Corrigendum to “Adipose tissue, metabolic syndrome and polycystic ovary syndrome: from pathophysiology to treatment” [Reprod. Biomed. Online 19 (2009) 552–563]

2012 ◽  
Vol 25 (3) ◽  
pp. 335
Author(s):  
Gabriella Garruti ◽  
Raffaella Depalo ◽  
Maria Grazia Vita ◽  
Filomenamila Lorusso ◽  
Federica Giampetruzzi ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.


2011 ◽  
Vol 165 (2) ◽  
pp. 283-292 ◽  
Author(s):  
Alessandra Gambineri ◽  
Federica Tomassoni ◽  
Alessandra Munarini ◽  
Roland H Stimson ◽  
Roberto Mioni ◽  
...  

ObjectiveRegeneration of cortisol by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) within liver and adipose tissue may be of pathophysiological importance in obesity and the metabolic syndrome. single nucleotide polymorphisms (SNPs) in HSD11B1, the gene encoding 11β-HSD1, have been associated with type 2 diabetes and hypertension in population-based cohort studies, and with hyperandrogenism in patients with the polycystic ovary syndrome (PCOS). However, the functional consequences of these SNPs for in vivo 11β-HSD1 expression and activity are unknown.MethodsWe explored associations of well-characterised hormonal and metabolic phenotypes with two common SNPs (rs846910 and rs12086634) in HSD11B1 in 600 women (300 with PCOS) and investigated 11β-HSD1 expression and activity in a nested study of 40 women from this cohort.ResultsHSD11B1 genotypes (as single SNPs and as the combination of the two minor allele SNPs) were not associated with PCOS. Women who were heterozygous for rs846910 A and homozygous for rs12086634 T (GA, TT genotype) had a higher risk of metabolic syndrome, regardless of the diagnosis of PCOS (odds ratio in the whole cohort=2.77 (95% confidence interval (CI) 1.16–6.67), P=0.023). In the nested cohort, women with the GA, TT genotype had higher HSD11B1 mRNA levels in adipose tissue, and higher rates of appearance of cortisol and d3-cortisol (16.1±0.7 nmol/min versus 12.1±1.1, P=0.044) during 9,11,12,12-2H4-cortisol (d4-cortisol) steady-state infusion.ConclusionsWe conclude that, in a population of Southern European Caucasian women with and without PCOS, alleles of HSD11B1 containing the two SNPs rs846910 A and rs12086634 T confer increased 11β-HSD1 expression and activity, which associates with the metabolic syndrome.


2017 ◽  
Vol 296 (3) ◽  
pp. 405-419 ◽  
Author(s):  
Alessandro P. Delitala ◽  
Giampiero Capobianco ◽  
Giuseppe Delitala ◽  
Pier Luigi Cherchi ◽  
Salvatore Dessole

2009 ◽  
Vol 19 (4) ◽  
pp. 552-563 ◽  
Author(s):  
Gabriella Garruti ◽  
Raffaella Depalo ◽  
Maria Grazia Vita ◽  
Filomenamila Lorusso ◽  
Federica Giampetruzzi ◽  
...  

2013 ◽  
Author(s):  
Antic Ivana Bozic ◽  
Jelica Bjekic-Macut ◽  
Dimitrios Panidis ◽  
Danijela Vojnovic Milutinovic ◽  
Biljana Kastratovic ◽  
...  

2014 ◽  
Author(s):  
Ivana Bozic Antic ◽  
Djuro Macut ◽  
Jelica Bjekic-Macut ◽  
Danijela Vojnovic Milutinovic ◽  
Milan Petakov ◽  
...  

Author(s):  
Soulmaz Shorakae ◽  
Eveline Jona ◽  
Courten Barbora de ◽  
Gavin Lambert ◽  
Elisabeth Lambert ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2494
Author(s):  
Małgorzata Kałużna ◽  
Magdalena Czlapka-Matyasik ◽  
Aleksandra Bykowska-Derda ◽  
Jerzy Moczko ◽  
Marek Ruchala ◽  
...  

Visceral adipose tissue (VAT) accumulation, is a part of a polycystic ovary syndrome (PCOS) phenotype. Dual-energy x-ray absorptiometry (DXA) provides a gold standard measurement of VAT. This study aimed to compare ten different indirect methods of VAT estimation in PCOS women. The study included 154 PCOS and 68 age- and BMI-matched control women. Subjects were divided into age groups: 18–30 y.o. and 30–40 y.o. Analysis included: body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), waist/height 0.5 (WHT.5R), visceral adipose index (VAI), lipid accumulation product (LAP), and fat mass index (FMI). VAT accumulation, android-to-gynoid ratio (A/G), and total body fat (TBF) was measured by DXA. ROC analysis revealed that WHtR, WHT.5R, WC, BMI, and LAP demonstrated the highest predictive value in identifying VAT in the PCOS group. Lower cut-off values of BMI (23.43 kg/m2) and WHtR (0.45) were determined in the younger PCOS group and higher thresholds of WHtR (0.52) in the older PCOS group than commonly used. Measuring either: WHtR, WHT.5R, WC, BMI, or LAP, could help identify a subgroup of PCOS patients at high cardiometabolic risk. The current observations reinforce the importance of using special cut-offs to identify VAT, dependent on age and PCOS presence.


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