Kangping Yang

Professor, Departments of Obstetrics & Gynaecology and Physicology & Phamacology, the University of Western Ontario.

Lecture for Students and Teachers

Topic: Bisphenol A Disrupts Fetal Development in the Mouse

Time: Nov. 26, 2014, 2:00 pm.
Place: Room 203, School of Food and Biological Engineering

Introduction to prof. Kangping Yang

Kaiping Yang is a professor at the University of Western Ontario, He received his Ph.D. from University of Nottingham, UK. His major achievement as follows,

April 2004: Demonstrated for the first time in the rat model that protein restriction during pregnancy resulted in low birth weight and central obesity later in adult life.

April 2008: Made a seminal discovery that neuropeptide Y (NPY), a neuropeptide thought only produced by both central and peripheral nervous systems, is produced by abdominal fat.

July 2008: Appointed as Chair of the Maternal, Fetal and newborn Health Division, which comprises of 25 research scientists and over 80 research staff and trainees, one of the three Divisions at Children’s Health Research Institute and Lawson Health Research Institute.

October 2008: Edited and published the second edition of a book called “Adipose Tissue Protocols”, as a volume in the popular and prestigious Methods in Molecular Biology series. The success and popularity of this book is attested by its reaching to the Top 100 Books in Biology several times on Amazon.com.

June 2012: Identified for the first time a plausible molecular mechanism by which maternal caffeine consumption may lead to fetal growth restriction, a leading cause of perinatal morbidity and mortality.

Abstract

Prenatal exposure to bisphenol A (BPA), one of the most prevalent endocrine disrupting chemicals in the environment, is associated with a wide range of disorders in both humans and animal models, including reproductive, metabolic, cardiovascular, respiratory and neurological disorders as well as certain cancers. However, the effects of BPA on fetal development are not well understood. We addressed this important question using the mouse as an experimental model. Various key organs from fetuses exposed to BPA via maternal diet were collected at embryonic day 18.5, and subjected to histological and molecular analysis. We found that BPA profoundly disrupted fetal development, as evidenced by impaired organ maturation and altered gene expression. Furthermore, these BPA-induced phenotypes were manifested in a organ- and gender-specific manner.Thus, our findings highlight the potential adverse effects of BPA exposure in utero on human fetal development. They may also provide a fetal origin for the previously reported adult phenotypes following prenatal exposure to BPA.Importantly, these findings provide an entry point through which novel therapeutic interventions may be developed to prevent and/or reverse the adverse effects of BPA.

(School of Food and Biological Engineering)