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• W1976745100 abstract "The prevalence of obesity is growing among reproductive-age women. This is concerning because obesity has significant health-related consequences. Aside from the long-term risks of diabetes, heart disease, and some types of cancer, obesity poses immediate threats for young women including subfertility and adverse early and late pregnancy outcomes. Epidemiologic and experimental studies demonstrate associations between prepregnancy obesity and poor reproductive outcomes; however, the mechanisms involved are poorly understood. We discuss current knowledge of the pathophysiology of obesity in early reproductive events and how these events may affect reproductive outcomes including fertility and miscarriage risk. We also discuss avenues for future research and interventions to improve reproductive outcomes for obese women. The prevalence of obesity is growing among reproductive-age women. This is concerning because obesity has significant health-related consequences. Aside from the long-term risks of diabetes, heart disease, and some types of cancer, obesity poses immediate threats for young women including subfertility and adverse early and late pregnancy outcomes. Epidemiologic and experimental studies demonstrate associations between prepregnancy obesity and poor reproductive outcomes; however, the mechanisms involved are poorly understood. We discuss current knowledge of the pathophysiology of obesity in early reproductive events and how these events may affect reproductive outcomes including fertility and miscarriage risk. We also discuss avenues for future research and interventions to improve reproductive outcomes for obese women. Almost a quarter of reproductive-age women in the United States are obese, with a body mass index (BMI) of 30 kg/m2 or greater.1Vahratian A. Prevalence of overweight and obesity among women of childbearing age: results from the 2002 National Survey of Family Growth.Matern Child Health J. 2009; 13: 268-273Crossref PubMed Scopus (156) Google Scholar This figure is worrisome because obesity may jeopardize long-term health with increased risks of type 2 diabetes, cardiovascular disease, and some types of cancer.2Flegal K.M. Graubard B.I. Williamson D.F. Gail M.H. Cause-specific excess deaths associated with underweight, overweight, and obesity.JAMA. 2007; 298: 2028-2037Crossref PubMed Scopus (1163) Google ScholarSee related editorial, page 522 See related editorial, page 522 Of more immediate concern for reproductive-age women, obesity is associated with increased risks of subfertility.3Gesink Law D.C. Maclehose R.F. Longnecker M.P. Obesity and time to pregnancy.Hum Reprod. 2007; 22: 414-420Crossref PubMed Scopus (299) Google Scholar, 4Ramlau-Hansen C.H. Thulstrup A.M. Nohr E.A. Bonde J.P. Sorensen T.I. Olsen J. Subfecundity in overweight and obese couples.Hum Reprod. 2007; 22: 1634-1637Crossref PubMed Scopus (310) Google Scholar, 5Wise L.A. Rothman K.J. Mikkelsen E.M. Sorensen H.T. Riis A. Hatch E.E. An internet-based prospective study of body size and time to pregnancy.Hum Reprod. 2010; 25: 253-264Crossref PubMed Scopus (177) Google Scholar For those who do conceive, obesity has been associated with increased risks of miscarriage,6Metwally M. Ong K.J. Ledger W.L. Li T.C. Does high body mass index increase the risk of miscarriage after spontaneous and assisted conception? A meta-analysis of the evidence.Fertil Steril. 2008; 90: 714-726Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar preeclampsia,7O'Brien T.E. Ray J.G. Chan W.S. Maternal body mass index and the risk of preeclampsia: a systematic overview.Epidemiology. 