Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome

Kiddy, D.; Hamilton‐Fairley, Diana; Bush, Anne; Short, Frances; Anyaoku, V.; Reed, Michael J.; Franks, Stephen

doi:10.1111/j.1365-2265.1992.tb02909.x

Cited by 828 publications

(411 citation statements)

References 28 publications

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“…Evidence that the case-control association was far weaker when restricted to the leaner PCOS patients supports this interpretation. To the extent that adjustment for BMI diminishes the PCOS association, our data provide further evidence, complementing that from epidemiology and the effects of weight reduction on PCOS risk [4][5][6][7], that obesity and PCOS are causally related. Since the mechanism(s) by which FTO variants affect fat mass are not currently known, other possible causal relationships (such as a direct effect of FTO variants on the development of PCOS, independent of the effects on fat mass) cannot be excluded, although a distinct non-adiposity effect of FTO variants on PCOS susceptibility would seem unlikely.…”

Section: Discussionsupporting

confidence: 60%

“…Substantial evidence implicates obesity as an important factor in the aetiology of PCOS [4][5][6][7], though the mechanistic links between these conditions and how they interact with type 2 diabetes mellitus are poorly understood. Both obesity and PCOS are highly heritable [8][9][10], raising the possibility that a shared genetic predisposition contributes to their cooccurrence.…”

Section: Introductionmentioning

confidence: 99%

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Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

et al. 2008

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Aims/hypothesis Variants in the fat-mass and obesityassociated gene (FTO) influence susceptibility to type 2 diabetes via an effect on adiposity/obesity. Given the important role of obesity in the aetiology of both polycystic ovary syndrome (PCOS) and type 2 diabetes mellitus, our aim was to establish whether FTO variants are also implicated in PCOS susceptibility. MethodsWe performed a genetic association study of FTO variant rs9939609 using case-control analyses, conducted in 463 PCOS patients (geometric mean BMI 27.5 kg/m 2 ) and 1,336 female controls (geometric mean BMI 25.3 kg/ m 2 ) of UK British/Irish origin. We also sought evidence for associations between FTO variation and circulating testosterone levels in 324 UK PCOS patients and 1,000 women from the Northern Finland Birth Cohort of 1966. Outcome Diabetologia (2008) [adjusted]). This association was most evident in obese PCOS patients (PCOS patients below median BMI vs UK controls, p=0.11; above median BMI vs controls, p=2.9× 10 −4 ). No relationship between FTO genotype and androgen levels was seen. Conclusions/interpretation We provide the first evidence that variants that predispose to common obesity also result in altered susceptibility to PCOS, confirming the mechanistic link between these conditions. The predominant effect of FTO variants on PCOS susceptibility is probably mediated through adiposity.

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Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

et al. 2008

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“…An excess of body fat among women with PCOS accentuates insulin resistance and its associated clinical sequelae [18,19]. Since obesity exacerbates the signs and symptoms of insulin resistance, weight loss can improve ovarian function and the associated hormonal abnormalities [20,21]. Therefore, weight loss should be the first line treatment in obese women with anovulatory infertility associated with PCOS.…”

Section: Introductionmentioning

confidence: 99%

The effects of metformin or orlistat on obese women with polycystic ovary syndrome: a prospective randomized open-label study

Ghandi

Aflatoonian

Tabibnejad

et al. 2011

J Assist Reprod Genet

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Purpose Comparing the effects of metformin or orlistat on hormone, lipid profile and ovulation status in obese women with polycystic ovary syndrome. Methods A total of 80 women were prospectively recruited to receive either metformin (n=40) or orlistat (n=40). Weight, BMI, waist, serum LH, total serum testosterone and lipid profile were assessed at baseline and after 3 months. The subjects' ovulatory status was assessed after 3 months. Results There was no significant difference in ovulation between the two treatment groups (30% vs 15%). Treatment with either drug showed a significant decline in body weight, BMI (Body Mass Index), and waist circumference, but the degree of decline in both groups was the same. Patients who were treated with orlistat, showed a significant reduction in total testosterone and serum lipid. Women in metformin group showed a significant reduction in serum LH.Conclusions Both metformin and orlistat showed a similar effect on weight loss and ovulation rates.

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“…Calorie restriction (and lifestyle modification) in obese women with PCOS results in improvement in metabolic indices and in fertility with as little as a 5% reduction in body weight. [71][72][73][74][75] The increasing prevalence of overweight and obesity in children has given rise to numerous concerns about shortand longer-term effects. It is even more problematical for girls with a predisposition to PCOS.…”

Section: Introductionmentioning

confidence: 99%

Polycystic ovary syndrome in adolescents

2008

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Background: Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder in women and typically presents during adolescence. The clinical and biochemical presentation is heterogeneous, but elevated serum concentrations of androgens are the most consistent biochemical abnormality and may be considered to be the hallmark of the syndrome. Many women with PCOS also have insulin resistance and hyperinsulinaemia, which may contribute to the clinical and endocrine abnormalities. The aetiology of PCOS is not clear but studies in the Rhesus monkey suggest that exposure to excess androgen during intrauterine life results in many of the features of human PCOS, including ovarian dysfunction, abnormal LH secretion and insulin resistance. Objective: To review the studies from the literature, including those of the author, regarding aetiology, presentation and management of PCOS in adolescents. Results and conclusions: We have proposed that PCOS in adolescents arises as a result of a genetically determined disorder of ovarian function that results in hyper-secretion of androgens, possibly during fetal life and also during physiological activation of the hypothalamic-pituitary-ovarian in infancy and at the onset of puberty. There is plentiful evidence for a genetic basis for PCOS (it appears to be a complex endocrine disorder resulting from the effects of a several genes), but environmental factors, notably nutrition, influence the clinical and biochemical phenotype. Obesity unmasks or amplifies symptoms, endocrine and metabolic abnormalities. The increasing incidence of childhood obesity has resulted in an alarming Increase not only in distressing symptoms but also impaired glucose tolerance and even diabetes among adolescent girls with PCOS. The search for PCOS genes in this condition, that is not only heterogeneous but also presents only in women of reproductive age, is not straightforward and has produced few convincing candidates so far. In due course, however, identification of the major susceptibility loci is likely to provide key insight into the aetiology of the syndrome and improve diagnosis and management.

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Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome

Cited by 828 publications

References 28 publications

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

The effects of metformin or orlistat on obese women with polycystic ovary syndrome: a prospective randomized open-label study

Polycystic ovary syndrome in adolescents

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