FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2007288539> ?p ?o ?g. }

• W2007288539 endingPage "17" @default.
• W2007288539 startingPage "13" @default.
• W2007288539 abstract "Women with PCOS are often obese and there is debate in the literature regarding whether women are obese because of their PCOS status or if those who become obese are more predisposed to PCOS. There is support for a predisposition to obesity by some data indicating impaired metabolism in PCOS women compared to weight matched controls but this data is limited. Contrary data also exist that adiposity rates do not vary between women with PCOS and those without, and that differences in obesity rates between countries are more likely due to environmental and lifestyle factors. Until further data are available, lifestyle recommendations for weight reduction in women with PCOS should be similar to those for women without PCOS. Women with PCOS are often obese and there is debate in the literature regarding whether women are obese because of their PCOS status or if those who become obese are more predisposed to PCOS. There is support for a predisposition to obesity by some data indicating impaired metabolism in PCOS women compared to weight matched controls but this data is limited. Contrary data also exist that adiposity rates do not vary between women with PCOS and those without, and that differences in obesity rates between countries are more likely due to environmental and lifestyle factors. Until further data are available, lifestyle recommendations for weight reduction in women with PCOS should be similar to those for women without PCOS. While, there is considerable evidence that obesity plays a negative role in the pathophysiology of PCOS (1Diamanti-Kandarakis E. Role of obesity and adiposity in polycystic ovary syndrome.Int J Obes. 2007; 31 (discussion S31–2): S8-13Crossref Scopus (90) Google Scholar), it is not clear if women with PCOS harbor a unique predisposition to obesity, or if obesity is a secondary factor exacerbating the condition. It has been estimated that as many as 38–88% of women with PCOS are overweight or obese (2Legro R.S. The genetics of obesity. Lessons for polycystic ovary syndrome.Ann N Y Acad Sci. 2000; 900: 193-202Crossref PubMed Scopus (67) Google Scholar, 3Balen A.H. Conway G.S. Kaltsas G. Techatrasak K. Manning P.J. West C. et al.Polycystic ovary syndrome: the spectrum of the disorder in 1741 patients.Hum Reprod. 1995; 10: 2107-2111Crossref PubMed Scopus (15) Google Scholar). Indeed, the rates of obesity across all populations worldwide have increased significantly in the last 30 years (4Kosti R.I. Panagiotakos D.B. The epidemic of obesity in children and adolescents in the world.Cent Eur J Public Health. 2006; 14: 151-159PubMed Google Scholar, 5Popkin B.M. Gordon-Larsen P. The nutrition transition: worldwide obesity dynamics and their determinants.Int J Obes Relat Metab Disord. 2004; 28: S2-S9Crossref PubMed Scopus (1021) Google Scholar). In the United States, the majority of the adult population is now overweight or obese (6Ogden C.L. Carroll M.D. Curtin L.R. McDowell M.A. Tabak C.J. Flegal K.M. Prevalence of overweight and obesity in the United States, 1999–2004.JAMA. 2006; 295: 1549-1555Crossref PubMed Scopus (7323) Google Scholar). Reasons for the continued growth in obesity prevalence are multifaceted. Energy intake has significantly increased in the last several decades, particularly the consumption of more calorie dense food. This increase is paralleled by a corresponding decline in energy expenditure through daily activity and physical exercise (7Trends in leisure-time physical inactivity by age, sex, and race/ethnicity–United States, 1994–2004.MMWR Morb Mortal Wkly Rep. 2005; 54: 991-994PubMed Google Scholar). The conditions that contribute to increased obesity prevalence impact women both with and without PCOS, making the relative contribution of obesity predisposition in PCOS difficult to assess. Obesity has been a common feature of PCOS since the original description of the Stein-Leventhal syndrome in the 1930s (8Stein I.F. Levinthal M. Amenorrhea associated with bilateral polycystic ovaries.Am J Obstet Gynecol. 1935; : 181-191Google Scholar). However, obesity is not a defining feature of the syndrome as PCOS is seen in both normal weight and obese women. There is nonetheless evidence that obesity, particularly abdominal obesity, worsens both the clinical and endocrine features of the syndrome. Variation in the prevalence of obesity in the syndrome across different populations has been attributed to lifestyle factors as well as genetic factors (9Carmina E. Genetic and environmental aspect of polycystic ovary syndrome.J Endocrinol Invest. 