ECE2015 Guided Posters Reproduction: Male and endocrine disruptors (8 abstracts)
Cord blood insulin-like peptide 3 is reduced in idiopathic cryptorchidism and inversely related to free bisphenol A: a marker and/or an actor of foetal exposure to endocrine disruptors?
Patrick Fenichel 1, , Najiba Lahlou 3 , Nicolas Chevalier 1, , Patrick Coquillard 4 , Patricia Panaia-Ferrari 5 , Kathy Wagner-Mahler 6 , Michel Pugeat 7 & Francoise Brucker-Davis 1,
1Department of Endocrinology, Diabetology and Reproductive Medicine CHU de Nice, Nice, France; 2Institut National de la Recherche Médicale, UMR U1065, Université Nice-Sophia Antipolis, Nice, France; 3Department of Hormonology and Metabolic Disorders, Hôpital Cochin, APHP, Paris-Descartes University, Paris, France; 4Institut Sophia-Agrobiotech [INRA-CNRS- Nice University], Sophia-Antipolis, France; 5Department of Biochemistry, CHU Nice, Nice, France; 6Department of Paediatrics, CHU Nice, Nice, France; 7Fédération d’Endocrinologie, hospices civils de Lyon-1, Bron, France.
Introduction: Cryptorchidism, the most frequent congenital malformation in full-term male newborns, increases risk of infertility and testicular cancer. Most cases remain idiopathic but epidemiological and experimental studies have suggested the role of both genetic and environmental factors. Physiological testicular descent is regulated by two major Leydig cell hormones: Insulin-like peptide 3 (INSL3) and testosterone.
Methods and results: From a prospective case control study, 52 idiopathic non syndromic, cryptorchid newborns were compared to 118 matched controls, all born after 34 weeks pregnancy. Cord blood (cb) INSL3 (modified validated enzyme-linked immune-sorbent assay) but not cb testosterone (ultrapressure liquid chromatography-tandem mass spectrometry) was decreased in unilateral idiopathic cryptorchidism (P=0.03) especially in transient forms (P=0.02) and in the subgroup of non-palpable testis compared to the subgroup of palpable testes (supra-scrotal, inguinal or high scrotal) according to Scorer classification (P=0.01). cb free bisphenol A (BPA) (RIA validated by High Pressure Liquid Chromatography-tandem Mass Spectrometry) in cryptorchid boys was not significantly increased (P=0.1). However, in the whole study population (cryptorchid and control), cb free BPA correlated negatively with INSL3 (P=0.01; R2=0.05) but not with testosterone.
Conclusion: INSL3, a major actor of foetal testicular descent, but not testosterone, is decreased at birth in idiopathic cryptorchidism. This hormonal decrease may have contributed earlier in foetal development, to the impaired testicular descend. The inverse correlation we found between cbINSL3 and cbBPA is strengthened by the paper reporting that INSL3 gene is negatively regulated by BPA in ex vitro cultivated foetal human testes. While measurements of cb BPA and cb INSL3 may not exactly reflect earlier foetal production or exposure, our results support the role of INSL3 as a marker and/or an actor of foetal exposure to endocrine disruptors such as BPA.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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