Comparison of MRI-assessed body fat content between lean women with polycystic ovary syndrome (PCOS) and matched controls: less visceral fat with PCOS

Dolfing, Jacoba G.; Stassen, C. M.; Haard, P.M.M. van; Wolffenbuttel, Bruce H. R.; Schweitzer, Dave H.

doi:10.1093/humrep/der070

Cited by 53 publications

(36 citation statements)

References 24 publications

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“…Considering that the prenatal T-treated female sheep mimic the phenotype of women with PCOS at the reproductive and metabolic level (12) and that these females are kept on a maintenance diet and not allowed to become obese (69), the metabolic phenotype of prenatal T-treated sheep described in this study, namely reduced fat mass lack of insulin resistance, is similar to those reported for the lean-PCOS phenotype (10). Because lean PCOS women are not insulin resistant (42,43), insulin resistance in PCOS women (44 -46) appears to be a trait strongly influenced by obesity (6,65).…”

Section: Translational Relevancesupporting

confidence: 57%

“…Prenatal T treatment was from day 30 to day 90 gestation for all time points except the 22-month time point, which involved T treatment from day 60 to day 90 of gestation. B, Comparison of directionality of changes in insulin homeostasis (gray boxes) and visceral adiposity (open boxes) after prenatal exposure to T in sheep (our studies) with outcomes from perinatal T/DHT exposure in other species pre-or perinatal T/DHT-treated mice (36), rats (20,(37)(38)(39), cows (40), rhesus monkeys (18,19,41), and women with PCOS (10,(42)(43)(44)(45)(46). Note the differences in age and reproductive status of animals undergoing the tests.…”

Section: Effects Of Prenatal T On Free Fatty Acid Metabolismmentioning

confidence: 99%

“…Because most studies in PCOS include overweight and obese subjects, the actual impact of PCOS on visceral adiposity is unclear. Interestingly, recent studies looking at visceral fat deposition have found either no difference between PCOS women and control subjects (9) or the lean PCOS women to have lower fat mass compared with controls (10).…”

mentioning

confidence: 98%

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Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

et al. 2013

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Prenatal T excess causes reproductive and metabolic disruptions including insulin resistance, attributes of women with polycystic ovary syndrome. This study tested whether increases in visceral adiposity, adipocyte size, and total free fatty acids underlie the insulin resistance seen in prenatal T-treated female sheep. At approximately 16 months of age, insulin resistance and adipose tissue partitioning were determined via hyperinsulinemic euglycemic clamp and computed tomography, respectively, in control and prenatal T-treated females. Three months later, adipocyte size and free fatty acid composition were determined. Results revealed that at the postpubertal time points tested, insulin sensitivity was increased, visceral adiposity and adipocyte size in both the sc and the visceral compartments were reduced, and circulating palmitic acid was increased in prenatal T-treated females relative to controls. In parallel studies, 20-month-old prenatal T-treated females tended to have increased basal insulin to glucose ratio. Relative to earlier findings of reduced insulin sensitivity of prenatal T-treated females during early life and adulthood, these findings of increased insulin sensitivity and reduced adiposity postpubertally are suggestive of a period of developmental adaptation. The disruption observed in free fatty acid metabolism a few months later correspond to a time point when the insulin sensitivity indices of prenatal T-treated animals appear to shift toward insulin resistance. In summary, current findings of improved insulin sensitivity and reduced visceral adiposity in postpubertal prenatal T-treated sheep relative to our earlier findings of reduced insulin sensitivity during early postnatal life and adulthood are indicative of a period of developmental adaptation.