2003; 14: 368-374Crossref PubMed Scopus (629) Google Scholar, 8Dokras A. Baredziak L. Blaine J. Syrop C. VanVoorhis B.J. Sparks A. Obstetric outcomes after in vitro fertilization in obese and morbidly obese women.Obstet Gynecol. 2006; 108: 61-69Crossref PubMed Scopus (204) Google Scholar and congenital anomalies in the offspring.9Stothard K.J. Tennant P.W. Bell R. Rankin J. Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis.JAMA. 2009; 301: 636-650Crossref PubMed Scopus (835) Google Scholar Of further concern, emerging evidence suggests that children born to obese mothers are at increased risk for obesity,10Chang G.Q. Gaysinskaya V. Karatayev O. Leibowitz S.F. Maternal high-fat diet and fetal programming: increased proliferation of hypothalamic peptide-producing neurons that increase risk for overeating and obesity.J Neurosci. 2008; 28: 12107-12119Crossref PubMed Scopus (298) Google Scholar, 11Catalano P.M. Farrell K. Thomas A. et al.Perinatal risk factors for childhood obesity and metabolic dysregulation.Am J Clin Nutr. 2009; 90: 1303-1313Crossref PubMed Scopus (362) Google Scholar, 12Nohr E.A. Timpson N.J. Andersen C.S. Davey Smith G. Olsen J. Sorensen T.I. Severe obesity in young women and reproductive health: the Danish National Birth Cohort.PLoS One. 2009; 4: e8444Crossref PubMed Scopus (73) Google Scholar type 2 diabetes,13Catalano P.M. Presley L. Minium J. Hauguel-de Mouzon S. Fetuses of obese mothers develop insulin resistance in utero.Diabetes Care. 2009; 32: 1076-1080Crossref PubMed Scopus (473) Google Scholar and cardiovascular disease later in life,14Symonds M.E. Sebert S.P. Hyatt M.A. Budge H. Nutritional programming of the metabolic syndrome.Nat Rev Endocrinol. 2009; 5: 604-610Crossref PubMed Scopus (280) Google Scholar perhaps the result of epigenetic modification of the embryonic genome in response to the alterations of the in utero environment in the setting of maternal obesity14Symonds M.E. Sebert S.P. Hyatt M.A. Budge H. Nutritional programming of the metabolic syndrome.Nat Rev Endocrinol. 2009; 5: 604-610Crossref PubMed Scopus (280) Google Scholar (Table 1).TABLE 1Epidemiologic studies of adverse reproductive outcomes in obese womenOutcomeOdds ratio (95% CI)ReferenceType of studyPatients, nSubfertility2.2 (1.8–2.6)Nohr et al12Nohr E.A. Timpson N.J. Andersen C.S. Davey Smith G. Olsen J. Sorensen T.I. Severe obesity in young women and reproductive health: the Danish National Birth Cohort.PLoS One. 2009; 4: e8444Crossref PubMed Scopus (73) Google ScholarProspective cohort4901Miscarriage1.67 (1.25–2.25)Metwally et al6Metwally M. Ong K.J. Ledger W.L. Li T.C. Does high body mass index increase the risk of miscarriage after spontaneous and assisted conception? A meta-analysis of the evidence.Fertil Steril. 2008; 90: 714-726Abstract Full Text Full Text PDF PubMed Scopus (327) Google ScholarMetaanalysis2257Various fetal anomalies1.2 (1.03–1.4, cleft lip and palate); 2.24 (1.86–2.69, spina bifida)Stothard et al9Stothard K.J. Tennant P.W. Bell R. Rankin J. Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis.JAMA. 2009; 301: 636-650Crossref PubMed Scopus (835) Google ScholarMetaanalysis863; 1188Large for gestational age2.3 (1.9–2.7)Nohr et al12Nohr E.A. Timpson N.J. Andersen C.S. Davey Smith G. Olsen J. Sorensen T.I. Severe obesity in young women and reproductive health: the Danish National Birth Cohort.PLoS One. 2009; 4: e8444Crossref PubMed Scopus (73) Google ScholarProspective cohort4901Preeclamspia1.6 (1.1–2.25, obese vs nonobese); 3.3 (2.4–4.5, morbidly obese vs nonobese)Weiss et al68Weiss J.L. Malone F.D. Emig D. et al.Obesity, obstetric complications and cesarean delivery rate—a population-based screening study.Am J Obstet Gynecol. 