Transgenerational Effects of Prenatal Exposure to Environmental Obesogens in Rodents
1:00 pm US Eastern Time
Slides & Resources
Transgenerational Inheritance of Increased Fat Depot Size, Stem Cell Reprogramming, and Hepatic Steatosis Elicited by Prenatal Obesogen Tributyltin in Mice.
Chamorro-García R, Sahu M, Abbey RJ, Laude J, Pham N, Blumberg B. 2013.
Environ Health Perspect: .doi:10.1289/ehp.1205701
Plastics Derived Endocrine Disruptors (BPA, DEHP and DBP) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations.
Manikkam M, Tracey R, Guerrero-Bosagna C, Skinner MK. 2013.
Hydrocarbons (jet fuel JP-8) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations, Reproductive Toxicology, In Press, Available online 25 January 2013.
Rebecca Tracey, Mohan Manikkam, Carlos Guerrero-Bosagna, Michael K. Skinner
Epigentic transgenerational actions of envirnmental factors in disease etiology
Michael K. Skinner, Mohan Manikkam and Carols Guerrero-Bosagna.
Trends Endocrinol Metab. 2010 April; 21(4): 214–222.
Environmental epigentic transgenerational inheritance and somatic epigentic mitotic stability
Epigentics 6:7, 838-842; July 2011
More information, including paper summaries, are available on Michael Skinner's lab website
CHE blog: You Are What Your Great-Grandmother Ate: Transmission of Obesity Across Generations
Environmental Health News: Tributyltin promotes obesity in mice generations
This call was hosted by the CHE Diabetes-Obesity Spectrum and CHE Fertility and Reproductive Health Working Groups
Accumulating scientific research suggests that exposure to environmental chemicals early in life can affect the risk of obesity in later life. Chemicals that can increase the risk of obesity are known as “obesogens.” Two recently published animal studies take obesogen research one step further: both found that the obesity-related effects of prenatal exposure to environmental chemicals were passed down to the third generation descendants of the exposed animals.
On this call we heard the authors of these studies discuss their results. Dr. Bruce Blumberg, who coined the term “obesogen” and has done extensive research on the topic, discussed his work on prenatal exposure to the obesogen tributyltin and its effects on fat cells in mice and their offspring. Dr. Michael Skinner, who has conducted extensive research on the transgenerational effects of various chemical exposures, discussed his findings on the transgenerational effects in rats of prenatal exposure to a mixture of BPA and phthalates.
This call was moderated by Sarah Howard, national coordinator of CHE Diabetes-Obesity Spectrum Working Group, and Karin Russ, national coordinator of CHE Fertility and Reproductive Health Working Group.
Bruce Blumberg, PhD, is a professor in the Department of Developmental and Cell Biology at the University of California, Irvine. Dr. Blumberg’s laboratory investigates the role of nuclear hormone receptors in development, physiology and disease. Dr. Blumberg and his colleagues originated the obesogen hypothesis which holds that developmental exposure to endocrine disrupting chemicals (EDCs) can induce permanent physiological changes. EDC exposure elicits epigenetic alterations in gene expression that reprograms the fate of mesenchymal stem cells, predisposing them to become fat cells. Exposed animals develop more and larger fat cells, despite normal diet and exercise, which is likely to lead to weight gain and obesity over time.
Michael Skinner, PhD, is a professor in the School of Biological Sciences at Washington State University. Dr. Skinner’s research is focused on the investigation of how different cell types in a tissue interact and communicate to regulate gonadal growth and differentiation, with emphasis in the area of reproductive biology. Recent studies have elucidated several critical events in the initiation of male sex differentiation, testis development and ovarian primordial follicle development. His current research has demonstrated the ability of endocrine disrupting chemicals to promote transgenerational epigenetic disease phenotypes due to abnormal germ line programming in gonadal development.