2021
DOI: 10.1016/j.mce.2020.111042
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Polycystic ovary syndrome (PCOS) affects over 10% of women. Insulin resistance, elevated free fatty acids (FFAs) and increased adiposity are key factors contributing to metabolic dysfunction in PCOS. We hypothesised that aberrant adipogenesis during adolescence, and downstream metabolic perturbations, contributes to the metabolic phenotype of adult PCOS. We used prenatally androgenized (PA) sheep as a clinically realistic model of PCOS. During adolescence, but not during fetal or early life of PA sheep, adipog… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

1
11
0

Year Published

2021
2021
2022
2022

Publication Types

Select...
6
1

Relationship

2
5

Authors

Journals

citations
Cited by 13 publications
(12 citation statements)
references
References 75 publications
(66 reference statements)
1
11
0
Order By: Relevance
“…A sequelae to such exposure is adipose tissue dysfunction in adulthood, which is implicated in the pathophysiology of PCOS. It was recently demonstrated, in a prenatally androgenized sheep model of PCOS, that adipogenesis is impaired in subcutaneous tissues during adolescence only to undergo compensatory hypertrophy during adulthood, paralleled with an overexpression of various inflammatory mediators in concert with dyslipidemia indicators of visceral fat accumulation [106]. Finally, thrombophilia and recurrent pregnancy loss are more extreme features of PCOS prevalent across different ethnic populations and highly correlated with genetic variants in specific folate cycle enzymes (Figure 3), plasma concentrations of tHcy, testosterone and measures of insulin resistance and obesity [107][108][109][110].…”
Section: Prenatal Metabolism and Stressmentioning
confidence: 99%
“…A sequelae to such exposure is adipose tissue dysfunction in adulthood, which is implicated in the pathophysiology of PCOS. It was recently demonstrated, in a prenatally androgenized sheep model of PCOS, that adipogenesis is impaired in subcutaneous tissues during adolescence only to undergo compensatory hypertrophy during adulthood, paralleled with an overexpression of various inflammatory mediators in concert with dyslipidemia indicators of visceral fat accumulation [106]. Finally, thrombophilia and recurrent pregnancy loss are more extreme features of PCOS prevalent across different ethnic populations and highly correlated with genetic variants in specific folate cycle enzymes (Figure 3), plasma concentrations of tHcy, testosterone and measures of insulin resistance and obesity [107][108][109][110].…”
Section: Prenatal Metabolism and Stressmentioning
confidence: 99%
“…Other factors may also contribute towards the establishment of insulin resistance in women with PCOS. These include increased levels of plasma testosterone (both in adulthood and prenatally, with evidence of the latter from an ovine model of PCOS 34 ) and enhanced sensitivity of the androgen receptor (determined by the androgen receptor CAG repeat number) 35 . Furthermore, suppressed levels of serum adiponectin in women with PCOS compared with BMI‐matched control women (demonstrated in a large meta‐analysis on >3400 subjects) may further contribute towards the establishment of insulin resistance in PCOS 36 .…”
Section: Introductionmentioning
confidence: 99%
“…Early hyperandrogenism during fetal life in animal models has been related to PCOS, influencing balance between prenatal adipogenesis and lipogenesis [49]; it could induce a mismatch between subcutaneous and visceral adipose tissue. As underpinning mechanisms, low levels of adiponectin, and increased fatty acid levels, magnified by both genetic and epigenetic factors, lead to decreased storage capacity and ectopic fat deposition (liver, visceral adipose tissue).…”
Section: Mechanism Of Oxidative Stress In Pcosmentioning
confidence: 99%
“…As underpinning mechanisms, low levels of adiponectin, and increased fatty acid levels, magnified by both genetic and epigenetic factors, lead to decreased storage capacity and ectopic fat deposition (liver, visceral adipose tissue). Adiponectin decrease, due to the key anti-inflammatory and insulin-sensitizing effect of the hormone, contributes to IR starting from childhood [49][50][51]; furthermore, during adulthood, upregulation of fat promoting genes in visceral adipose tissue could ensue. Recently animal models as a tool for understanding physiopathology of PCOS confirmed such view [52].…”
Section: Mechanism Of Oxidative Stress In Pcosmentioning
confidence: 99%