2004; 190: 1091-1097Abstract Full Text Full Text PDF PubMed Scopus (798) Google ScholarProspective cohort15,225; 14,629Obesity in the offspring at age 1 y (BMI ≥95th percentile)1.9 (1.3–2.6)Nohr et al12Nohr E.A. Timpson N.J. Andersen C.S. Davey Smith G. Olsen J. Sorensen T.I. Severe obesity in young women and reproductive health: the Danish National Birth Cohort.PLoS One. 2009; 4: e8444Crossref PubMed Scopus (73) Google ScholarProspective cohort4901BMI, body mass index; CI, confidence interval.Jungheim. Obesity and reproduction. Am J Obstet Gynecol 2010. Open table in a new tab BMI, body mass index; CI, confidence interval. Jungheim. Obesity and reproduction. Am J Obstet Gynecol 2010. Interventions aimed at improving reproductive outcomes for obese pregnant women often focus on limiting weight gain during pregnancy15Chang A.S. Dale A.N. Moley K.H. Maternal diabetes adversely affects preovulatory oocyte maturation, development, and granulosa cell apoptosis.Endocrinology. 2005; 146: 2445-2453Crossref PubMed Scopus (141) Google Scholar; however, many of the risks of obesity in pregnancy may be linked to abnormalities in reproductive events occurring preconceptionally and early in pregnancy including abnormalities in events of oocyte recruitment and development, ovulation, preimplantation embryonic development, and implantation,16Jungheim E.S. Moley K.H. The impact of type 1 and type 2 diabetes mellitus on the oocyte and the preimplantation embryo.Semin Reprod Med. 2008; 26: 186-195Crossref PubMed Scopus (41) Google Scholar, 17Wyman A. Pinto A.B. Sheridan R. Moley K.H. One-cell zygote transfer from diabetic to nondiabetic mouse results in congenital malformations and growth retardation in offspring.Endocrinology. 2008; 149: 466-469Crossref PubMed Scopus (92) Google Scholar, 18Norman R.J. Chura L.R. Robker R.L. Effects of obesity on assisted reproductive technology outcomes.Fertil Steril. 2008; 89: 1611-1612Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar Although managing weight gain during pregnancy may be helpful in preventing some adverse outcomes in obese pregnancy,19Artal R. Lockwood C.J. Brown H.L. Weight gain recommendations in pregnancy and the obesity epidemic.Obstet Gynecol. 2010; 115: 152-155Crossref PubMed Scopus (100) Google Scholar such intervention does not address abnormalities in events that have already occurred. Accordingly, increased intervention for weight loss and increased efforts in counseling of the risks of obesity to reproductive potential and outcome should also be undertaken by clinicians working with reproductive-age women. For obese women who do conceive, research elucidating the pathophysiology of obesity in early reproductive events may help shed light on effective interventions for preventing the adverse pregnancy outcomes that weight management in pregnancy has not been able to address. Increased incidence of subfertility among obese women may be attributed in part to the frequent cooccurrence of obesity with polycystic ovary syndrome (PCOS),20Alvarez-Blasco F. Botella-Carretero J.I. San Millan J.L. Escobar-Morreale H.F. Prevalence and characteristics of the polycystic ovary syndrome in overweight and obese women.Arch Intern Med. 2006; 166: 2081-2086Crossref PubMed Scopus (245) Google Scholar a relatively common condition characterized by hyperandrogenism and anovulation and associated with insulin resistance.21Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop GroupRevised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome.Fertil Steril. 2004; 81: 19-25Scopus (0) Google Scholar, 22Azziz R. Carmina E. Dewailly D. et al.The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report.Fertil Steril. 