J. Andrew Pospisilik receives Prize by the GlaxoSmithKline Foundation

The young researcher is awarded for his work in the field of metabolic diseases

July 09, 2015

The GlaxoSmithKline (GSK) Foundation annually awards two scientific prizes to young researchers in Germany. Outstanding achievements in the categories "Medical Basic Research" and "Clinical Research" are honored. An important criterion is one or two pioneering scientific publications in the previous year. One of this year’s awards for "Basic Medical Research" goes to Dr. J. Andrew Pospisilik, a junior research group leader at the MPI-IE. The prize, endowed with 7500 Euros, will be presented at a ceremony of the GSK Foundation on July 9, 2015.

Dr. Pospisilik heads his own laboratory at the Max Planck Institute of Immunobiology and Epigenetics since 2010. His main research interest is to study the causes and underlying mechanisms of metabolic disorders. "Obesity and its associated secondary diseases such as diabetes, heart disease and cancer are a ever-growing socio-economic problem of modern society." Dr. Pospisilik points out. "In my laboratory we want to figure out why we are fat (and sick) and which mechanisms influence this."

In 2014 the Pospisilik group in close collaboration with Austrian scientists identified the enzyme heme oxygenase 1 (HO-1) as a factor affecting the health of obese people. The evaluation of liver and fat biopsies from obese individuals showed that patients with low HO-1 values very rarely developed secondary diseases. This finding was also supported in mouse models. When the enzyme HO-1 was specifically removed from macrophages or hepatocytes, these mice remained healthy despite obesity. This can be explained by a lower inflammatory state and increased insulin sensitivity within the body. These findings provide new approaches for diagnosis and treatment of secondary diseases in overweight and obese patients.

The major research focus in the Pospisilik laboratory aims to uncover the epigenetic component of metabolic diseases. In particular, this relates to environmental influences that may lead to changes in gene expression without mutations in the DNA sequence. "We wanted to know whether diet-induced changes in metabolism can be inherited." Dr. Pospisilik outlines the goal of another recently published study. This time the researchers used fruit flies as model organisms, also due to their short generation time. Two days before the mating male files were fed a diet with varying sugar content. Sons resulting from these matings were then tested for their susceptibility to obesity. Only animals, whose fathers ate either too much or too little sugar, tended to be overweight. Further tests with several mutant lines allowed the researchers to identify multiple genes that are essential for the inheritance of obesity. These epigenetic factors are responsible for compact packaging of DNA and are also less abundant in obese humans and mice.

"Our findings are part of a rapid ongoing discovery in our field of research. We are learning that obesity associated metabolic syndrome truly is an inflammatory disease. Moreover, our understanding of why we develop such diseases is also changing rapidly. The focus is shifting way form the dogma that everything lies in our DNA and moving towards an appreciation for substantial influences of our own early lives, in the womb, and even to the health and stress conditions of our parents.” Dr. Pospisilik summarizes the insights of recent years. He expects that "these ideas will reshape how we approach treatment and, especially, prevention.

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