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Endocrine parameters and ovarian dynamics in Ossabaw miniature swine with metabolic syndrome suggest a model for polycystic ovary syndrome
Author(s) -
Krisher Rebecca L,
Lowe Jennifer,
Bailey Amanda,
Sturek Michael
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.757.24
Subject(s) - androstenedione , polycystic ovary , medicine , endocrinology , waist , follicular phase , testosterone (patch) , ovary , metabolic syndrome , endocrine system , biology , insulin resistance , androgen , obesity , hormone
We describe characterization of the Ossabaw pig as a model of polycystic ovary syndrome (PCOS). Gilts (n=17) were fed either a control (lean) or excess kcal atherogenic diet for 22 weeks that elicits metabolic syndrome (MetS). Blood free testosterone and androstenedione were measured by RIA and ovarian activity monitored by ultrasound twice a week. Ovarian follicles were measured individually and area, circumference and diameter recorded. Across the period of the study, androstenedione values did not differ between groups. However, androstenedione was significantly higher in the last third of the study period in MetS gilts, suggesting the onset of hyperandrogenemia. Free testosterone was higher in lean gilts. There were no differences in follicular circumference or diameter between groups. MetS had significantly greater follicular area than lean gilts (MetS = 0.044±0.002, lean = 0.037±0.001), more follicles with an area ≥0.1 cm 2 (MetS = 4.98%, lean = 3.54%), more follicles with circumference ≥2 cm (MetS = 1.68%, lean = 0.65%) and more follicles with circumference <0.5 cm (lMetS=16.91%, lean=14.59%), suggesting that MetS gilts produce more small follicles that in turn grow larger than those in lean gilts. We propose that Ossabaw swine with MetS develop reproductive parameters reminiscent of PCOS, and thus may represent a complete animal model of the disease. Support: CBR2‐IUPU, RR013223 , HL062552.