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Section: Translational Relevancesupporting

confidence: 57%

Section: Effects Of Prenatal T On Free Fatty Acid Metabolismmentioning

confidence: 99%

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Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

et al. 2013

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“…Two MRI studies demonstrated that although increased waist: hip ratio measurements indicated abdominal/visceral fat accumulation, MRI did not show this accumulation (104, 105). Subsequently, one study demonstrated lower visceral fat among lean women with PCOS (353), and another found larger accumulations of visceral fat among both normal-weight and overweight women with PCOS (354). However, these studies used different imaging protocols (ie, single slice vs multislice) and differing PCOS inclusion criteria, which may explain the conflicting results.…”

Section: F Obesity Fat Distribution and Adipose Tissue Function Anmentioning

confidence: 99%

Scientific Statement on the Diagnostic Criteria, Epidemiology, Pathophysiology, and Molecular Genetics of Polycystic Ovary Syndrome

et al. 2015

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Polycystic ovary syndrome (PCOS) is a heterogeneous and complex disorder that has both adverse reproductive and metabolic implications for affected women. However, there is generally poor understanding of its etiology. Varying expert-based diagnostic criteria utilize some combination of oligo-ovulation, hyperandrogenism, and the presence of polycystic ovaries. Criteria that require hyperandrogenism tend to identify a more severe reproductive and metabolic phenotype. The phenotype can vary by race and ethnicity, is difficult to define in the perimenarchal and perimenopausal period, and is exacerbated by obesity. The pathophysiology involves abnormal gonadotropin secretion from a reduced hypothalamic feedback response to circulating sex steroids, altered ovarian morphology and functional changes, and disordered insulin action in a variety of target tissues. PCOS clusters in families and both female and male relatives can show stigmata of the syndrome, including metabolic abnormalities. Genome-wide association studies have identified a number of candidate regions, although their role in contributing to PCOS is still largely unknown.

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“…In a further study by Huang et al [54] on mainly nonobese women with PCOS vs. control women, MRI did show a significant increase in central (including visceral) fat depots in the PCOS group independent of BMI. In a further study using MRI in a comparison of lean women with PCOS and matched control women, Dolfing et al [55] demonstrated that the PCOS group had less visceral fat than the controls. It is possible that some of the controversy in the current literature regarding BFD in PCOS is related to differences in BMI of the subjects between studies [54].…”

Section: Effects Of Female Obesity On Androgen Levelsmentioning

confidence: 99%

The impact of hyperandrogenism in female obesity and cardiometabolic diseases associated with polycystic ovary syndrome

Barber

Vojtechova

2013

Hormone Molecular Biology and Clinical Investigation

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Polycystic ovary syndrome (PCOS) is a common condition characterized by reproductive and hyperandrogenic features and is often associated with obesity and metabolic dysfunction. Overall, women with PCOS have a substantially greater prevalence of metabolic syndrome than women from the general population. Furthermore, PCOS per se (independent of its frequent association with obesity) often confers cardiometabolic risk (including insulin resistance), and its concurrence with obesity often represents a metabolic "double-whammy" from the adverse effects of PCOS and obesity. The introduction of the Rotterdam diagnostic criteria for PCOS in 2003 has broadened the scope of this condition. The Rotterdam diagnostic criteria have also introduced two new phenotypic subgroups (including normoandrogenemic women with PCOS) that have provided novel insights into a potential role for hyperandrogenism in the development of adverse cardiometabolic risk in women with PCOS. Based on evidence from cross-sectional and interventional studies, hyperandrogenism, obesity, and cardiometabolic risk in women appear to be linked through complex and multidirectional pathways. Furthermore, data from obese women without a formal diagnosis of PCOS also suggest that these interrelationships often exist in female obesity per se (in milder forms than occurs in PCOS). Data from female-to-male transsexuals are particularly informative because these show direct effects of hyperandrogenism (induced through exogenous use of androgenic therapies) on fat distribution and cardiometabolic risk in women. A challenge for the future will be to disentangle and improve our understanding of this complex pathogenic web, thereby facilitating novel and targeted therapies for the hyperandrogenic and adverse cardiometabolic manifestations of PCOS.

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Comparison of MRI-assessed body fat content between lean women with polycystic ovary syndrome (PCOS) and matched controls: less visceral fat with PCOS

Cited by 53 publications

References 24 publications

Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

Scientific Statement on the Diagnostic Criteria, Epidemiology, Pathophysiology, and Molecular Genetics of Polycystic Ovary Syndrome

The impact of hyperandrogenism in female obesity and cardiometabolic diseases associated with polycystic ovary syndrome

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