Our team aims to identify new hormonal systems, which coordinate insulin sensitivity and energy expenditure across tissues. More specifically we study novel hormones and blood factors mediating the cross talk between liver and adipose tissue in response to feeding cues, such as fasting-refeeding, time restricted feeding and obesigenic diets. Our research aims to increase the understanding of the complex physiology of feeding and energy balance and directly works on the development of new therapeutics factors of Type 2 diabetes and the new diagnostic biomarkers of early diabetes. In hypothesis-driven approaches we perform all steps from the discovery to preclinical testing of novel metabolic factors.
Development of novel hormones-based therapeutics against insulin resistance and Type 2 diabetes
The successful candidate for this project will utilize recombinant protein techniques to design and purify novel therapeutic proteins and peptides, which he/she will test on mouse models of obesity and Type 2 diabetes. In addition, the PhD candidate will employ classical biochemistry, molecular biology and state of the art high throughput methods (proteomics, phoshoproteomics, metabolomics) to identify signaling receptors and novel molecular pathways to understand the function of the studied novel hormones. Finally characterization of mouse models of loss and gain of function, as well as work with adenoviruses and adenoassociated viruses (AAV) will be part of the PhD training. The candidate will work with a young PI, who offers extensive training and mentoring in a highly equipped and multidisciplinary environment.
Your profil: Masters degree in biology, biochemistry, molecular medicine or related fields. Previous exposure to and experience with basic biochemical and molecular biology techniques is essential.
2016: Bosma M, Gerling M, Pasto J, Georgiadi A, Graham E, Shilkova O, Iwata Y, Almer S, Söderman J, Toftgård R, Wermeling F, Boström EA, Boström PA. FNDC4 acts as an antiinflammatory factor on macrophages and improves colitis in mice. Nat Commun. 2016 Apr 12;7:11314
2014: Tjeerdema N, Georgiadi A, Jonker JT, van Glabbeek M, Alizadeh Dehnavi R, Tamsma JT, Smit JW, Kersten S, Rensen PC. Inflammation increases plasma angiopoietin-like protein 4 in patients with the metabolic syndrome and type 2 diabetes. BMJ Open Diabetes Res Care. 2014 Dec 3;2(1):e000034.
2014: Mattijssen F, Georgiadi A, Andasarie T, Szalowska E, Zota A, Krones-Herzig A, Heier C, Ratman D, De Bosscher K, Qi L, Zechner R, Herzig S, Kersten S. Hypoxia-inducible lipid dropletassociated (HILPDA) is a novel peroxisome proliferator-activated receptor (PPAR) target involved in hepatic triglyceride secretion. J Biol Chem. 2014 Jul 11;289(28):19279-93.
2014: Roberts LD, Boström P, O'Sullivan JF, Schinzel RT, Lewis GD, Dejam A, Lee YK, Palma MJ, Calhoun S, Georgiadi A, Chen MH, Ramachandran VS, Larson MG, Bouchard C, Rankinen T, Souza AL, Clish CB, Wang TJ, Estall JL, Soukas AA, Cowan CA, Spiegelman BM, Gerszten RE. β- Aminoisobutyric acid induces browning of white fat and hepatic β-oxidation and is inversely correlated with cardiometabolic risk factors. Cell Metab. 2014 Jan 7;19(1):96-108.
2013: Georgiadi A, Wang Y, Stienstra R, Tjeerdema N, Janssen A, Stalenhoef A, van der Vliet JA, de Roos A, Tamsma JT, Smit JW, Tan NS, Müller M, Rensen PC, Kersten S. Overexpression of angiopoietin-like protein 4 protects against atherosclerosis development. Arterioscler Thromb Vasc Biol. 2013 Jul;33(7):1529-37
2012: Georgiadi A, Boekschoten MV, Müller M, Kersten S. Detailed transcriptomics analysis of the effect of dietary fatty acids on gene expression in the heart. Physiol Genomics. 2012 Mar 19;44(6):352-61.
2010: Georgiadi A, Lichtenstein L, Degenhardt T, Boekschoten MV, van Bilsen M, Desvergne B, Müller M, Kersten S. Induction of cardiac Angptl4 by dietary fatty acids is mediated by peroxisome proliferator-activated receptor beta/delta and protects against fatty acid-induced oxidative stress. Circ Res. 2010 Jun 11;106(11):1712-21