will take place on Tuesday, May 10, 2016 from 17:15 to 18:15 hours in CBBM, Ground Floor, Room 50/51.
Host: Prof. Hendrik Lehnert,
Department of Internal Medicine I,
Universität zu Lübeck
Abstract
The vast majority of obese subjects suffer from hypothalamic leptin resistance, which impedes sustainable weight loss and mediates weight regain after dieting. Dr. Pfluger and his team aim to delineate the underpinnings of hypothalamic leptin resistance and leptin re-sensitization by pharmacological and dietary intervention, which is key to develop an efficient therapy against obesity and its comorbid diseases. Using diet-induced obese mice as model system, they observe superior restoration of leptin sensitivity after pharmacologically induced weight loss by Exendin-4 (Ex-4) compared to weight loss induced by calorie restriction (CR). Next generation sequencing in combination with the phosphorylated ribosome capture technique further identified novel genes that associate with hypothalamic leptin sensitivity. Commencing studies unraveled class IIa histone deacetylase 5 (HDAC5) as essential component of hypothalamic leptin action that directly interacts with STAT3 to fine-tune its transactivation activity.
CV
Dr. Pfluger earned his Master in Human and Environmental Toxicology at the University of Konstanz, Germany, in 2000. He subsequently graduated in Biochemistry of Micronutrients at the German Institute of Human Nutrition, University of Potsdam, Germany, and continued his education as postdoctoral fellow at the Dept. of Psychiatry, University of Cincinnati. In summer 2009, he was awarded a faculty position at the Dept. of Internal Medicine, University of Cincinnati, OH, and subsequently worked as Research Assistant Professor at the UC Metabolic Diseases Institute. In October 2011 he returned to Europe to serve as Associate Director of the Institute for Diabetes and Obesity at the Helmholtz Centre Munich, Germany. In April 2015, he was appointed head of the Research Unit NeuroBiology of Diabetes at the Helmholtz Center Munich, Germany.
Research Topic:
Gene - environment interactions in the hypothalamic control of energy and glucose homeostasis
Five most important publications:
- Kabra DG, Pfuhlmann K, García-Cáceres C, Schriever SC, Casquero García V, Kebede AF, Fuente-Martin E, Trivedi C, Heppner K, Uhlenhaut NH, Legutko B, Kabra UD, Gao Y, Yi CX, Quarta C, Clemmensen C, Finan B, Müller TD, Meyer CW, Paez-Pereda M, Stemmer K, Woods SC, Perez-Tilve D, Schneider R, Olson EN, Tschöp MH, Pfluger PT. Hypothalamic leptin action is mediated by histone deacetylase 5. Nat Commun. 2016 Feb 29;7:10782.
- Pfluger PT, Kabra DG, Aichler M, Schriever SC, Pfuhlmann K, García VC, Lehti M, Weber J, Kutschke M, Rozman J, Elrod JW, Hevener AL, Feuchtinger A, Hrabě de Angelis M, Walch A, Rollmann SM, Aronow BJ, Müller TD, Perez-Tilve D, Jastroch M, De Luca M, Molkentin JD, Tschöp MH. Calcineurin Links Mitochondrial Elongation with Energy Metabolism. Cell Metab. 2015 Nov 3;22(5):838-50.
- Stemmer K, Perez-Tilve D, Ananthakrishnan G, Bort A, Seeley RJ, Tschöp MH, Dietrich DR, Pfluger PT. High-fat-diet-induced obesity causes an inflammatory and tumor-promoting microenvironment in the rat kidney. Dis Model Mech. 2012 Sep;5(5):627-35.
- Perez-Tilve D, Heppner K, Kirchner H, Lockie SH, Woods SC, Smiley DL, Tschöp M, Pfluger P. Ghrelin-induced adiposity is independent of orexigenic effects. FASEB J. 2011 Aug;25(8):2814-22.
- Pfluger PT, Herranz D, Velasco-Miguel S, Serrano M, Tschöp MH. Sirt1 protects against high-fat diet-induced metabolic damage. Proc Natl Acad Sci U S A. 2008 Jul 15;105(28):9793-8.