2009; 91: 456-488Abstract Full Text Full Text PDF PubMed Scopus (1350) Google Scholar PCOS is not uncommon in women of normal weight; however, in obese women insulin resistance may lead to clinical features consistent with PCOS.23Yildiz B.O. Azziz R. Ovarian and adipose tissue dysfunction in polycystic ovary syndrome: report of the 4th special scientific meeting of the Androgen Excess and PCOS Society.Fertil Steril. 2010; 94: 690-693Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 24Chang R.J. Polycystic ovary syndrome and hyperandtrogenic states.in: Strauss J.F. Barbieri R.L. Yen and Jaffe's reproductive endocrinology. Saunders, Philadelphia, PA2009: 489-516Crossref Scopus (5) Google Scholar Insulin resistance and hyperinsulinemia consequent of obesity hamper hepatic production of steroid hormone-binding globulin (SHBG) with subsequent hyperandrogenemia. Lower SHBG levels and increased peripheral aromatization of androgens to estrogens in obese women also result in higher free circulating estrogen levels, which may lead to increased negative feedback on the hypothalamic-pituitary axis. This increased negative feedback adversely affects the gonadotropin secretion that is needed for adequate ovarian follicular recruitment and subsequent ovulation.24Chang R.J. Polycystic ovary syndrome and hyperandtrogenic states.in: Strauss J.F. Barbieri R.L. Yen and Jaffe's reproductive endocrinology. Saunders, Philadelphia, PA2009: 489-516Crossref Scopus (5) Google Scholar, 25Nestler J.E. Obesity, insulin, sex steroids and ovulation.Int J Obes Relat Metab Disord. 2000; 24: S71-S73Crossref PubMed Scopus (55) Google Scholar, 26Santoro N. Lasley B. McConnell D. et al.Body size and ethnicity are associated with menstrual cycle alterations in women in the early menopausal transition: the Study of Women's Health across the Nation (SWAN) daily hormone study.J Clin Endocrinol Metab. 2004; 89: 2622-2631Crossref PubMed Scopus (178) Google Scholar, 27Rachon D, Teede H. Ovarian function and obesity—interrelationship, impact on women's reproductive lifespan and treatment options. Mol Cell Endocrinol;316:172–9.Google Scholar Weight loss among obese women with PCOS often helps in restoring ovulation and improving chances of conception.28Norman R.J. Dewailly D. Legro R.S. Hickey T.E. Polycystic ovary syndrome.Lancet. 2007; 370: 685-697Abstract Full Text Full Text PDF PubMed Scopus (1047) Google Scholar, 29Teitelman M. Grotegut C.A. Williams N.N. Lewis J.D. The impact of bariatric surgery on menstrual patterns.Obes Surg. 2006; 16: 1457-1463Crossref PubMed Scopus (136) Google Scholar Independent of PCOS, obesity is associated with abnormalities of the hypothalamic-pituitary-ovarian (HPO) axis that may affect the quality of follicular development and ovulation.26Santoro N. Lasley B. McConnell D. et al.Body size and ethnicity are associated with menstrual cycle alterations in women in the early menopausal transition: the Study of Women's Health across the Nation (SWAN) daily hormone study.J Clin Endocrinol Metab. 2004; 89: 2622-2631Crossref PubMed Scopus (178) Google Scholar, 30Helm K.D. Ness R.M. Evans W.S. Physiologic and pathophysiologic alternations of the neuroendocrine components of the reproductive axis.in: Strauss J.F. Barbieri R.L. Yen and Jaffe's reproductive endocrinology. Saunders, Philadelphia, PA2009: 441-488Crossref Scopus (6) Google Scholar, 31Jain A. Polotsky A.J. Rochester D. et al.Pulsatile luteinizing hormone amplitude and progesterone metabolite excretion are reduced in obese women.J Clin Endocrinol Metab. 2007; 92: 2468-2473Crossref PubMed Scopus (142) Google Scholar As a consequence, fertility is decreased, even among obese women with regular menses.3Gesink Law D.C. Maclehose R.F. Longnecker M.P. Obesity and time to pregnancy.Hum Reprod. 