Endocrine Abstracts

S Hillier, University of Edinburgh, Edinburgh, United Kingdom AbstractSteve Hillier is Professor of Reproductive Endocrinology at the University of Edinburgh, where he has directed infertility laboratory services at the Royal Infirmary of Edinburgh and undertaken research at the Centre for Reproductive Biology for over 20 years. Previously (1982–1985), working with Robert (now Lord) Winston, he established the <i...

G Risbridger, Monash University, Melbourne, Australia AbstractProfessor Risbridger, a founding member of the Monash Institute of Medical Research, currently heads the Institute's Centre for Urological Research (CURe). She leads a team of investigators who aim to better understand prostate disease leading to better diagnosis and treatment of both benign and malignant prostate disease. Professor Risbridger is a Fulbright...

VKK Chatterjee, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom AbstractKrishna Chatterjee graduated from Cambridge and completed his clinical training in Oxford. He first trained in endocrinology at Hammersmith Hospital, London and subsequently undertook research in the Thyroid Unit at Massachusetts General Hospital, Boston. In 1990, he returned to Cambridge as a Wellcome Senior Clinical Res...

C Strasburger, Charite Campus Mitte, Berlin, Germany AbstractSince 2003 Christian J Strasburger has been Division Chief and Professor of Clinical Endocrinology at the Department of Medicine at Charité-Universitätsmedizin Berlin, Germany. He graduated from the Medizinische Universität Lübeck, Germany and trained in internal medicine and endocrinology at the Universities of Lübeck and Munich. He ...

Recent studies suggest TSH inhibits bone remodeling, indicating that TSH deficiency rather than thyroid hormone excess could cause bone loss in thyrotoxicosis. The findings predict that TSH receptor (TSHR) stimulating antibodies (TSHRAb) should inhibit bone turnover, whereas Graves’ disease patients exhibit high bone turnover with increased fracture susceptibility. We characterized TSH-action in primary human and mouse osteoblasts and osteoclasts, and explored whether a p...

Studies of TSHR−/− mice suggest that TSH inhibits bone turnover, but these mice have congenital hypothyroidism and the actions of TSH cannot be separated from effects of thyroid hormone deficiency. We characterised skeletal development in hyt/hyt mice, which have a point mutation in the Tshr gene, and Pax8−/− mice with thyroid gland agenesis. Hyt/hyt mice have a 100-fold increase in TSH but inactive TSHRs, whereas Pax8&...