2003; 26: 1151-1159PubMed Google Scholar). Obesity in PCOS has a marked impact on the features of the syndrome. In addition to the metabolic consequences including a high prevalence of type 2 diabetes in obese women with PCOS (10Moran L.J. Misso M.L. Wild R.A. Norman R.J. Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis.Hum Reprod Update. 2010; 16: 347-363Crossref PubMed Scopus (711) Google Scholar), the reproductive consequences of obesity in PCOS include a higher prevalence of irregular menses and menorrhagia, an increase in serum androgen concentrations, and a significantly reduced response to ovulation induction regimens as well as reduced success of fertility treatments when compared to lean women with the condition (11Pasquali R. Gambineri A. Pagotto U. The impact of obesity on reproduction in women with polycystic ovary syndrome.BJOG. 2006; 113: 1148-1159Crossref PubMed Scopus (257) Google Scholar, 12Hoeger K. Obesity and weight loss in polycystic ovary syndrome.Obstet Gynecol Clin North Am. 2001; 28: 85-97Abstract Full Text Full Text PDF PubMed Scopus (74) Google Scholar). This review examines the evidence both for and against the predisposition towards obesity in women with PCOS. Given the impact of obesity in PCOS, the question as to whether women with PCOS have a unique predisposition to obesity is critical to our understanding of the pathophysiology of the condition, as well as insight into the best treatment options. While all individuals with obesity face potential barriers to effective weight management, it is possible that women with PCOS face additional barriers. Women with PCOS who are enrolled in a lifestyle program demonstrate high rates of failure to lose weight and dropout from these studies. Dropout rates in excess of 40% are noted in these studies (13Thomson R.L. Buckley J.D. Noakes M. Clifton P.M. Norman R.J. Brinkworth G.D. The effect of a hypocaloric diet with and without exercise training on body composition, cardiometabolic risk profile, and reproductive function in overweight and obese women with polycystic ovary syndrome.J Clin Endocrinol Metab. 2008; 93: 3373-3380Crossref PubMed Scopus (176) Google Scholar, 14Hoeger K.M. Kochman L. Wixom N. Craig K. Miller R.K. Guzick D.S. A randomized, 48-week, placebo-controlled trial of intensive lifestyle modification and/or metformin therapy in overweight women with polycystic ovary syndrome: a pilot study.Fertil Steril. 2004; 82: 421-429Abstract Full Text Full Text PDF PubMed Scopus (211) Google Scholar). As stated above, there is some evidence that prevalence of obesity is increased in PCOS populations when compared to general populations. In the North Finland birth cohort, a study of over 2000 women born in 1966 and followed prospectively, women were contacted at ages 14 and 31. If individuals were obese at age 31 there was an increased relative risk of self reported symptoms of PCOS of 1.44. If there was obesity present at both 14 and 31 years of age the relative risk of PCOS increased to 1.71 (15Laitinen J. Taponen S. Martikainen H. Pouta A. Millwood I. Hartikainen A.L. et al.Body size from birth to adulthood as a predictor of self-reported polycystic ovary syndrome symptoms.Int J Obes Relat Metab Disord. 2003; 27: 710-715Crossref PubMed Scopus (115) Google Scholar). In an unselected Spanish cohort, the prevalence of PCOS in an obese population was 28.3% which was significantly increased over the rate of PCOS in the general population (16Asuncion M. Calvo R.M. San Millan J.L. Sancho J. Avila S. Escobar-Morreale H.F. A prospective study of the prevalence of the polycystic ovary syndrome in unselected Caucasian women from Spain.J Clin Endocrinol Metab. 2000; 85: 2434-2438Crossref PubMed Scopus (1140) Google Scholar). However in an unselected US population the rate of PCOS in lean women with BMI <25 kg/m2 did not differ from that in women with BMI 35 kg/m2 or higher (9.8% versus 12.5%, NS) (17Yildiz B.O. Knochenhauer E.S. Azziz R. Impact of obesity on the risk for polycystic ovary syndrome.J Clin Endocrinol Metab. 2008; 93: 162-168Crossref PubMed Scopus (242) Google Scholar). This may reflect however a smaller portion of women in the higher BMI categories with a trend noted to increased diagnosis of PCOS in those with BMI over 35 kg/m2. Obesity itself is associated with an increase in androgen concentration in children. While this is not clearly associated with an increase in the diagnosis of PCOS, premenarchal obesity is associated with significantly higher androgen concentrations in early puberty (18Burt Solorzano C.M. McCartney C.R. Obesity and the pubertal transition in girls and boys.Reproduction. 