2007; 22: 414-420Crossref PubMed Scopus (299) Google Scholar, 32van der Steeg J.W. Steures P. Eijkemans M.J. et al.Obesity affects spontaneous pregnancy chances in subfertile, ovulatory women.Hum Reprod. 2008; 23: 324-328Crossref PubMed Scopus (293) Google Scholar In a large study of women participating in the Study of Women's Health Across the Nation (SWAN), a BMI increasing greater than 25 kg/m2 was associated with a longer follicular phase and a shortened luteal phase.26Santoro N. Lasley B. McConnell D. et al.Body size and ethnicity are associated with menstrual cycle alterations in women in the early menopausal transition: the Study of Women's Health across the Nation (SWAN) daily hormone study.J Clin Endocrinol Metab. 2004; 89: 2622-2631Crossref PubMed Scopus (178) Google Scholar A further detailed study conducted by some of the same researchers demonstrated decreased luteinizing hormone (LH) amplitude and mean serum LH levels in cycling obese women compared with women of normal weight, possibly leading to a shortened luteal phase.30Helm K.D. Ness R.M. Evans W.S. Physiologic and pathophysiologic alternations of the neuroendocrine components of the reproductive axis.in: Strauss J.F. Barbieri R.L. Yen and Jaffe's reproductive endocrinology. Saunders, Philadelphia, PA2009: 441-488Crossref Scopus (6) Google Scholar, 31Jain A. Polotsky A.J. Rochester D. et al.Pulsatile luteinizing hormone amplitude and progesterone metabolite excretion are reduced in obese women.J Clin Endocrinol Metab. 2007; 92: 2468-2473Crossref PubMed Scopus (142) Google Scholar Whereas the concept and definition of the luteal phase deficiency and its role in fertility have long been debated, shorter luteal phases theoretically could affect endometrial development and subsequent embryo implantation.33Speroff L. Fritz M. Clinical gynecologic endocrinology and infertility.in: Lippincott Williams & Wilkins, Philadelphia, PA2005: 1033-1035Google Scholar If this problem did exist in obese women, it could explain in part findings demonstrating that obesity may be associated with increased risk of miscarriage in spontaneous conceptions6Metwally M. Ong K.J. Ledger W.L. Li T.C. Does high body mass index increase the risk of miscarriage after spontaneous and assisted conception? A meta-analysis of the evidence.Fertil Steril. 2008; 90: 714-726Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar and decreased embryonic implantation rates in obese women receiving donor oocytes after in vitro fertilization (IVF).34Dessolle L. Darai E. Cornet D. et al.Determinants of pregnancy rate in the donor oocyte model: a multivariate analysis of 450 frozen-thawed embryo transfers.Hum Reprod. 2009; 24: 3082-3089Crossref PubMed Scopus (71) Google Scholar The mechanism responsible for the observed decreased LH pulse amplitude in obese women is unknown. Several theories exist including interference of adipokine hormones or hormones made by adipose tissue, including leptin, tumor necrosis factor (TNF)-alpha, or interleukin-1beta, with the pituitary response to gonadotropin-releasing hormone.23Yildiz B.O. Azziz R. Ovarian and adipose tissue dysfunction in polycystic ovary syndrome: report of the 4th special scientific meeting of the Androgen Excess and PCOS Society.Fertil Steril. 2010; 94: 690-693Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 30Helm K.D. Ness R.M. Evans W.S. Physiologic and pathophysiologic alternations of the neuroendocrine components of the reproductive axis.in: Strauss J.F. Barbieri R.L. Yen and Jaffe's reproductive endocrinology. Saunders, Philadelphia, PA2009: 441-488Crossref Scopus (6) Google Scholar, 31Jain A. Polotsky A.J. Rochester D. et al.Pulsatile luteinizing hormone amplitude and progesterone metabolite excretion are reduced in obese women.J Clin Endocrinol Metab. 