{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T15:38:38Z","timestamp":1759333118904},"reference-count":45,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2010,1,12]],"date-time":"2010-01-12T00:00:00Z","timestamp":1263254400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p> <jats:bold>Citation<\/jats:bold> Wiedemann A, Vocke F, Fitzgerald JS, Markert UR, Jeschke U, Lohse P, Toth B. Leptin gene (TTTC)<jats:sub>n<\/jats:sub> microsatellite polymorphism as well as Leptin receptor R223Q and PPAR\u03b32 P12A substitutions are not associated with hypertensive disorders in pregnancy. Am J Reprod Immunol 2010; 63: 310\u2013317<\/jats:p><jats:p><jats:bold>Problem\u2002<\/jats:bold> Pregnancy\u2010induced hypertension (PIH) affects up to 15% of all pregnancies. Disturbed placentation is one factor associated with PIH. Leptin and peroxisome proliferator activator receptors (PPAR) seem to play an important role in placentation, fetal development, and blood pressure regulation. Therefore, we investigated polymorphisms in the genes encoding leptin, the leptin receptor, and PPAR\u03b32 in patients with PIH.<\/jats:p><jats:p><jats:bold>Method of study\u2002<\/jats:bold> In this retrospective case\u2013control study, 103 patients with PIH [gestational hypertension (GH) <jats:italic>n<\/jats:italic>\u2003=\u200339; preeclampsia <jats:italic>n<\/jats:italic>\u2003=\u200327; eclampsia <jats:italic>n<\/jats:italic>\u2003=\u20035; HELLP <jats:italic>n<\/jats:italic>\u2003=\u200332] and 100 controls were analyzed for the <jats:italic>LEP<\/jats:italic> tetranucleotide repeat (TTTC)<jats:sub>n<\/jats:sub> and the leptin receptor (LEPR) R223Q and PPAR\u03b32 P12A substitutions. Statistical analysis was performed using the chi\u2010square, Mann\u2013Whitney <jats:italic>U<\/jats:italic>\u2010, and Kruskal\u2013Wallis tests (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05 significant).<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> The frequency of the three possible genotypes did not differ significantly between patients and controls [<jats:italic>LEP<\/jats:italic> (TTTC)<jats:sub>n<\/jats:sub>: <jats:italic>P<\/jats:italic>\u2003=\u20030.43; LEPR R223Q: <jats:italic>P<\/jats:italic>\u2003=\u20030.94; PPAR\u03b32 P12A: <jats:italic>P<\/jats:italic>\u2003=\u20030.94]. However, postpartal diastolic blood pressure of PIH patients was significantly higher in homozygous carriers of the LEPR Q223\u2010encoding allele as compared with patients carrying the wild\u2010type allele (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.01).<\/jats:p><jats:p><jats:bold>Conclusion\u2002<\/jats:bold> Hypertensive disorders in pregnancy were not associated with the <jats:italic>LEP<\/jats:italic>, LEPR, and PPAR\u03b32 polymorphisms studied. The role of other variations in the <jats:italic>LEP<\/jats:italic> and <jats:italic>PPAR<\/jats:italic> genes in the pathophysiology of PIH and in exacerbations are the objective of ongoing research.<\/jats:p>","DOI":"10.1111\/j.1600-0897.2009.00799.x","type":"journal-article","created":{"date-parts":[[2010,1,13]],"date-time":"2010-01-13T02:41:47Z","timestamp":1263350507000},"page":"310-317","source":"Crossref","is-referenced-by-count":9,"title":["ORIGINAL ARTICLE: Leptin Gene (TTTC)<sub>n<\/sub> Microsatellite Polymorphism as well as Leptin Receptor R223Q and PPAR\u03b32 P12A Substitutions are not Associated with Hypertensive Disorders in Pregnancy"],"prefix":"10.1111","volume":"63","author":[{"given":"Annette","family":"Wiedemann","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Franziska","family":"Vocke","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Justine 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