2010; 140: 399-410Crossref PubMed Scopus (246) Google Scholar). It is not possible from these studies to interpret whether a predisposition to obesity is associated with PCOS early in development but it is suggested that obesity primarily is associated with elevated ovarian androgen production which may predispose to PCOS. If women with PCOS have an increased risk of obesity compared to women without PCOS, it is possible that this may manifest as a difference in either basal metabolic rate (BMR) or in utilization of calories after consumption. There have been only a few studies that have attempted to assess the basal metabolic rate and postprandial thermogenesis in women with PCOS compared to control women matched for body weight. The studies available in the literature were all performed with indirect calorimetry and show mixed results. Segal and Dunaif studied 10 obese women with PCOS and 9 obese controls and compared to lean controls. They demonstrated decreased resting metabolic rate in obese versus lean control women but there was no difference between obese with and without PCOS (19Segal K.R. Dunaif A. Resting metabolic rate and postprandial thermogenesis in polycystic ovarian syndrome.Int J Obes. 1990; 14: 559-567PubMed Google Scholar). Robinson et al., however, found decreased postprandial thermogenesis in women with PCOS compared to control women in both obese and lean PCOS (20Robinson S. Chan S.P. Spacey S. Anyaoku V. Johnston D.G. Franks S. Postprandial thermogenesis is reduced in polycystic ovary syndrome and is associated with increased insulin resistance.Clin Endocrinol. 1992; 36: 537-543Crossref PubMed Scopus (110) Google Scholar). More recently a study of 62 women with PCOS and 23 control women matched for body weight demonstrated decreased basal metabolic rate in all PCOS women compared to controls, although women with PCOS who were classified as insulin resistant had the lowest BMR (21Georgopoulos N.A. Saltamavros A.D. Vervita V. Karkoulias K. Adonakis G. Decavalas G. et al.Basal metabolic rate is decreased in women with polycystic ovary syndrome and biochemical hyperandrogenemia and is associated with insulin resistance.Fertil Steril. 2009; 92: 250-255Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar). Overall these studies suggest that there are differences in caloric utilization in women with PCOS when matched for body weight. Unfortunately there are no studies that examine metabolic rates in women with PCOS using more rigorous methodology and carefully controlled direct observation of dietary intakes, leaving the question of basal metabolic rates in PCOS unresolved. It is possible that either energy intake or energy expenditure differ between women with and without PCOS. With respect to energy intake, a study of 84 women with PCOS and 79 controls, part of a long-term PCOS cohort study in Pittsburgh, suggested that lean women (BMI <25 kg/m2) with PCOS restricted calories significantly more than BMI matched control women to maintain the same weight (1398 versus 1792 kcal/day) (22Wright C.E. Zborowski J.V. Talbott E.O. McHugh-Pemu K. Youk A. Dietary intake, physical activity, and obesity in women with polycystic ovary syndrome.Int J Obes Relat Metab Disord. 2004; 28: 1026-1032Crossref PubMed Scopus (70) Google Scholar). This relationship was not seen in the overweight and obese women, as similar caloric intake was seen between the cases and controls in women with BMI >25 kg/m2. In that study there was no difference in physical activity scores between the groups as measured in a survey questionnaire. In a contrary study looking a prospective food diary collection, Douglas et al studied 30 overweight women with PCOS compared to weight matched controls (BMI 29 kg/m2) and did not show any difference in caloric intake between the groups, but women with PCOS consumed more foods with high glycemic content (23Douglas C.C. Norris L.E. Oster R.A. Darnell B.E. Azziz R. Gower B.A. Difference in dietary intake between women with polycystic ovary syndrome and healthy controls.Fertil Steril. 