Aging and bacterial endotoxin

Applicants: Prof. Dr. Ina Bergheim, University of Vienna, Dept. of Nutritional Sciences, Research Sector Molecular Nutritional Science, Althanstr. 14/UZA2, A-1090 Vienna, Austria Dr. Annika Höhn, German Institute of Human Nutrition, Department of Molecular Toxicology, Arthur- Scheunert-Allee 114-116, 14558 Nuthetal, Germany Average life expectancy has increased dramatically over the past century and senior people constitute the fastest growing segment of the population, not only in Austria and Germany but also many other industrialized countries. Chronic and non-communicable diseases are now the leading causes of death and long periods of moderate and severe illness often precede death. Additionally, human aging is associated with a wide range of physiological changes limiting normal functions and presumably all organ systems of the human body are affected, including key regulators of digestion and metabolism such as liver and pancreas. Despite intense research efforts throughout the last decades molecular mechanisms involved in aging-associated organ degeneration are not fully understood and prevention strategies are still lacking. Results of several studies suggest that aging is associated with alterations of intestinal barrier function and subsequently elevated bacterial endotoxin levels. Elevated bacterial endotoxin levels are discussed to be critical in the development of various liver diseases among them also aging-associated liver degenerations but also the development of pancreatic fibrosis. To date, systematic studies assessing when elevated endotoxin levels occur during healthy aging and if they are causally involved in liver and pancreatic decline as well as histological alterations are lacking. Therefore, the project aims to investigate the role of bacterial toxin in the development of aging- associated liver and pancreas degeneration and to lay the basis for new nutrition-based prevention strategies targeting these alterations thereby also aiming to extend healthy life-span.