Objective-To determine if follicular free fatty acid (FFA) levels are associated with cumulus oocyte complex morphology
Design-Prospective cohort study
Setting-University in vitro fertilization (IVF) practice
Patients-102 women undergoing IVF
Interventions-Measurement of FFAs in serum and ovarian follicular fluidMain Outcome Measures-Total and specific follicular and serum FFA levels, correlations between follicular and serum FFAs, and associations between follicular FFA levels and markers of oocyte quality including cumulus oocyte complex (COC) morphology Results-Predominant follicular fluid and serum FFAs were oleic, palmitic, linoleic and stearic acids. Correlations between follicular and serum FFA concentrations were weak (r=0.252, 0.288, 0.236, 0.309 respectively for specific FFAs; r=0.212 for total FFAs). A receiver operator characteristic curve determined total follicular FFAs ≥ 0.232 µmol/ml distinguished women with lower versus higher percentage COCs with favorable morphology. Women with elevated follicular FFAs (n=31) were more likely to have COCs with poor morphology than others (n=71) (OR 3.3, 95% CI:1.2-9.2). This relationship held after adjusting for potential confounders including age, BMI, endometriosis and amount of gonadotropin administered (β=1.2; OR 3.4, 95% CI:1.1-10.4).Conclusions-Elevated follicular FFA levels are associated with poor COC morphology. Further work is needed to determine what factors influence follicular FFA levels and if these factors impact fertility.
Oocyte loss, either directly through attrition (germ cell death) or indirectly through follicular atresia (somatic or granulosa cell death), is a fundamental event associated with defining the time of normal or premature reproductive senescence in females. Although apoptosis has been reported to function as the underlying mechanism responsible for death of both germ cells and somatic cells in the ovary, the final molecular steps which commit ovarian cells to death have not been fully elucidated. To examine if death repressor activity of the bcl-2 gene product is important for germ cell survival, we conducted studies using a Bcl-2 loss-of-function (bcl-2 -/-) transgenic mouse model. Histological analyses revealed that ovaries collected from bcl-2 -/- mice possessed numerous aberrantly formed primordial follicle-like structures containing a single layer of granulosa cells without an oocyte. Additionally, the total number of primordial follicles present which contained a healthy oocyte was markedly reduced in bcl-2 -/- mice as compared to heterozygote (bcl-2 -/+) or wild-type (bcl-2 +/+) mice, suggesting that expression of the bcl-2 death repressor gene is critical for endowment of a normal complement of germ cells and primordial follicles in the mammalian ovary.
Oocyte loss, either directly through attrition (germ cell death) or indirectly through follicular atresia (somatic or granulosa cell death), is a fundamental event associated with defining the time of normal or premature reproductive senescence in females. Although apoptosis has been reported to function as the underlying mechanism responsible for death of both germ cells and somatic cells in the ovary, the final molecular steps which commit ovarian cells to death have not been fully elucidated. To examine if death repressor activity of the bcl-2 gene product is important for germ cell survival, we conducted studies using a Bcl-2 loss-of-function (bcl-2 -/-) transgenic mouse model. Histological analyses revealed that ovaries collected from bcl-2 -/- mice possessed numerous aberrantly formed primordial follicle-like structures containing a single layer of granulosa cells without an oocyte. Additionally, the total number of primordial follicles present which contained a healthy oocyte was markedly reduced in bcl-2 -/- mice as compared to heterozygote (bcl-2 -/+) or wild-type (bcl-2 +/+) mice, suggesting that expression of the bcl-2 death repressor gene is critical for endowment of a normal complement of germ cells and primordial follicles in the mammalian ovary.
Objective
To determine if morbid obesity is associated with decreased pregnancy and live birth rates after IVF in women with PCOS
Design
Retrospective cohort study
Setting
University-based fertility center
Patients
72 women with PCOS who completed their first IVF cycle between 2001 and 2007
Interventions
IVF outcomes were compared between women with a BMI of less than 40 kg/m2 versus those women with a BMI of 40 kg/m2 or greater
Main outcome measures
Clinical pregnancy rate, live birth rate
Results
Morbidly obese women with PCOS (n=19) had significantly lower clinical pregnancy rates after IVF than PCOS patients who were not morbidly obese (n=53) (32% vs. 72%, RR 0.44, 95% confidence interval 0.22 to 0.87). Their live birth rates were lower too, although this difference was not statistically significant (32% vs. 60%, RR 0.52, 95% confidence interval 0.26 to 1.05).
Conclusions
Morbid obesity is associated with lower pregnancy rates in women with PCOS after IVF raising the question if weight loss may improve IVF success rates for morbidly obese PCOS patients.
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