2006; 86: 411-417Abstract Full Text Full Text PDF PubMed Scopus (97) Google Scholar). It is possible that differences in caloric intake and BMI may be most revealing however in women with normal body weight. Unfortunately there are no studies with a large enough lean population of PCOS women to adequate answer the question as to whether maintaining a normal body mass index in PCOS requires either more dietary restriction or increased energy utilization. There is evidence that obesity prevalence varies between different ethnic populations of women with PCOS (9Carmina E. Genetic and environmental aspect of polycystic ovary syndrome.J Endocrinol Invest. 2003; 26: 1151-1159PubMed Google Scholar). This may indeed be due to the impact of different lifestyle characteristics within different geographic areas but may also reflect genetic predisposition to obesity within populations. While there are yet no definitive genetic markers that define PCOS, it is possible that genes for obesity may track in PCOS populations and therefore predispose women with PCOS to obesity. Evidence for this was reported with the fat mass and obesity associated gene (FTO) which has been shown to influence susceptibility to type 2 DM through a substantial impact on BMI and adiposity in a general European population (24Frayling T.M. Timpson N.J. Weedon M.N. Zeggini E. Freathy R.M. Lindgren C.M. et al.A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.Science. 2007; 316: 889-894Crossref PubMed Scopus (3250) Google Scholar). Barber et al. studied a variant of FTO, rs9939609 in 436 women with PCOS and 1336 controls. They found a significant association between this FTO genotype and PCOS status (25Barber T.M. Bennett A.J. Groves C.J. Sovio U. Ruokonen A. Martikainen H. et al.Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome.Diabetologia. 2008; 51: 1153-1158Crossref PubMed Scopus (94) Google Scholar). There was no association however with androgens in that study. This study would need to be expanded to other populations to assess the possibility of increased prevalence of obesity genes in women with PCOS. Androgen excess itself may predispose to abdominal fat deposition. In women androgen excess has been associated in some studies with increased risk of metabolic syndrome (26Pasquali R. Obesity and androgens: facts and perspectives.Fertil Steril. 2006; 85: 1319-1340Abstract Full Text Full Text PDF PubMed Scopus (308) Google Scholar). Coviello et al. (27Coviello A.D. Legro R.S. Dunaif A. Adolescent girls with polycystic ovary syndrome have an increased risk of the metabolic syndrome associated with increasing androgen levels independent of obesity and insulin resistance.J Clin Endocrinol Metab. 2006; 91: 492-497Crossref PubMed Scopus (349) Google Scholar) reported higher prevalence of metabolic syndrome in PCOS adolescents than in the general population. They demonstrated a higher prevalence of metabolic syndrome using pediatric standards with increasing levels of testosterone. Interestingly this was independent of both obesity and insulin resistance, although abdominal adiposity specifically was not examined. Given the dysregulation of sex steroids in PCOS as demonstrated by androgen excess, this may play a fundamental role in the development and expression of obesity phenotypes as well as metabolic dysfunction. An area of relatively new investigation is the influence of prenatal exposures on adult diseases. It is possible that predisposition to obesity begins antenatally. The intrauterine environment, particularly over nutrition prenatally, may predispose to adult diseases (28Dyer J.S. Rosenfeld C.R. Metabolic imprinting by prenatal, perinatal, and postnatal overnutrition: a review.Semin Reprod Med. 2011; 29: 266-276Crossref PubMed Scopus (112) Google Scholar). For instance, there is evidence that maternal obesity predisposes to risk for childhood metabolic syndrome. In a study of children at 11 years of age, maternal obesity predicted presence of metabolic syndrome in childhood, independently of gestational diabetes, a known risk factor for metabolic dysfunction in childhood (29Boney C.M. Verma A. Tucker R. Vohr B.R. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus.Pediatrics. 2005; 115: e290-e296Crossref PubMed Scopus (1696) Google Scholar). It is also possible that insulin resistance itself, a feature in the majority of individuals with PCOS, may predispose to obesity and this may be predetermined in the intrauterine environment. In a study of 301 pregnant women, evidence for insulin resistance as measured by oral glucose tolerance test in pregnancy was associated with infant weight gain in the first year of life as well as increased infant adiposity. This was independent of maternal glucose status (30Hamilton J.K. Odrobina E. Yin J. Hanley A.J. Zinman B. Retnakaran R. Maternal insulin sensitivity during pregnancy predicts infant weight gain and adiposity at 1 year of age.Obesity. 