Body size from birth to adulthood as a predictor of self-reported polycystic ovary syndrome symptoms

Laitinen, Jaana; Taponen, Saara; Martikainen, Hannu; Pouta, Anneli; Millwood, Iona Y.; Al, Hartikainen; Ruokonen, Aimo; Sovio, Ulla; McCarthy, Mark I.; Järvelin, Marjo‐Riitta

doi:10.1038/sj.ijo.0802301

Cited by 154 publications

(109 citation statements)

References 35 publications

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“…More recently, human studies (Jarvelin et al, 1997;Laitinen et al, 2003 and have demonstrated that body shape at birth, rather than weight Litten-Brown, Corson and Clarke per se, may be a better indicator of future health and development of the human infant. The modern domestic pig, rather than the ancient domestic pig or minipig, is an excellent model for developmental programming due to the 2-to 3-fold variation in BW among littermates, which provides a naturally occurring form of foetal growth restriction with less genetic variation than seen in man or other monotocous species (Bauer et al, 1998;Corson et al, 2008a).…”

Section: Litten-brown Corson and Clarkementioning

confidence: 99%

Porcine models for the metabolic syndrome, digestive and bone disorders: a general overview

Litten-Brown

Corson

Clarke

2010

Animal

147

136

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The aim of this review article is to provide an overview of the role of pigs as a biomedical model for humans. The usefulness and limitations of porcine models have been discussed in terms of metabolic, cardiovascular, digestive and bone diseases in humans. Domestic pigs and minipigs are the main categories of pigs used as biomedical models. One drawback of minipigs is that they are in short supply and expensive compared with domestic pigs, which in contrast cost more to house, feed and medicate. Different porcine breeds show different responses to the induction of specific diseases. For example, ossabaw minipigs provide a better model than Yucatan for the metabolic syndrome as they exhibit obesity, insulin resistance and hypertension, all of which are absent in the Yucatan. Similar metabolic/physiological differences exist between domestic breeds (e.g. Meishan v. Pietrain). The modern commercial (e.g. Large White) domestic pig has been the preferred model for developmental programming due to the 2-to 3-fold variation in body weight among littermates providing a natural form of foetal growth retardation not observed in ancient (e.g. Meishan) domestic breeds. Pigs have been increasingly used to study chronic ischaemia, therapeutic angiogenesis, hypertrophic cardiomyopathy and abdominal aortic aneurysm as their coronary anatomy and physiology are similar to humans. Type 1 and II diabetes can be induced in swine using dietary regimes and/or administration of streptozotocin. Pigs are a good and extensively used model for specific nutritional studies as their protein and lipid metabolism is comparable with humans, although pigs are not as sensitive to protein restriction as rodents. Neonatal and weanling pigs have been used to examine the pathophysiology and prevention/treatment of microbial-associated diseases and immune system disorders. A porcine model mimicking various degrees of prematurity in infants receiving total parenteral nutrition has been established to investigate gut development, amino acid metabolism and non-alcoholic fatty liver disease. Endoscopic therapeutic methods for upper gastrointestinal tract bleeding are being developed. Bone remodelling cycle in pigs is histologically more similar to humans than that of rats or mice, and is used to examine the relationship between menopause and osteoporosis. Work has also been conducted on dental implants in pigs to consider loading; however with caution as porcine bone remodels slightly faster than human bone. We conclude that pigs are a valuable translational model to bridge the gap between classical rodent models and humans in developing new therapies to aid human health.

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Section: Litten-brown Corson and Clarkementioning

confidence: 99%

Porcine models for the metabolic syndrome, digestive and bone disorders: a general overview

Litten-Brown

Corson

Clarke

2010

Animal

147

136

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“…25,62 On the other hand, a survey of a large population in the north of Finland concluded that there was no association between birth weight and symptoms of PCOS in adolescents and adults. 63 For the time being then, it is important to keep an open mind about the possible non-genetic, intrauterine factors that could impact on development of 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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“…During the third decade of life, this risk can be twice as high in women born SGA as it is in women born AGA (Melo et al 2010). However, PCOS does not occur in all women born SGA (Laitinen et al 2003, Mumm et al 2013, and …”

