{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T21:40:56Z","timestamp":1787002856486,"version":"build-2736575974"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2012,9,6]],"date-time":"2012-09-06T00:00:00Z","timestamp":1346889600000},"content-version":"vor","delay-in-days":920,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Obesity"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:p>Hyperandrogenemia predisposes an organism toward developing impaired insulin sensitivity. The aim of our study was to evaluate endocrine and metabolic effects during early allostasis induced by a fructose\u2010rich diet (FRD) in normal (control; CT) and neonatal\u2010androgenized (testosterone propionate; TP) female adult rats. CT and TP rats were fed either a normal diet (ND) or an FRD for 3 weeks immediately before the day of study, which was at age 100 days. Energy intake, body weight (BW), parametrial (PM) fat characteristics, and endocrine\/metabolic biomarkers were then evaluated. Daily energy intake was similar in CT and TP rats regardless of the differences in diet. When compared with CT\u2010ND rats, the TP\u2010ND rats were heavier, had larger PM fat, and were characterized by basal hypoadiponectinemia and enhanced plasma levels of non\u2010esterified fatty acid (NEFA), plasminogen activator inhibitor\u20101 (PAI\u20101), and leptin. FRD\u2010fed CT rats, when compared with CT\u2010ND rats, had high plasma levels of NEFA, triglyceride (TG), PAI\u20101, leptin, and adiponectin. The TP\u2010FRD rats, when compared with TP\u2010ND rats, displayed enhanced leptinemia and triglyceridemia, and were hyperinsulinemic, with glucose intolerance. The PM fat taken from TP rats displayed increase in the size of adipocytes, decrease in adiponectin (protein\/gene), and a greater abundance of the leptin gene. PM adipocyte response to insulin was impaired in CT\u2010FRD, TP\u2010ND, and TP\u2010FRD rats. A very short duration of isocaloric FRD intake in TP rats induced severe metabolic dysfunction at the reproductive age. Our study supports the hypothesis that the early\u2010androgenized female rat phenotype is highly susceptible to developing endocrine\/metabolic dysfunction. In turn, these abnormalities enhance the risk of metabolic syndrome, obesity, type 2 diabetes, and cardiovascular disease.<\/jats:p>","DOI":"10.1038\/oby.2009.255","type":"journal-article","created":{"date-parts":[[2009,8,20]],"date-time":"2009-08-20T10:31:16Z","timestamp":1250764276000},"page":"441-448","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Parametrial Adipose Tissue and Metabolic Dysfunctions Induced by Fructose\u2010rich Diet in Normal and Neonatal\u2010androgenized Adult Female Rats"],"prefix":"10.1002","volume":"18","author":[{"given":"Ana","family":"Alzamendi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Castrogiovanni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hugo 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