2007; 92: 2468-2473Crossref PubMed Scopus (142) Google Scholar, 35Fenichel R.M. Dominguez J.E. Mayer L. Walsh B.T. Boozer C. Warren M.P. Leptin levels and luteinizing hormone pulsatility in normal cycling women and their relationship to daily changes in metabolic rate.Fertil Steril. 2008; 90: 1161-1168Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, 36Moschos S. Chan J.L. Mantzoros C.S. Leptin and reproduction: a review.Fertil Steril. 2002; 77: 433-444Abstract Full Text Full Text PDF PubMed Scopus (399) Google Scholar Although some work has been done to investigate the effects of obesity on the HPO axis and infertility in animal models, further work examining these relationships in women is needed.37Tortoriello D.V. McMinn J. Chua S.C. Dietary-induced obesity and hypothalamic infertility in female DBA/2J mice.Endocrinology. 2004; 145: 1238-1247Crossref PubMed Scopus (135) Google Scholar Insight into the importance of maternal physiology on oocyte quality can be demonstrated in experimental animal models of maternal diabetes in which there is an increase in granulosa cell apoptosis of the ovarian follicle and impaired oocyte maturation.15Chang A.S. Dale A.N. Moley K.H. Maternal diabetes adversely affects preovulatory oocyte maturation, development, and granulosa cell apoptosis.Endocrinology. 2005; 146: 2445-2453Crossref PubMed Scopus (141) Google Scholar, 16Jungheim E.S. Moley K.H. The impact of type 1 and type 2 diabetes mellitus on the oocyte and the preimplantation embryo.Semin Reprod Med. 2008; 26: 186-195Crossref PubMed Scopus (41) Google Scholar, 38Ratchford A.M. Chang A.S. Chi M.M. Sheridan R. Moley K.H. Maternal diabetes adversely affects AMP-activated protein kinase activity and cellular metabolism in murine oocytes.Am J Physiol Endocrinol Metab. 2007; 293: E1198-E1206Crossref PubMed Scopus (70) Google Scholar Similar to diabetes, obesity is a condition marked by aberrations in circulating levels of substrates for energy production, and it too appears to have effects on oocyte quality. Visually, these effects appear to be primarily on oocyte maturation,39Wittemer C. Ohl J. Bailly M. Bettahar-Lebugle K. Nisand I. Does body mass index of infertile women have an impact on IVF procedure and outcome?.J Assist Reprod Genet. 2000; 17: 547-552Crossref PubMed Scopus (179) Google Scholar, 40Robker R.L. Evidence that obesity alters the quality of oocytes and embryos.Pathophysiology. 2008; 15: 115-121Abstract Full Text Full Text PDF PubMed Scopus (141) Google Scholar, 41Jungheim E.S. Schoeller E.L. Marquard K.L. Louden E.D. Schaffer J.E. Moley K.H. Diet induced obesity model: abnormal oocytes and persistent growth abnormalities in the offspring.Endocrinology. 2010; 151: 3475-3476Crossref PubMed Scopus (250) Google Scholar although there are data suggesting that even subjectively normal oocytes are altered at the molecular level by conditions like PCOS.42Wood J.R. Dumesic D.A. Abbott D.H. Strauss 3rd, J.F. Molecular abnormalities in oocytes from women with polycystic ovary syndrome revealed by microarray analysis.J Clin Endocrinol Metab. 2007; 92: 705-713Crossref PubMed Scopus (224) Google Scholar These alterations are in genes associated with chromosome alignment and segregation during mitosis and/or meiosis and in genes associated with peroxisome proliferator-activated receptors, receptors important to cellular growth and development in the fetus43Rees W.D. McNeil C.J. Maloney C.A. The roles of PPARs in the fetal origins of metabolic health and disease.PPAR Res. 2008; 2008: 459030Crossref PubMed Scopus (61) Google Scholar and known to be activated by thiazolidinedione drugs. Thiazolidinedione drugs have been shown to improve oocyte competence as measured by embryonic development in mouse models of maternal obesity44Minge C.E. Bennett B.D. Norman R.J. Robker R.L. Peroxisome proliferator-activated receptor-gamma agonist rosiglitazone reverses the adverse effects of diet-induced obesity on oocyte quality.Endocrinology. 