2010; 18: 340-346Crossref PubMed Scopus (34) Google Scholar). In summary, PCOS is highly linked to obesity in all populations studied. Insulin resistance or androgen excess may predispose to changes in body composition independently. While the evidence is limited due to small studies or preliminary data, there appears to be support for the hypothesis that women with PCOS demonstrate a predisposition to obesity. It is possible this predisposition is related to prenatal events, genetic predisposition or both, but more study is needed. There is little doubt that PCOS and obesity are highly correlated, but the evidence for a unique predisposition to obesity in PCOS is not strong. Environmental factors, hence modifiable factors, are more likely to play a role in the high prevalence of obesity that is seen in the condition. This is evidenced by the fact that the prevalence of obesity varies greatly between countries (31Moran L.J. Pasquali R. Teede H.J. Hoeger K.M. Norman R.J. Treatment of obesity in polycystic ovary syndrome: a position statement of the Androgen Excess and Polycystic Ovary Syndrome Society.Fertil Steril. 2009; 92: 1966-1982Abstract Full Text Full Text PDF PubMed Scopus (272) Google Scholar). It is likely that the environmental and lifestyle differences between countries account for population based differences in obesity reported, but due to the lack of population based data it is not possible to directly compare obesity rates between countries. It is also clear that obese women with PCOS enrolled in a lifestyle treatment program have high dropout rates from the program and demonstrate only modest weight reduction. Whether this is distinct, however, from the general obese population with respect to degree of weight reduction or success with lifestyle programs is unclear (32Ayyad C. Andersen T. Long-term efficacy of dietary treatment of obesity: a systematic review of studies published between 1931 and 1999.Obes Rev. 2000; 1: 113-119Crossref PubMed Scopus (267) Google Scholar). Long-term rates of success in weight reduction using lifestyle modification and diet in the general population are low and estimated to be approximately 15%. This is likely similar to that seen in studies in women with PCOS. While this review focuses on obesity in general, body weight alone may not be the best measure of the metabolic impact. Actually what may be more important and germane to this discussion than total body weight, is fat distribution in women with PCOS. Insulin resistance is a hallmark feature of PCOS and abdominal obesity is associated with greater insulin resistance as well as diabetes emphasizing the importance of abdominal fat in the discussion of obesity’s impact (33Carey D.G. Jenkins A.B. Campbell L.V. Freund J. Chisholm D.J. Abdominal fat and insulin resistance in normal and overweight women: Direct measurements reveal a strong relationship in subjects at both low and high risk of NIDDM.Diabetes. 1996; 45: 633-638Crossref PubMed Google Scholar). Although an older study by Goode et al. (34Good C. Tulchinsky M. Mauger D. Demers L.M. Legro R.S. Bone mineral density and body composition in lean women with polycystic ovary syndrome.Fertil Steril. 1999; 72: 21-25Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar) did not demonstrate differences in fat distribution between PCOS and lean controls, Kirchengast and Huber (35Kirchengast S. Huber J. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome.Hum Reprod. 2001; 16: 1255-1260Crossref PubMed Scopus (233) Google Scholar) showed a significantly higher amount of body fat and lower amount of lean body mass than did age, weight and BMI matched controls. They found that the FDI (fat distribution index), which equals the upper body fat mass in kg divided by the lower body fat mass in kg, to be of an android, or intermediate versus gynoid pattern in 7/10 of their small study population. The role of androgens themselves in the propagation or development of an android body fat distribution over the life span is beyond the scope of this review, but clearly a link between central adiposity and hyperandrogenism has been suggested. Abbott et al showed that the prenatally virilized female rhesus monkey had an increase in abdominal obesity in adulthood (36Abbott D.H. Tarantal A.F. Dumesic D.A. Fetal, infant, adolescent and adult phenotypes of polycystic ovary syndrome in prenatally androgenized female rhesus monkeys.Am J Primatol. 