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Background Polycystic ovary syndrome (PCOS) is a common endocrine condition in women associated with obesity, reproductive and metabolic abnormalities. It improves with weight loss, however currently no specific dietary recommendations exist and there may be abnormalities in appetite regulation in PCOS that contribute to difficulty in weight management. Aims To assess the effect of 1) short and long-term weight loss and weight maintenance strategies on weight loss, reproductive and metabolic parameters in overweight women with PCOS and to 2) assess the relative effect of weight loss on cardiovascular risk factors and 3) postprandial appetite, appetite hormones (ghrelin, CCK, PYY) and food intake in overweight women with and without PCOS. Results Overweight women with PCOS followed an 8-week weight loss (2 meal replacements/day, 4904.4±127 kJ, n=32) followed by a 6 month carbohydrate (<120 g/day) or fat restricted (<50 g/day) weight maintenance regime (n=23). Reductions in weight (5.6±2.4 kg) and improvements in body composition, insulin, reproductive hormones and menstrual cyclicity occurred and were sustained equivalently for both diet groups. We then assessed the effect of weight loss (4.2±0.7 kg over 8 weeks as described above) in overweight women with (n=15) and without (n=17) PCOS on cardiovascular risk factors. All subjects had similar improvements in body composition, triglycerides, reproductive hormones and fasting and post-prandial insulin. C-reactive protein decreased with weight loss for non-PCOS women (-1.2±0.5 mg/L, P=0.025) but not for PCOS women. We finally assessed appetite regulation in PCOS. Women with (n=20) and without (n=12) PCOS followed a standard protein (55% carbohydrate, 15% protein) or high protein diet (40% carbohydrate, 30% protein) for 16 weeks (~6000 kJ/day). Non-PCOS subjects were more satiated (P=0.001) and less hungry (P=0.007) after the test meals and had a 70% higher fasting baseline ghrelin (P=0.011), a greater increase in fasting ghrelin (57.5 versus 34.0%, P=0.033), a greater post-prandial ghrelin decrease at week 16 (113.5±46.3 versus 49.3±12.2 pg/mL, P=0.05) and a greater maximal decrease in post-prandial ghrelin (-144.1±58.4 versus -28.9±14.2 pg/mL, P=0.02) following weight loss than subjects with PCOS. Lastly, women with (n=14) and without (n=14) PCOS undertook an 8-week weight loss regime (4.2±0.7 kg as described above). At week 0 and 8, women with PCOS again displayed lower ghrelin levels (P=0.01 and P=0.097 respectively) and a lesser post-prandial ghrelin decrease (P=0.048 and P=0.069 respectively) but similar post-prandial appetite, buffet consumption and fasting or post-prandial peptide YY and cholecystokinin compared to women without PCOS. Conclusion Meal replacements and moderate macronutrient restriction are effective strategies for the dietary management of PCOS. Equivalent weight losses improved cardiovascular risk factors similarly for overweight women with and without PCOS with the exception of CRP which did not decrease with weight loss for overweight women with PCOS. PCOS status is associated with altered fasting and post-prandial ghrelin levels but is not consistently associated with other impairments in post-prandial gut peptides or food intake. Further investigation is required to assess if appetite regulation is impaired in PCOS and the optimal strategies and amount of weight loss for improvement of reproductive and metabolic parameters in PCOS. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1282329 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2007

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Paper III reprinted with kind permission of Elsevier, sciencedirect.com

Paper III reprinted with kind permission of Elsevier, sciencedirect.com

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Polycystic ovary syndrome (PCOS) is a common and complex endocrine condition with reproductive and metabolic complications, affecting up to 10% of reproductive-age women. Hyperandrogenemia, ovulatory dysfunction, and luteinising hormone hypersecretion are characteristic traits of PCOS however, it seems that the most concerning long-term key issues are metabolic problems associated with the syndrome, such as hyperinsulinemia, insulin resistance, obesity, dyslipidaemia and non-alcoholic liver disease. Despite the numerous studies on PCOS, its origin and pathophysiology are still not fully understood. However, there is increasing evidence that the adult PCOS phenotype is programmed in fetal life by androgen excess. Exposure to increased levels of testosterone in utero in rodents, sheep and monkeys result in adult reproductive and metabolic pathologies that parallel those seen in PCOS women. Since hyperandrogenemia is a hallmark of PCOS and daughters of PCOS mothers have elevated levels of androgens at birth, it is likely that prenatal androgenisation during early life predispose to the future development of PCOS. Animal models of PCOS provide an opportunity to examine the developmental aetiology and molecular mechanisms underlying the pathogenesis of this condition. Over last 10 years our lab has successfully utilised a well-established ovine model of PCOS, where pregnant ewes were treated with testosterone propionate (TP) through mid-gestation. From this model, we had a large sample bank of fixed and frozen tissues from the fetal, lamb and adolescent prenatally androgenised animals that allowed to carry a broad range of experiments. In addition, a new cohort of prenatally androgenised adult sheep enabled additional in vivo analysis. Past research documented that prenatal androgenisation result in hyperinsulinemia with altered pancreas structure and function, and early fatty liver without difference in body weight in adolescent sheep. This thesis examines the effects and consequences of increased in utero androgen exposure on metabolic dysregulation in adolescent and adult female sheep. During puberty, but not fetal or early life, there was decreased adipogenesis in subcutaneous adipose tissue (SAT), but not visceral adipose tissue (VAT), accompanied by decreased circulating concentrations of fibroblast growth factor 21 (FGF21), leptin and adiponectin, and increased concentrations of fasting free fatty acids (FFA) in prenatally androgenised sheep. This was countered by upregulated expression of FFA transporters in liver. As adults, TP-exposed animals had increased body weight, elevated fasting insulin and FFA concentrations but normal FGF21, leptin and adiponectin levels. Histological analysis revealed that adult TP-exposed animals had SAT hypertrophy, which was associated with increased expression of inflammatory markers and correlated with increased fasting FFA. Therefore, it is likely that impaired preadipocyte differentiation in SAT during adolescence resulted in hypertrophy and inflammation of adult SAT. This consequently lowered capacity of SAT to safely store fat and potentially explains metabolic perturbations observed in PCOS-like female sheep. To further investigate potential causes of obesity in adult PCOS-like sheep postprandial thermogenesis (PPT), an important constituent of energy expenditure, was measured through implantation of datalogger thermometers into interscapular adipose tissue. Adult prenatally androgenised sheep had decreased amplitude of PPT, without difference in basal body temperature, despite receiving the same caloric intake, and independent of obesity. These findings indicate that adult PCOS-like sheep have reduced capacity for energy expenditure, which is mirrored in women with PCOS. This reduced capacity for postprandial thermogenesis was correlated with hyperinsulinemia decreased noradrenaline levels and reduced thermogenic potential of brown and/or beige adipose tissue. This suggests that women with PCOS might be prenatally programmed to become obese. In summary, findings documented in this thesis provide better understanding into the pathophysiology of PCOS from puberty to adulthood and give opportunities for early clinical intervention to ameliorate the metabolic phenotype of PCOS.