2008; 149: 2646-2656Crossref PubMed Scopus (176) Google Scholar and to induce ovulation in women with PCOS.45Azziz R. Ehrmann D. Legro R.S. et al.Troglitazone improves ovulation and hirsutism in the polycystic ovary syndrome: a multicenter, double blind, placebo-controlled trial.J Clin Endocrinol Metab. 2001; 86: 1626-1632Crossref PubMed Scopus (525) Google Scholar There are a variety of factors that may impair oocyte maturation in obese women including abnormalities in ovarian follicular recruitment and development due to blunted LH amplitude as discussed earlier.26Santoro N. Lasley B. McConnell D. et al.Body size and ethnicity are associated with menstrual cycle alterations in women in the early menopausal transition: the Study of Women's Health across the Nation (SWAN) daily hormone study.J Clin Endocrinol Metab. 2004; 89: 2622-2631Crossref PubMed Scopus (178) Google Scholar, 31Jain A. Polotsky A.J. Rochester D. et al.Pulsatile luteinizing hormone amplitude and progesterone metabolite excretion are reduced in obese women.J Clin Endocrinol Metab. 2007; 92: 2468-2473Crossref PubMed Scopus (142) Google Scholar On the other hand, there is evidence that the follicular environment in which the oocyte develops and matures is altered in obese women compared with nonobese women. Because these differences are noted in women undergoing IVF during which exogenous gonadotropins are used to achieve follicular recruitment and development, it is unlikely that the abnormalities are the result of obesity-related HPO axis dysfunction. Instead, it may be that some component of obesity alters composition of the follicular fluid directly, which could influence oocyte metabolism or metabolism of the cells that support the developing oocyte and follicle including granulosa cells, cumulus cells, and theca cells.46Sutton-McDowall M.L. Gilchrist R.B. Thompson J.G. The pivotal role of glucose metabolism in determining oocyte developmental competence.Reproduction. 2010; 139: 685-695Crossref PubMed Scopus (310) Google Scholar Changes in the metabolism of these cells could further alter the composition of follicular fluid. Alterations noted in follicular fluid from obese women include increased insulin, glucose and lactate, increased androgen activity, increased C-reactive protein, and decreased human chorionic gonadotropin levels.47Robker R.L. Akison L.K. Bennett B.D. et al.Obese women exhibit differences in ovarian metabolites, hormones, and gene expression compared with moderate-weight women.J Clin Endocrinol Metab. 2009; 94: 1533-1540Crossref PubMed Scopus (260) Google Scholar, 48Carrell D.T. Jones K.P. Peterson C.M. Aoki V. Emery B.R. Campbell B.R. Body mass index is inversely related to intrafollicular HCG concentrations, embryo quality and IVF outcome.Reprod Biomed Online. 2001; 3: 109-111Abstract Full Text PDF PubMed Google Scholar There is also evidence that follicular leptin levels correlate with BMI.49Hill M.J. Uyehara C.F. Hashiro G.M. Frattarelli J.L. The utility of serum leptin and follicular fluid leptin, estradiol, and progesterone levels during an in vitro fertilization cycle.J Assist Reprod Genet. 2007; 24: 183-188Crossref PubMed Scopus (26) Google Scholar In vitro studies have shown that leptin impairs steroidogenesis in granulosa cells,50Lin Q. Poon S.L. Chen J. Cheng L. HoYuen B. Leung P.C. Leptin interferes with 3',5'-cyclic adenosine monophosphate (cAMP) signaling to inhibit steroidogenesis in human granulosa cells.Reprod Biol Endocrinol. 