Low birth weight and later development of insulin resistance and biochemical/clinical features of polycystic ovary syndrome

Pandolfi, C; Zugaro, Antonella; Lattanzio, Francesca; Necozione, Stefano; Barbonetti, Arcangelo; Colangeli, Maria Simonetta; Francavilla, Sandro; Francavilla, Felice

doi:10.1016/j.metabol.2008.02.018

Cited by 48 publications

(42 citation statements)

References 32 publications

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“…However, studies with experimental animals have found that foetuses with IUGR caused by placental insufficiency or maternal malnutrition were born SGA and that these animals showed a predisposition to developing pathologies in postnatal life after compensatory growth during the first 2 years of life (Bloomfield et al 2003, Reynolds 2012. Clinical data show that compensatory growth might also be associated with the development of comorbidities in humans, such as precocious puberty (Ibáñez et al 1998), SAH (Elting et al 2001), cardiovascular disease (Bonamy et al 2008), type 2 DM, glucose intolerance (Willemsen et al 2008), dyslipidaemia, obesity (Martinez-Aguayo et al 2007), R16 A S Melo and others metabolic syndrome (Jaquet et al 2005) and PCOS (Pandolfi et al 2008, Melo et al 2010, Hizli et al 2012. Thus, children born SGA would exhibit a clinical marker of developmental programming by glucocorticoids associated with the development of PCOS and its associated comorbidities, although SGA may also be constitutional (variation of normal).…”

Section: Developmental Programming By Glucocorticoid Excessmentioning

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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Section: Developmental Programming By Glucocorticoid Excessmentioning

confidence: 99%

Section: Genetic Predispositionmentioning

confidence: 99%

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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“…Interestingly, treatment of adult monkeys with androgens in various forms and regimens failed to induce PCOS (Billiar et al 1985). An association between low birthweight and PCOS has been reported in human studies (Ibanez et al 1998, Pandolfi et al 2008, although more comprehensive analyses failed to support these findings (Sadrzadeh et al 2003, Legro et al 2010. Fibrillin 3, an ECM protein that regulates TGFB bioactivity, has been shown to be expressed in the stroma of foetal ovaries during the period when follicles are forming (Hatzirodos et al 2011).…”

Section: Foxl2: a Key Regulator Of Ovarian Developmentmentioning

confidence: 99%

Mammalian foetal ovarian development: consequences for health and disease

Sarraj¹,

Drummond

2012

Reproduction

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The development of a normal ovary during foetal life is essential for the production and ovulation of a high-quality oocyte in adult life. Early in embryogenesis, the primordial germ cells (PGCs) migrate to and colonise the genital ridges. Once the PGCs reach the bipotential gonad, the absence of the sex-determining region on the Y chromosome (SRY) gene and the presence of female-specific genes ensure that the indifferent gonad takes the female pathway and an ovary forms. PGCs enter into meiosis, transform into oogonia and ultimately give rise to oocytes that are later surrounded by granulosa cells to form primordial follicles. Various genes and signals are implicated in germ and somatic cell development, leading to successful follicle formation and normal ovarian development. This review focuses on the differentiation events, cellular processes and molecular mechanisms essential for foetal ovarian development in the mice and humans. A better understanding of these early cellular and morphological events will facilitate further study into the regulation of oocyte development, manifestation of ovarian disease and basis of female infertility.

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“…Poor fetal growth, as measured by LBW and small for gestational age (SGA), is also linked with growth retardation and adult chronic diseases (Barker, 2007, Bonamy et al, 2008, Meas et al, 2008, Pandolfi et al, 2008. For girls, the lower their birthweight, the smaller their offspring will be at birth (Victora et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Modifying effect of maternal nutritional status on the impact of maternal multiple micronutrient supplementation on birthweight in Indonesia

et al. 2011

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Background/Objective: Low birthweight (LBW) and intrauterine growth restriction are linked with maternal nutritional status during pregnancy, and maternal supplementation with multiple micronutrients (MMNs) is reported to increase birthweight. Responses to MMN, however, might be modified by maternal nutrition. Subjects/Methods: To examine the differential effects of maternal nutritional status on birthweight responses to prenatal MMN supplementation, data from the Supplementation with Multiple Micronutrient Intervention Trial, a cluster-randomized trial in Indonesia was analyzed. Birthweight outcomes of 7001 infants whose mothers received iron/folic acid were compared with 7292 infants whose mothers received MMN. The modifying effects of maternal short-term nutritional status (mid-upper arm circumference (MUAC) and long-term nutritional status (height) on the birthweight response to MMN supplementation were assessed. Results: For women with higher MUAC (X23.5 cm), MMN increased mean birthweight by 33 g (95% confidence interval (CI): À1 to 66, P ¼ 0.06) and significantly reduced LBW by 21% (relative risk: 0.79, 95% CI: 0.64-0.99, P ¼ 0.04). The modifying effect of MUAC on mean birthweight, LBW and small for gestational age was significant. There was no evidence of a modifying effect of maternal height on the response to MMN. Conclusions: Supplementation with MMN in pregnancy increased birthweight, but maternal nutritional status modified this response, with infants born to women with better short-term nutrition having greater birthweight response.

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Low birth weight and later development of insulin resistance and biochemical/clinical features of polycystic ovary syndrome

Cited by 48 publications

References 32 publications

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

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

Mammalian foetal ovarian development: consequences for health and disease

Modifying effect of maternal nutritional status on the impact of maternal multiple micronutrient supplementation on birthweight in Indonesia

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