【目的】从整体上把握多囊卵巢综合征的发生、发展及其规律, 为临床进一步诊断治疗提供整体思路和文献学基础。【方法】收集整理近10 年与多囊卵巢综合征研究相关的中、英文献，归纳和总结该病的病因病机、诊断、治疗，找出存在问题，提出发展方向。【结果】①多囊卵巢综合征主要病因为：肾虚、脾虚、肝郁、痰湿、痕血，并与饮食、环境、精神、遗传具有相尖性；②多囊卵巢综合征基本病机：本虚标实，肾虚、脾虚为本’肝郁、气滞、血痕、痰浊、痰湿为标；③PCOS 的分型大致有：肾虚血脐型、肾虚血痕痰浊型；脾肾阳虚型；痕血内阻型；肝气郁结型；脾肾阳虚型；痰湿阻滞型；④PCOS 的治疗以辨证分型论治为主，参考名老中医经验、专方专药、针灸、周期疗法、辨体质进行诊治，重视中西医结合在治疗中的应用。⑤PCOS 仍存在病因、病机认识不一，诊断存在争议’辨证分型众说纷纭等问题。⑥PCOS 发展方向：找出与PCOS 相尖性最强的病因，明确中西医发病机制，规范PCOS 诊断’研发有效药物，加强临床及实验研究，注重基础治疗和健康宣敦。【结论】多囊卵巢综合征的病因、病机、诊断及治疗研究已取得可喜的成绩，形成了完整的体系。但仍存在具体病因不明’发病机制不清，缺乏有效治疗方法等问题。今后应加强高级别基础和临床研究’尽快明确病因病机’找出有效治疗方案。关键词：多囊卵巢综合征；中医；病因病机；证治规律；药物

目的： PCOS 是女性最常见的内分泌疾病, 其症状与并发症严重危害了女性的身心健康。本研究通过收集整体近10 年关于PCOS 的中医临床研究类文献，对本病的证型、治法，尤其是用药处方进行统计、归纳、分析’从而总结出该病的病因病机分布及治疗规律，为PCOS 下一步的临床治疗及用药提供思路和依据。方法：以“多囊卵巢综合征”、“PCOS”、“多囊卵巢”、“不孕症”、“闭经”“中医” 、“中医治疗”、“中医药”等为关键词’搜索2006 年1 月至2016 年12 月刊登在中文学术期刊上有关多囊卵巢综合征中医临床研究类文献，通过建立数据库，对其中医证型及使用方药进行统计分析’归纳总结出多囊卵巢综合征的主要病因病机及治疗用药规律。结果：经过筛选最终得到120 篇文献，共记录病例5670 例，明确治法4616 例，明确证型3778 例。肾虚证型2598 例（ 68. 8% ）；痰湿阻滞型613 例(16. 2%)占84.8% 侨肾3172 例（ 68. 7% ）补肾法中辅以活血化痰之法者也497 例（ 78. 7% ）。药物使用频共中’补虚药（ 43. 7% ）、活血化痕药（ 16.1% ），占59.8% 。归纳的两种疗效评判标准中，总有效率分别为87.9% 、88.9% 。结论： 1. 肾、肝、脾功能失调为PCOS 的发病之源。2. 肾虚、痰湿、血痕是PCOS 的基本病机。3. 补肾健脾，活血化痰是治疗PCOS 的根本大法。4. 补虚药、活血化寐药为治疗PCOS 的主导药物类别。5 中医药治疗PCOS 有副作用小基本黛痛苦璧幢调筒H p O 轴的功能。6. 不同年龄段治疗目的不同导致疗效评判标准尚不统一。关键词：多囊卵巢综合征，中医，用药规律，文献研究