Publications
355 results found
Lajunen TK, Purhonen A-K, Haapea M, et al., 2012, Full-length visfatin levels are associated with inflammation in women with polycystic ovary syndrome, EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Vol: 42, Pages: 321-328, ISSN: 0014-2972
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- Citations: 25
Barber TM, Franks S, 2012, The link between polycystic ovary syndrome and both Type 1 and Type 2 diabetes mellitus: what do we know today?, Womens Health (Lond), Vol: 8, Pages: 147-154
Polycystic ovary syndrome (PCOS) and Type 2 diabetes mellitus (T2D) are both obesity-related conditions that share epidemiological and pathophysiological factors. Insulin resistance is a key factor whereby obesity influences the expression of each condition. However, the mechanisms by which insulin resistance contributes towards the manifestation of PCOS and T2D differ in important ways: in PCOS, compensatory hyperinsulinemia results in pleiotropic effects including co-gonadotrophic stimulation of ovarian and adrenal steroidogenesis; in T2D, insulin resistance contributes towards β-cell exhaustion and ultimately to hyposecretion of insulin with resultant dysglycemia. The link between PCOS and Type 1 diabetes mellitus is believed to implicate supraphysiological concentrations of insulin within the systemic circulation. Further progression of the obesity epidemic will ensure even greater prominence of important obesity-related conditions such as PCOS and T2D. Research to gain a clearer understanding of the mechanisms linking each condition should be a priority.
Fauser BCJM, Tarlatzis BC, Rebar RW, et al., 2012, Consensus on women's health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group, FERTILITY AND STERILITY, Vol: 97, Pages: 28-U84, ISSN: 0015-0282
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- Citations: 974
Franks S, Berga SL, 2012, Does PCOS have developmental origins?, FERTILITY AND STERILITY, Vol: 97, Pages: 2-6, ISSN: 0015-0282
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- Citations: 40
Fauser BCJM, Tarlatzis BC, Rebar RW, et al., 2012, Consensus on women's health aspects of polycystic ovary syndrome (PCOS), HUMAN REPRODUCTION, Vol: 27, Pages: 14-24, ISSN: 0268-1161
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- Citations: 231
Fenwick MA, Mansour YT, Franks S, et al., 2011, Identification and Regulation of Bone Morphogenetic Protein Antagonists Associated with Preantral Follicle Development in the Ovary, ENDOCRINOLOGY, Vol: 152, Pages: 3515-3526, ISSN: 0013-7227
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- Citations: 30
Torvinen A, Koivunen R, Pouta A, et al., 2011, Metabolic and reproductive characteristics of first-degree relatives of women with self-reported oligo-amenorrhoea and hirsutism, GYNECOLOGICAL ENDOCRINOLOGY, Vol: 27, Pages: 630-635, ISSN: 0951-3590
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- Citations: 5
Fowler PA, Anderson RA, Saunders PT, et al., 2011, Development of Steroid Signaling Pathways during Primordial Follicle Formation in the Human Fetal Ovary, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 96, Pages: 1754-1762, ISSN: 0021-972X
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- Citations: 76
Joharatnam J, Barber TM, Webber L, et al., 2011, Determinants of dyslipidaemia in probands with polycystic ovary syndrome and their sisters, CLINICAL ENDOCRINOLOGY, Vol: 74, Pages: 714-719, ISSN: 0300-0664
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- Citations: 15
Hickey M, Doherty DA, Atkinson H, et al., 2011, Clinical, ultrasound and biochemical features of polycystic ovary syndrome in adolescents: implications for diagnosis, HUMAN REPRODUCTION, Vol: 26, Pages: 1469-1477, ISSN: 0268-1161
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- Citations: 107
Hart R, Doherty DA, Mori T, et al., 2011, Extent of metabolic risk in adolescent girls with features of polycystic ovary syndrome, FERTILITY AND STERILITY, Vol: 95, Pages: 2347-U268, ISSN: 0015-0282
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- Citations: 54
Pasquali R, Stener-Victorin E, Yildiz BO, et al., 2011, PCOS Forum: research in polycystic ovary syndrome today and tomorrow, CLINICAL ENDOCRINOLOGY, Vol: 74, Pages: 424-433, ISSN: 0300-0664
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- Citations: 110
Franks S, 2011, When should an insulin sensitizing agent be used in the treatment of polycystic ovary syndrome?, CLINICAL ENDOCRINOLOGY, Vol: 74, Pages: 148-151, ISSN: 0300-0664
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- Citations: 25
Hart R, Doherty DA, Norman RJ, et al., 2010, Serum antimullerian hormone (AMH) levels are elevated in adolescent girls with polycystic ovaries and the polycystic ovarian syndrome (PCOS), FERTILITY AND STERILITY, Vol: 94, Pages: 1118-1121, ISSN: 0015-0282
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- Citations: 89
Barber TM, Franks S, 2010, Genetic basis of polycystic ovary syndrome., Expert Rev Endocrinol Metab, Vol: 5, Pages: 549-561
Polycystic ovary syndrome (PCOS) is associated with obesity and manifests with reproductive, hyperandrogenic and metabolic features. Although the etiology of PCOS is complex and incompletely understood, genetics plays an important role (heritability: ∼70%). Potential problems with studying the genetics of PCOS include the heterogeneity of the condition and associated sub-fertility. A candidate gene approach has been used in over 70 published studies on PCOS, most of which have been inadequately powered to detect a statistically meaningful association. Furthermore, these studies often fail to replicate prior published studies on the same candidate gene in different populations. The first genome-sequence variant (identified from a genome-wide association study in subjects with Type 2 diabetes mellitus) to be studied in PCOS (FTO gene) has been shown by our group to associate with susceptibility for the development of PCOS. This is the first genetic corroboration of a link between PCOS and obesity. Future directions include a genome-wide association study in PCOS.
