>\n                    <jats:list list-type=\"simple\">\n                      <jats:list-item>\n                        <jats:label>\u2022<\/jats:label>\n                        <jats:p>Rates of obesity, type 2 diabetes, and fatty liver disease are rising in children, in part due to maternal obesity and insulin resistance that program offspring metabolic risk during the perinatal period.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:label>\u2022<\/jats:label>\n                        <jats:p>We asked whether the GLP-1 receptor agonist (GLP-1 RA), semaglutide, administered during critical developmental windows could prevent adverse outcomes in offspring using a diet-induced mouse model of maternal obesity.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:label>\u2022<\/jats:label>\n                        <jats:p>Semaglutide, given to dams from preconception through lactation, improved maternal metabolism and ameliorated metabolic dysfunction in offspring caused by maternal high-fat diet.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:label>\u2022<\/jats:label>\n                        <jats:p>These findings highlight a potential role for perinatal GLP-1 receptor agonism to improve maternal metabolic health and reduce metabolic risk in offspring.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.06.07.730723","type":"posted-content","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T15:05:19Z","timestamp":1781190319000},"source":"Crossref","is-referenced-by-count":0,"title":["Perinatal Semaglutide Treatment Improves Maternal Health and Mitigates Offspring Metabolic Dysfunction in a Mouse Model of Maternal Obesity"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-8936-8325","authenticated-orcid":false,"given":"Ananthi","family":"Rajamoorthi","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, The Children\u2019s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taylor","family":"Hollingsworth","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Neonatology, The Children\u2019s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuxia","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Neonatology, The Children\u2019s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara E.","family":"Pinney","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Endocrinology, The Children\u2019s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca A.","family":"Simmons","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Neonatology, The Children\u2019s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"issue":"3","key":"2026061502250990000_2026.06.07.730723v1.1","doi-asserted-by":"crossref","first-page":"158","DOI":"10.1016\/S2352-4642(21)00374-6","article-title":"Global, regional, and country estimates of metabolic syndrome burden in children and adolescents in 2020: a systematic review and modelling analysis","volume":"6","year":"2022","journal-title":"Lancet Child Adolesc Health"},{"issue":"7","key":"2026061502250990000_2026.06.07.730723v1.2","doi-asserted-by":"crossref","first-page":"e2521170","DOI":"10.1001\/jamanetworkopen.2025.21170","article-title":"Prevalence of Extremely Severe Obesity and Metabolic Dysfunction Among US Children and Adolescents","volume":"8","year":"2025","journal-title":"JAMA Netw 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MASLD in children: integrating epidemiological trends with mechanistic and translational advances. J Clin Invest. 2025;135(13).","DOI":"10.1172\/JCI186422"},{"key":"2026061502250990000_2026.06.07.730723v1.6","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2012.08.043"},{"key":"2026061502250990000_2026.06.07.730723v1.7","doi-asserted-by":"crossref","unstructured":"Bomberg EM , Kyle T , Stanford FC . Considering Pediatric Obesity as a US Public Health Emergency. 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High-fat diet disrupts metabolism in two generations of rats in a parent-of-origin specific manner. 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