66 research outputs found
Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan
Polycystic ovary syndrome (PCOS) is of clinical and public health importance as it is very common, affecting up to one in five women of reproductive age. It has significant and diverse clinical implications including reproductive (infertility, hyperandrogenism, hirsutism), metabolic (insulin resistance, impaired glucose tolerance, type 2 diabetes mellitus, adverse cardiovascular risk profiles) and psychological features (increased anxiety, depression and worsened quality of life). Polycystic ovary syndrome is a heterogeneous condition and, as such, clinical and research agendas are broad and involve many disciplines. The phenotype varies widely depending on life stage, genotype, ethnicity and environmental factors including lifestyle and bodyweight. Importantly, PCOS has unique interactions with the ever increasing obesity prevalence worldwide as obesity-induced insulin resistance significantly exacerbates all the features of PCOS. Furthermore, it has clinical implications across the lifespan and is relevant to related family members with an increased risk for metabolic conditions reported in first-degree relatives. Therapy should focus on both the short and long-term reproductive, metabolic and psychological features. Given the aetiological role of insulin resistance and the impact of obesity on both hyperinsulinaemia and hyperandrogenism, multidisciplinary lifestyle improvement aimed at normalising insulin resistance, improving androgen status and aiding weight management is recognised as a crucial initial treatment strategy. Modest weight loss of 5% to 10% of initial body weight has been demonstrated to improve many of the features of PCOS. Management should focus on support, education, addressing psychological factors and strongly emphasising healthy lifestyle with targeted medical therapy as required. Monitoring and management of long-term metabolic complications is also an important part of routine clinical care. Comprehensive evidence-based guidelines are needed to aid early diagnosis, appropriate investigation, regular screening and treatment of this common condition. Whilst reproductive features of PCOS are well recognised and are covered here, this review focuses primarily on the less appreciated cardiometabolic and psychological features of PCOS
Altered D-Chiro-inositol urinary clearance in women with polycystic ovary syndrome
OBJECTIVE - Evidence suggests that some actions of insulin are effected
by inositolphosphoglycan (IPG) mediators. We hypothesize that a
deficiency in D-chiro-inositol (DCI) and/or a DCI-containing IPG
(DCI-IPG) may contribute to insulin resistance in humans.
RESEARCH DESIGN AND METHODS - To assess this possibility in polycystic
ovary syndrome (PCOS), we determined insulin sensitivity (Si by
frequently sampled intravenous glucose tolerance test), plasma and
urinary DCI and myo-inositol (MYO) levels (by gas chromatography/mass
spectrometry), and the release of insulin and DCI-IPG during the oral
glucose tolerance test (area under the curve [AUC]) in 23 women with
PCOS and 26 normal women.
RESULTS - Women with PCOS were heavier than control subjects (P = 0.002
for BMI), but also had decreased S-1 (P < 0.001) and increased
AUC(insulin) (P < 0.001) compared with normal women, even when corrected
for BMI. The urinary clearance of DCI.(uCl(DCl)) was increased almost
sixfold in PCOS compared with normal women (P = 0.001), but not MYO
clearance (P = 0.10) uCl(DCI), correlated inversely with S-1 when all
women were analyzed together (n = 49, r = 0.50, P < 0.001) and was one
of the three best independent parameters predicting S-1. Finally, the
ratio of AUC(DCl-IPG) to AUC(insulin) was decreased threefold in women
with PCOS (P < 0.001).
CONCLUSIONS - uCl(DCI) is inversely correlated with insulin sensitivity
in women and is a strong independent predictor of insulin resistance in
multivariate models. PCOS, which is characterized by insulin resistance,
is associated with a selective increase in uCl(DCI) and impaired DCI-IPG
release in response to insulin. These findings are consistent with a
defect in tissue availability or utilization of DCI in PCOS that may
contribute to the insulin resistance of the syndrome
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