Franks S, Hardy K, 2010, Aberrant follicle development and anovulation in polycystic ovary syndrome, ANNALES D ENDOCRINOLOGIE, Vol: 71, Pages: 228-230, ISSN: 0003-4266
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- Citations: 22
Franks S, Joharatnam J, 2010, Pathogenesis and Management of Adiposity and Insulin Resistance in PCOS: Prevention and Treatment of the Metabolic Disease Components, PEDIATRIC OBESITY: ETIOLOGY, PATHOGENESIS, AND TREATMENT, Editors: Freemark, Publisher: HUMANA PRESS INC, Pages: 357-367, ISBN: 978-1-60327-873-7
Hickey M, Sloboda DM, Atkinson HC, et al., 2009, The relationship between maternal and umbilical cord androgen levels and polycystic ovary syndrome in adolescence: a prospective cohort study., Journal of Clincal Endocrinology and Metabolism, Vol: 94, Pages: 3714-3720
Franks S, 2009, Do Animal Models of Polycystic Ovary Syndrome Help to Understand Its Pathogenesis and Management? Yes, but Their Limitations Should be Recognized, ENDOCRINOLOGY, Vol: 150, Pages: 3983-3985, ISSN: 0013-7227
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- Citations: 28
Vassiliadi DA, Barber TM, Hughes BA, et al., 2009, Increased 5 alpha-reductase activity and adrenocortical drive in women with polycystic ovary syndrome., Journal of Clinical Endocrinology and Metabolism, Vol: 94, Pages: 3358-3366
Vassiliadi DA, Barber TM, Hughes BA, et al., 2009, Increased 5α-Reductase Activity and Adrenocortical Drive in Women with Polycystic Ovary Syndrome, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 94, Pages: 3558-3566, ISSN: 0021-972X
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- Citations: 68
Balen A, Homburg R, Franks S, 2009, Defining polycystic ovary syndrome, BMJ-BRITISH MEDICAL JOURNAL, Vol: 338, ISSN: 1756-1833
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- Citations: 28
Da Silva-Buttkus P, Marcelli G, Franks S, et al., 2009, Inferring biological mechanisms from spatial analysis: Prediction of a local inhibitor in the ovary, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 106, Pages: 456-461, ISSN: 0027-8424
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- Citations: 68
Da Silva-Buttkus P, Marcelli G, Franks S, et al., 2009, Inferring biological mechanisms from spatial analysis: prediction of a local inhibitor in the ovary, Proceedings of the National Academy of Sciences of USA, Vol: 106, Pages: 456-461
Da Silva-Buttkus P, Jayasooriya GS, Mora JM, et al., 2008, Effect of cell shape and packing density on granulosa cell proliferation and formation of multiple layers during early follicle development in the ovary, JOURNAL OF CELL SCIENCE, Vol: 121, Pages: 3890-3900, ISSN: 0021-9533
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- Citations: 85
Morin-Papunen L, Martikainen H, McCarthy MI, et al., 2008, Comparison of metabolic and inflammatory outcomes in women who used oral contraceptives and the levonorgestrel-releasing intrauterine device in a general population, American Journal of Obstetrics and Gynecology, Vol: 199, Pages: 529.e1-529.e10
Morin-Papunen L, Martikainen H, McCarthy MI, et al., 2008, Comparison of metabolic and inflammatory outcomes in women who used oral contraceptives and the levonorgestrel-releasing intrauterine device in a general population, 62nd Annual Meeting of the American-Society-for-Reproductive-Medicine, Publisher: MOSBY-ELSEVIER, ISSN: 0002-9378
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- Citations: 46
Morin-Papunen L, Martikainen H, McCarthy MI, et al., 2008, Comparison of metabolic and inflammatory outcomes in women who used oral contraceptives and the levonorgestrel-releasing intrauterine device in a general population., Am J Obstet Gynecol, Vol: 199, Pages: 529.e1-529.e10
