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André Marques-Pinto and Davide Carvalho

diseases and a consequent decline in reproductive function worldwide (3) . Given the short time frame, genetic changes cannot explain it. Thus, environmental substances may be accountable for the observed trends (4, 5) . Indeed, both humans and wildlife

Open access

Vittorio Unfer, Fabio Facchinetti, Beatrice Orrù, Barbara Giordani and John Nestler

endocrine, reproductive and metabolic disorder, affecting at least 5–10% of the total population of reproductive-age women, worldwide ( 14 ). Independently of body habitus ( 15 ), women with PCOS manifest a 50–70% incidence of IR, resulting in a compensatory

Open access

Kristian Almstrup, Hanne Frederiksen, Anna-Maria Andersson and Anders Juul

Puberty marks a transition period, which leads to the attainment of adult sexual maturity. Timing of puberty is a strongly heritable trait. However, large genetic association studies can only explain a fraction of the observed variability and striking secular trends suggest that lifestyle and/or environmental factors are important. Using liquid-chromatography tandem-mass-spectrometry, we measured endocrine disrupting chemicals (EDCs; triclosan, bisphenol A, benzophenone-3, 2,4-dichlorophenol, 11 metabolites from 5 phthalates) in longitudinal urine samples obtained biannually from peri-pubertal children included in the COPENHAGEN puberty cohort. EDC levels were associated with blood DNA methylation profiles from 31 boys and 20 girls measured both pre- and post-pubertally. We found little evidence of single methylation sites that on their own showed association with urinary excretion levels of EDCs obtained either the same day or measured as the yearly mean of dichotomized EDC levels. In contrast, methylation of several promoter regions was found to be associated with two or more EDCs, overlap with known gene-chemical interactions, and form a core network with genes known to be important for puberty. Furthermore, children with the highest yearly mean of dichotomized urinary phthalate metabolite levels were associated with higher promoter methylation of the thyroid hormone receptor interactor 6 gene (TRIP6), which again was mirrored by lower circulating TRIP6 protein levels. In general, the mean TRIP6 promoter methylation was mirrored by circulating TRIP6 protein levels. Our results provide a potential molecular mode of action of how exposure to environmental chemicals may modify pubertal development.

Open access

Josef Köhrle

authoritative review articles in all areas of endocrinology. Social media has become an inherent element of science communication in the 21st century; if you are eager to instantly follow novel trends, the latest endocrine information, or contribute to debates

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Malachi J McKenna, Barbara F Murray, Myra O'Keane and Mark T Kilbane

sunlight exposure have lesser dependence on oral sources. The recommended daily allowances specified by IOM in 2011 are between 30% and threefold higher than the 1997 recommended allowances (4) . Noting the trend for unsubstantiated claims regarding

Open access

Jes Sloth Mathiesen, Jens Peter Kroustrup, Peter Vestergaard, Kirstine Stochholm, Per Løgstrup Poulsen, Åse Krogh Rasmussen, Ulla Feldt-Rasmussen, Sten Schytte, Stefano Christian Londero, Henrik Baymler Pedersen, Christoffer Holst Hahn, Bjarki Ditlev Djurhuus, Jens Bentzen, Sören Möller, Mette Gaustadnes, Maria Rossing, Finn Cilius Nielsen, Kim Brixen, Anja Lisbeth Frederiksen, Christian Godballe and the Danish Thyroid Cancer Group (DATHYRCA)

thyroid cancer in the USA . Endocrine-Related Cancer 2016 23 313 – 322 . ( https://doi.org/10.1530/ERC-15-0445 ) 26917552 10.1530/ERC-15-0445 8 Randle RW Balentine CJ Leverson GE Havlena JA Sippel RS Schneider DF Pitt SC Trends in

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Louise Vølund Larsen, Delphine Mirebeau-Prunier, Tsuneo Imai, Cristina Alvarez-Escola, Kornelia Hasse-Lazar, Simona Censi, Luciana A Castroneves, Akihiro Sakurai, Minoru Kihara, Kiyomi Horiuchi, Véronique Dorine Barbu, Francoise Borson-Chazot, Anne-Paule Gimenez-Roqueplo, Pascal Pigny, Stephane Pinson, Nelson Wohllk, Charis Eng, Berna Imge Aydogan, Dhananjaya Saranath, Sarka Dvorakova, Frederic Castinetti, Attila Patocs, Damijan Bergant, Thera P Links, Mariola Peczkowska, Ana O Hoff, Caterina Mian, Trisha Dwight, Barbara Jarzab, Hartmut P H Neumann, Mercedes Robledo, Shinya Uchino, Anne Barlier, Christian Godballe and Jes Sloth Mathiesen

Introduction Multiple endocrine neoplasia type 2 (MEN 2) is an autosomal dominant inherited cancer syndrome caused by germline mutations of the rearranged during transfection ( RET ) proto-oncogene ( 1 , 2 , 3 , 4 , 5 , 6 ). The syndrome

Open access

Cristina Lamas, Elena Navarro, Anna Casterás, Paloma Portillo, Victoria Alcázar, María Calatayud, Cristina Álvarez-Escolá, Julia Sastre, Evangelina Boix, Lluis Forga, Almudena Vicente, Josep Oriola, Jordi Mesa and Nuria Valdés

Introduction Multiple endocrine neoplasia type 1 (MEN1) syndrome is a rare hereditary disease, with an estimated prevalence of 0.15–0.30 cases per 1000 in general population ( 1 , 2 ). Primary hyperparathyroidism (PHPT) is its most common

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Hanbaro Kim, Ki Byung Song, Dae Wook Hwang, Jae Hoon Lee, Shadi Alshammary and Song Cheol Kim

Introduction Pancreatic neuroendocrine tumors (PNETs), also known as islet cell tumors, are rare neoplasms arising from the endocrine pancreas, with a reported incidence of <1 per 100,000 persons per year ( 1 , 2 ). However, the incidence of

Open access

Kate E Lines, Mahsa Javid, Anita A C Reed, Gerard V Walls, Mark Stevenson, Michelle Simon, Kreepa G Kooblall, Sian E Piret, Paul T Christie, Paul J Newey, Ann-Marie Mallon and Rajesh V Thakker

BL/6 Men1 +/- mice were assessed by Chi-squared test for trend. Table 1 Occurrence of endocrine tumours observed in 12- to 26-month-old Men1 +/- mice in 129S6/SvEv and C57BL/6 strains. Tumours Strain P 129S6