{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T02:45:06Z","timestamp":1790217906875,"version":"4.1.0"},"reference-count":58,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"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. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The pathogenesis of gestational diabetes mellitus (GDM) is not fully understood, with gut microbiota dysbiosis emerging as a potential contributing factor. Existing animal models primarily mimic type 1 or type 2 diabetes, inadequately representing GDM. This study aimed to investigate whether fecal microbiota transplantation (FMT) from GDM patients is associated with the development of GDM-like phenotypes in mice, comparing this approach to traditional modeling methods.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Fecal microbiota from GDM patients and healthy controls were transplanted into antibiotic-treated pregnant mice, creating trimester-specific FMT models. Control groups included mice on a high-fat diet (HFD) and HFD combined with streptozotocin (STZ). Metabolic phenotypes were assessed via glucose and insulin tolerance tests, fasting blood glucose, and insulin measurements. Serum inflammatory markers were analyzed, and gut inflammation was evaluated. 16S rRNA sequencing was performed on key model groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Mice receiving FMT from mid-late trimester GDM donors or traditional treatments developed significant glucose intolerance, insulin resistance, and gestational weight gain. Serum levels of inflammatory factors (e.g., IL-1\u03b2, MMP-9) were elevated. 16S rRNA sequencing revealed markedly reduced gut microbiota diversity and increased Firmicutes\/Bacteroidota ratio in both GDM-FMT and traditional model groups, with similar microbial community structures and alterations in metabolic and inflammation-related pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Gut microbiota from GDM patients may disrupt glucose homeostasis and contribute to a pro-inflammatory state during pregnancy. The GDM-FMT model effectively recapitulates key metabolic, inflammatory, and microbial dysbiosis features of GDM, providing a novel and reliable experimental tool for mechanistic studies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fmicb.2025.1723816","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T22:58:37Z","timestamp":1769641117000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Fecal microbiota transplantation from gestational diabetes mellitus patients induces glucose intolerance and subclinical inflammation in mice"],"prefix":"10.3389","volume":"16","author":[{"given":"Junhua","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Nutrition, Endocrinology, and Metabolism, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Nutrition, Endocrinology, and Metabolism, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujie","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nutrition, Endocrinology, and Metabolism, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Nutrition, Endocrinology, and Metabolism, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guanghui","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Nutrition, Endocrinology, and Metabolism, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,1,28]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1174","DOI":"10.1136\/gutjnl-2020-323071","article-title":"Gut microbiota-derived metabolites as central regulators in metabolic disorders.","volume":"70","author":"Agus","year":"2021","journal-title":"Gut"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1723","DOI":"10.1242\/dev.122.6.1723","article-title":"Expression and function of matrix metalloproteinases and their inhibitors at the maternal-embryonic boundary during mouse embryo implantation.","volume":"122","author":"Alexander","year":"1996","journal-title":"Development"},{"key":"B3","doi-asserted-by":"publisher","first-page":"51","DOI":"10.2337\/diab.16.1.51","article-title":"Light and electron microscopy of lesions in rats rendered diabetic with streptozotocin.","volume":"16","author":"Arison","year":"1967","journal-title":"Diabetes"},{"key":"B4","doi-asserted-by":"publisher","first-page":"63","DOI":"10.1111\/dom.12716","article-title":"\u03b2-Cell adaptation in pregnancy.","volume":"18","author":"Baeyens","year":"2016","journal-title":"Diabetes Obes. 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