OBJECTIVE: We compared the metabolic and cardiovascular parameters of a reference group of women with those of women who used 2 contraceptive regimes that are used worldwide: the levonorgestrel-releasing intrauterine device and oral contraceptives. STUDY DESIGN: We investigated a cohort of 2814 women at age 31 years from the general population-based Northern Finland Birth Cohort who were born in 1966. Women were classified as oral contraceptive users (n = 687 women), levonorgestrel-releasing intrauterine device users (n = 168 women), or no use of hormonal contraception (reference group; n = 1959 women). The analyses were adjusted for body mass index, current alcohol use, household income, and area of residence. RESULTS: Compared with the reference group, oral contraceptive users had higher systolic and diastolic blood pressure, raised levels of inflammatory indices (C-reactive protein), and impaired insulin sensitivity. Levonorgestrel-releasing intrauterine device users displayed a lower high-density lipoprotein and total cholesterol, but a similar cholesterol/ high-density lipoprotein ratio, and higher leukocyte count compared with the reference group. Oral contraception users were insulin-resistant compared with levonorgestrel-releasing intrauterine device users with higher blood pressure, raised lipid levels (such as total cholesterol and triglycerides) and insulin levels, and lower homeostasis model assessment and insulin sensitivity, despite smaller waist and lower waist-hip ratio. CONCLUSION: Oral contraception usage was associated with adverse findings in several metabolic, cardiovascular, and inflammatory parameters, which is consistent with an increased future risk of cardiovascular and metabolic disease. These findings should invite more criticism of recent trends that encourage the prescription of oral contraceptives for years during reproductive life and especially in premenopausal women. In contrast, levonorgestrel-releasing intrauterine device or proge
Franks S, Webber LJ, Goh M, et al., 2008, Ovarian morphology is a marker of heritable biochemical traits in sisters with polycystic ovaries, Journal of Clinical Endocrinology and Metabolism, Vol: 93, Pages: 3396-3402
Context: Polycystic ovary syndrome (PCOS) is a common endocrinopathy ofuncertain etiology but with strong evidence for a genetic contribution. Objective: Totest the hypothesis that the typical polycystic ovarian morphology is a marker ofinherited biochemical features in families of women with PCOS. Design: A study ofprobands with PCOS and their sisters. Patients: 125 probands and 214 sisters. Allprobands had PCOS, defined by symptoms of anovulation and/or hyperandrogenismwith polycystic ovaries on ultrasound. Affected sisters were defined by polycysticovaries, regardless of symptoms, and unaffected sisters defined by normal ovarianmorphology. Setting: Clinic-based study. Main outcome measures: Clinical,endocrine and metabolic features in the various groups were compared and estimatesof broad-sense heritability were obtained using the quantitative transmissiondisequilibrium test (QTDT). Results: Although affected sisters had fewer symptomsthan probands (30% had no symptoms of PCOS), serum testosterone,androstenedione, LH, fasting insulin and insulin sensitivity (HOMA-S) were similarin the two groups with polycystic ovaries but significantly different from those inunaffected sisters or controls. We observed moderate to high heritabilities for all traitsstudied in affected sister pairs whereas heritabilities calculated from discordantsiblings were substantially lower. Conclusions: These data provide further evidencefor a genetic basis of PCOS. The high heritability of biochemical features in probandsand affected sisters, despite wide variation in symptoms shows that not only are thesebiochemical traits strongly influenced by genetic factors but also, importantly, thatpolycystic ovarian morphology is an index of inherited traits in families with PCOS.
Koivunen R, Pouta A, Franks S, et al., 2008, Fecundability and spontaneous abortions in women with self-reported oligo-amenorrhea and/or hirsutism:: Northern Finland Birth Cohort 1966 Study, HUMAN REPRODUCTION, Vol: 23, Pages: 2134-2139, ISSN: 0268-1161
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- Citations: 55
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