2009; 71: 776-784Crossref PubMed Scopus (132) Google Scholar). In this regard, abdominal adiposity may be more prevalent in women with PCOS however population based data are not available. Recently, Baranova et al. (37Baranova A. Tran T.P. Birerdinc A. Younossi Z.M. Systematic review: association of polycystic ovary syndrome with metabolic syndrome and non-alcoholic fatty liver disease.Aliment Pharmacol Ther. 2011; 33: 801-814Crossref PubMed Scopus (97) Google Scholar) reviewed the association of PCOS with metabolic syndrome and non-alcoholic fatty liver disease (NAFLD) in a systematic PubMed review from 1985–2010. It was evident that women with PCOS are at risk for NAFLD and that NAFLD may be a risk factor for PCOS. Additionally, NAFLD is thought to be the hepatic manifestation of metabolic syndrome- whereas PCOS is the ovarian manifestation. Rather than being causative it appears that the prevalence of both PCOS and NAFLD increases proportionally with the degree of insulin resistance and increase in the mass of adipose tissue, similarly to other conditions of obesity and not specifically for PCOS. Attempting further to assess whether obesity or the effects associated with obesity were more prevalent in PCOS, Rossi tried to determine if PCOS increased the risk of metabolic syndrome, a syndrome known to be strongly associated with obesity, in a group of obese adolescent women. When matched for obesity, PCOS defined by the NIH criteria, was not an increased risk factor for MBS using either pediatric or adult standards. As the number of metabolic syndrome factors increased, however, to three or more there was a significant association with increased visceral adipose tissue (VAT) as assessed by CT scan slice at L4–L5. Further assessment of the risk of obesity occurrence in those with PCOS has begun to be evaluated by Glueck et al. (38Glueck C.J. Morrison J.A. Daniels S. Wang P. Stroop D. Sex hormone-binding globulin, oligomenorrhea, polycystic ovary syndrome, and childhood insulin at age 14 years predict metabolic syndrome and class III obesity at age 24 years.J Pediatr. 2011; 159 (308–13.e2)PubMed Google Scholar). It did appear that if at age 14 years one had oligomennorhea and hyperandrogenism there was an increase risk of having severe obesity (BMI >40) and metabolic syndrome at age 24 years of age, supporting a temporal progressive association of PCOS with obesity, but not a predisposition to obesity primarily. PCOS is significantly associated with insulin resistance as noted previously in this review. Whether insulin resistance per se is associated with predisposition to weight gain is not clear however. Most studies that have associated insulin resistance with weight gain did not adequately control for dietary and lifestyle factors present. Therefore there are mixed data with respect to insulin resistance and weight gain in the general population (39Hivert M.F. Langlois M.F. Carpentier A.C. The entero-insular axis and adipose tissue-related factors in the prediction of weight gain in humans.Int J Obes. 2007; 31: 731-742Crossref Scopus (74) Google Scholar) and whether the insulin resistance in PCOS predisposes to weight gain and obesity is not clear. Basal metabolic rate has been previously examined in women with PCOS using indirect calorimetry. While two studies indicate either decreased BMR or decreased postprandial thermogeneis (20Robinson S. Chan S.P. Spacey S. Anyaoku V. Johnston D.G. Franks S. Postprandial thermogenesis is reduced in polycystic ovary syndrome and is associated with increased insulin resistance.Clin Endocrinol. 1992; 36: 537-543Crossref PubMed Scopus (110) Google Scholar, 21Georgopoulos N.A. Saltamavros A.D. Vervita V. Karkoulias K. Adonakis G. Decavalas G. et al.Basal metabolic rate is decreased in women with polycystic ovary syndrome and biochemical hyperandrogenemia and is associated with insulin resistance.Fertil Steril. 2009; 92: 250-255Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar), other studies do not support this finding (19Segal K.R. Dunaif A. Resting metabolic rate and postprandial thermogenesis in polycystic ovarian syndrome.Int J Obes. 1990; 14: 559-567PubMed Google Scholar, 40Cosar E. Koken G. Sahin F.K. Akgun L. Ucok K. Genc A. et al.Resting metabolic rate and exercise capacity in women with polycystic ovary syndrome.Int J Gynaecol Obstet. 