Section: )mentioning

confidence: 99%

“…Although SGA women in Brazil (Melo et al 2010) and those with LBW in Italy (Pandolfi et al 2008) and Turkey (Hizli et al 2012) present a higher risk for developing PCOS, these findings were not confirmed in individuals from the USA (Legro et al 2010), UK (Cresswell et al 1997, Michelmore et al 2001, Shayeb et al 2014, The Netherlands (Sadrzadeh et al 2003), Finland (Laitinen et al 2003), Spain (Ibáñ ez et al 2008) or Denmark (Mumm et al 2013). One study conducted in Australia analysed birth weight as a continuous variable and found that each 100 g increase in birth weight increased the risk of hyperandrogenism.…”

Section: Genetic Predispositionmentioning

confidence: 99%

“…The authors of that study also found that the subjects' thinness was related to PCOS symptoms and to IR (Davies et al 2012; Table 3). These apparent regional differences may result from the limitations of these studies, which include the use of varying definitions of PCOS (Cresswell et al 1997, Laitinen et al 2003, Sadrzadeh et al 2003, Ibáñ ez et al 2008, Hizli et al 2012, Mumm et al 2013, the inclusion of women using hormonal contraceptives (Ibáñ ez et al 2007, Davies et al 2012, Mumm et al 2013, the small numbers of participants (Ibáñez et al 2001, Pandolfi et al 2008, the use of self-reported birth data (Laitinen et al 2003, Sadrzadeh et al 2003, Legro et al 2010, Hizli et al 2012, the inclusion of women with immature HPG axes (Ibáñ ez et al 2001) and the absence of compensatory growth assessments (Cresswell et al 1997, Michelmore et al 2001, Laitinen et al 2003, Sadrzadeh et al 2003, Ibáñez et al 2008, Pandolfi et al 2008, Legro et al 2010, Melo et al 2010, Hizli et al 2012, Mumm et al 2013, Shayeb et al 2014. The use of birth weight classifications as an exposure factor across studies was perhaps the most important limitation, because not all of the studies adjusted the subjects' birth weight for GA. For that reason, some of the studies included preterm newborn infants.…”

Section: Genetic Predispositionmentioning

confidence: 99%

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Pathogenesis of polycystic ovary syndrome: multifactorial assessment from the foetal stage to menopause

Melo¹,

Dias²,

Cavalli³

et al. 2015

Reproduction

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Polycystic ovary syndrome (PCOS) is a multifactorial disorder that arises from interactions between genetic, environmental and intrauterine factors. Small-for-gestational-age (SGA) babies and the daughters of mothers with PCOS represent possible postnatal clinical targets for developmental programming by steroid excess. The presence of excess glucocorticoids and/or androgens during foetal organogenesis and growth might promote changes in gene expression, and these changes might be related to an increase in the risk of PCOS-like reproductive and metabolic disorders in postnatal life, such as rapid growth and weight gain during the first 2 years of life (only in SGA babies), hyperinsulinaemia, adipocyte dysfunction and childhood visceral obesity, premature pubarche and adrenarche (only in SGA babies) and PCOS. In the fourth decade of life, women who have PCOS may be at higher risk for type 2 diabetes mellitus, dyslipidaemia and systemic arterial hypertension, which suggests that these women are also at higher risk for cardiovascular disease during menopause. However, PCOS can also occur in women who were born at appropriate weight for GA or in newborns of women without PCOS, which suggests that genetic variation and environmental factors play important roles in the development and maintenance of PCOS in a population. Genome-wide association studies based on adequate population samples have shown a higher frequency of genetic polymorphisms of the LHCGR, THADA and DENND1A genes in women with PCOS. Genetic studies of PCOS have also included analyses of structural changes in the chromosome based on an assessment of telomere length in single, cross-sectional evaluations, and these studies have produced controversial results. The present narrative review assesses the multifactorial origins of PCOS (including environmental, genetic and intra-uterine factors) and the development of conditions associated with this disorder. It is concluded that although PCOS might originate in the intra-uterine environment through developmental programming by steroid excess, the interaction between genetic and environmental factors is crucial for its appearance. Follow-up studies should be conducted to assess the same populations over their entire lifespans while taking into account different aspects of the pathogenesis of PCOS.Reproduction (2015) 150 R11-R24

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Body size from birth to adulthood as a predictor of self-reported polycystic ovary syndrome symptoms

Cited by 154 publications

References 35 publications

Porcine models for the metabolic syndrome, digestive and bone disorders: a general overview

Porcine models for the metabolic syndrome, digestive and bone disorders: a general overview

Polycystic ovary syndrome in adolescents

Pathogenesis of polycystic ovary syndrome: multifactorial assessment from the foetal stage to menopause

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