2009; 7: 115Crossref PubMed Scopus (40) Google Scholar, 51Mantzoros C.S. Role of leptin in reproduction.Ann N Y Acad Sci. 2000; 900: 174-183Crossref PubMed Google Scholar and such an impairment could also have an impact on follicular development, oocyte quality, and ovulation in obese women.52Brannian J.D. Hansen K.A. Leptin and ovarian folliculogenesis: implications for ovulation induction and ART outcomes.Semin Reprod Med. 2002; 20: 103-112Crossref PubMed Scopus (76) Google Scholar Further work is needed to determine how oocyte quality specifically influences pregnancy outcome for obese women; however, as mentioned in previous text, data from animal models of obesity and type 1 diabetes mellitus demonstrate that poor maternal physiology affects oocyte quality. In the case of type 1 diabetes, these affected oocytes predispose to an increased risk of fetal abnormalities including congenital anomalies and fetal growth restriction,15Chang A.S. Dale A.N. Moley K.H. Maternal diabetes adversely affects preovulatory oocyte maturation, development, and granulosa cell apoptosis.Endocrinology. 2005; 146: 2445-2453Crossref PubMed Scopus (141) Google Scholar, 17Wyman A. Pinto A.B. Sheridan R. Moley K.H. One-cell zygote transfer from diabetic to nondiabetic mouse results in congenital malformations and growth retardation in offspring.Endocrinology. 2008; 149: 466-469Crossref PubMed Scopus (92) Google Scholar perhaps via adverse effects on the meiotic spindle of the oocyte or on mitochondrial structure and function.53Wang Q. Ratchford A.M. Chi M.M. et al.Maternal diabetes causes mitochondrial dysfunction and meiotic defects in murine oocytes.Mol Endocrinol. 2009; 23: 1603-1612Crossref PubMed Scopus (143) Google Scholar Similar to diabetes, obesity is also a condition of abnormal maternal physiology. Although laboratory evidence supports a role for poor oocyte quality as a factor in adverse reproductive outcomes in the setting of obesity,41Jungheim E.S. Schoeller E.L. Marquard K.L. Louden E.D. Schaffer J.E. Moley K.H. Diet induced obesity model: abnormal oocytes and persistent growth abnormalities in the offspring.Endocrinology. 2010; 151: 3475-3476Crossref PubMed Scopus (250) Google Scholar clinical evidence is lacking. One avenue to consider exploring for additional information regarding relationships between oocytes and pregnancy outcome is data from donor oocyte cycles in clinical IVF practice. One published abstract suggests donor oocytes taken from obese women do not affect live birth rates in recipient women of normal weight; however, the numbers of patients included in the study were too small (64 IVF cycles using oocytes from normal-weight women vs 8 IVF cycles using oocytes from donors who were obese) to adequately control for potential confounding factors.54Wu D.H. Griffin D. Eckert J. Aubuchon M. Williams D.B. Thomas M.A. Oocyte donors' body mass index (BMI) confers no adverse effect on recipients' pregnancy outcomes.Fertil Steril. 2009; 92: A15-A77Google Scholar On the other hand, some IVF centers may restrict oocyte donation to women of normal weight55Obeso I.S.R. Galache P. Sepulveda J. Diaz P. Patrizi P. The impact of body mass index (BMI) on ovarian stimulation in young oocyte donors.Fertil Steril. 2009; 92: S103Abstract Full Text Full Text PDF Google Scholar because overweight and obese women are known to require additional gonadotropin stimulation in their IVF cycles," @default.
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• W1976745100 date "2010-12-01" @default.
• W1976745100 modified "2023-10-12" @default.
• W1976745100 title "Current knowledge of obesity's effects in the pre- and periconceptional periods and avenues for future research" @default.
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