2008; 101: 31-34Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar). The lack of definitive study on BMR does not allow specific conclusion as to whether there is increased predisposition to obesity in PCOS. Obesity itself may be influenced by hormones involved with satiety and appetite. With respect to the influence of appetite regulators in PCOS, attention has focused on potential dysregulation of ghrelin, a gastric peptide that has appetite suppression and adipogenic properties and is felt to regulate food intake and body weight. In a study of 20 obese women with PCOS and 11 BMI matched controls, non-PCOS subjects had a greater fasting baseline ghrelin and a greater increase in ghrelin with diet induced weight loss, while PCOS subjects demonstrated increased hunger and decreased satiety during dieting (41Moran L.J. Noakes M. Clifton P.M. Wittert G. Tomlinson L. Galletly C. et al.Ghrelin and measures of satiety are altered in polycystic ovary syndrome but not differentially affected by diet composition.Asia Pac J Clin Nutr. 2003; 12: S52PubMed Google Scholar). However, other studies have not demonstrated differences between women with and without PCOS. In a study of 33 women with PCOS and 31 BMI matched controls, there was a significant inverse correlation between BMI and ghrelin but no difference between PCOS and controls (42Orio Jr., F. Lucidi P. Palomba S. Tauchmanova L. Cascella T. Russo T. et al.Circulating ghrelin concentrations in the polycystic ovary syndrome.J Clin Endocrinol Metab. 2003; 88: 942-945Crossref PubMed Scopus (77) Google Scholar). In another study of 20 non-obese women with PCOS compared with 45 lean controls and 37 obese controls, there were no baseline fasting differences in ghrelin between lean PCOS and lean controls, and both lean groups demonstrated increased ghrelin compared to obese women without PCOS (43Bik W. Baranowska-Bik A. Wolinska-Witort E. Chmielowska M. Martynska L. Baranowska B. The relationship between metabolic status and levels of adiponectin and ghrelin in lean women with polycystic ovary syndrome.Gynecol Endocrinol. 2007; 23: 325-331Crossref PubMed Scopus (38) Google Scholar). Overall there is no definitive evidence that women with PCOS are predisposed to obesity. While obesity is clearly highly prevalent in PCOS, attention to weight reduction efforts and maintenance of normal body weight in those who are not obese remains a high priority in the management of PCOS. Until there are definitive data available, techniques for weight reduction and lifestyle modification in the general population are likely the best management for women with PCOS as well. Obesity and excess body fat have been increasing dramatically across all populations in the developed world. Associated with the increase in obesity is an increase in obesity related diseases such as diabetes. While a high prevalence of obesity in PCOS is clear, the role that obesity plays in the fundamental pathophysiology of PCOS is still unclear. While the impact from obesity in PCOS is significant, notably women with PCOS have a high prevalence of obesity, abdominal obesity, insulin resistance and even metabolic syndrome, whether there is distinct predisposition to obesity remains uncertain. Evidence supporting the predisposition to obesity is limited to small studies without the gold standard for this determination, metabolic chamber assessment, to examine metabolic rates and energy utilization rigorously. The role for intrauterine environment provides the strongest data currently to suggest epigenetic causes for obesity but how this relates to development of PCOS is not yet clear. Population based studies that look longitudinally to assess the incidence of PCOS in relationship to development of obesity are needed. Research to define both basic metabolism in PCOS and potential impact of specific dietary and lifestyle factors is needed. Lifestyle modification based on the principles of caloric restriction and exercise remains a primary therapy for the management of obesity in PCOS." @default.
• W2007288539 created "2016-06-24" @default.
• W2007288539 creator A5065813469 @default.
• W2007288539 creator A5067531230 @default.
• W2007288539 date "2012-01-01" @default.
• W2007288539 modified "2023-10-08" @default.
• W2007288539 title "Do women with PCOS have a unique predisposition to obesity?" @default.
• W2007288539 cites W1964753360 @default.
• W2007288539 cites W1965636834 @default.
• W2007288539 cites W1971712685 @default.
• W2007288539 cites W1974716906 @default.
• W2007288539 cites W1977333932 @default.
• W2007288539 cites W1984524047 @default.
• W2007288539 cites W1989468609 @default.
• W2007288539 cites W1992527366 @default.
• W2007288539 cites W2001380683 @default.
• W2007288539 cites W2004708554 @default.
• W2007288539 cites W2007842092 @default.
• W2007288539 cites W2011637513 @default.
• W2007288539 cites W2016497833 @default.
• W2007288539 cites W2016548273 @default.
• W2007288539 cites W2036507326 @default.
• W2007288539 cites W2050998122 @default.
• W2007288539 cites W2052785258 @default.
• W2007288539 cites W2057326698 @default.
• W2007288539 cites W2067166016 @default.
• W2007288539 cites W2080464810 @default.
• W2007288539 cites W2089391845 @default.
• W2007288539 cites W2092509345 @default.
• W2007288539 cites W2097660065 @default.
• W2007288539 cites W2101316067 @default.
• W2007288539 cites W2101492737 @default.
• W2007288539 cites W2108833696 @default.
• W2007288539 cites W2124508331 @default.
• W2007288539 cites W2132082799 @default.
• W2007288539 cites W2135808538 @default.
• W2007288539 cites W2137461702 @default.
• W2007288539 cites W2140855573 @default.
• W2007288539 cites W2157068724 @default.
• W2007288539 cites W2160827694 @default.
• W2007288539 cites W2161862672 @default.
• W2007288539 cites W2166816901 @default.
• W2007288539 cites W2167631142 @default.
• W2007288539 cites W2170046777 @default.
• W2007288539 cites W2198261718 @default.
• W2007288539 cites W2249620842 @default.
• W2007288539 doi "https://doi.org/10.1016/j.fertnstert.2011.11.026" @default.
• W2007288539 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22192136" @default.
• W2007288539 hasPublicationYear "2012" @default.
• W2007288539 type Work @default.
• W2007288539 sameAs 2007288539 @default.
• W2007288539 citedByCount "30" @default.
• W2007288539 countsByYear W20072885392014 @default.
• W2007288539 countsByYear W20072885392015 @default.
• W2007288539 countsByYear W20072885392016 @default.
• W2007288539 countsByYear W20072885392017 @default.
• W2007288539 countsByYear W20072885392019 @default.
• W2007288539 countsByYear W20072885392020 @default.
• W2007288539 countsByYear W20072885392021 @default.
• W2007288539 countsByYear W20072885392022 @default.
• W2007288539 countsByYear W20072885392023 @default.
• W2007288539 crossrefType "journal-article" @default.
• W2007288539 hasAuthorship W2007288539A5065813469 @default.
• W2007288539 hasAuthorship W2007288539A5067531230 @default.
• W2007288539 hasBestOaLocation W20072885391 @default.
• W2007288539 hasConcept C126322002 @default.
• W2007288539 hasConcept C134018914 @default.
• W2007288539 hasConcept C2779134260 @default.
• W2007288539 hasConcept C511355011 @default.
• W2007288539 hasConcept C67636389 @default.
• W2007288539 hasConcept C71924100 @default.
• W2007288539 hasConceptScore W2007288539C126322002 @default.
• W2007288539 hasConceptScore W2007288539C134018914 @default.
• W2007288539 hasConceptScore W2007288539C2779134260 @default.
• W2007288539 hasConceptScore W2007288539C511355011 @default.
• W2007288539 hasConceptScore W2007288539C67636389 @default.
• W2007288539 hasConceptScore W2007288539C71924100 @default.
• W2007288539 hasIssue "1" @default.
• W2007288539 hasLocation W20072885391 @default.
• W2007288539 hasLocation W20072885392 @default.
• W2007288539 hasOpenAccess W2007288539 @default.
• W2007288539 hasPrimaryLocation W20072885391 @default.
• W2007288539 hasRelatedWork W1812775924 @default.
• W2007288539 hasRelatedWork W1963547220 @default.
• W2007288539 hasRelatedWork W1973602664 @default.
• W2007288539 hasRelatedWork W2017230043 @default.
• W2007288539 hasRelatedWork W2055618430 @default.
• W2007288539 hasRelatedWork W2430076739 @default.
• W2007288539 hasRelatedWork W2748952813 @default.
• W2007288539 hasRelatedWork W2898645499 @default.
• W2007288539 hasRelatedWork W4254531794 @default.
• W2007288539 hasRelatedWork W4297338646 @default.
• W2007288539 hasVolume "97" @default.
• W2007288539 isParatext "false" @default.
• W2007288539 isRetracted "false" @default.
• W2007288539 magId "2007288539" @default.
• W2007288539 workType "article" @default.