Robert Kleemann

Research area

After my academic training at the Universities of Tübingen and Freiburg (Physiological Chemistry, Biochemistry), I started my research career at the University of Stuttgart-Hohenheim and the Fraunhofer Institute Stuttgart, primarily investigating inflammation cascades and immunity (PhD; summa cum laude). In the last 20 years, I became interested in whole body physiology and extended my expertise to the fields of nutrition, metabolism and pharmacology. Over the years, I gained insight into the underlying mechanisms of a broad spectrum of metabolic and inflammatory diseases, including cardiovascular disease, NAFLD/NASH, and neurodegenerative disorders. My work at TNO focusses on the interface of metabolism & inflammation and has resulted in several patents, >130 publications (with >12,500 citations; H-factor: 59), and new technologies for biomedical research such as translational experimental models that reflect human pathophysiology and sophisticated analytical tools for biomarker profiling. In my research, I combine human and preclinical studies to study the effect of external factors (e.g. nutrition, exercise, stress) on our metabolism and how disturbance of the latter causes inflammation. This “metabolic inflammation” drives a plethora of diseases such as obesity, diabetes, atherosclerosis, frailty and dementia. In my work at TNO, I develop strategies to re-gain metabolic control to reduce chronic inflammation and treat these diseases using combinations of lifestyle, nutritional and pharmaceutical strategies. The required interdisciplinary mindset is also necessary for my ongoing work at the Leiden University Medical Center (Associate Professor at the Department of Vascular Surgery), the Wageningen University (Dept. Human and Animal Physiology) and the Radboud UMC (Dept. Translational Neuroanatomy).

Recent results

As a Principal Scientist, I am responsible for the establishment of large international consortia, often including multiple scientific disciplines and a broad spectrum of academic and private partners. Our main industrial partners are typically pharmaceutical companies, nutrition companies and medium-size enterprises with sophisticated diagnostic tools. Examples of recently established private public partnerships (PPS) and larger research programs (ERP; H2020) are:

• PPS ‘ProLiver’ (develops new technologies and treatments for fatty liver disease);
• PPS ‘Muscle Health’ (gender differences in muscle health/frailty and role of aging)
• PPS ‘GLoBAL’ (international consortium to investigate organ crosstalk along the gut-brain axis)
• ERP ‘Body Brain Interactions’ (development of new human and preclinical body-brain research platforms to study and predict cognitive performance).
• H2020 ‘Moon’ (development of Raman & OCT based apparatus for diagnosis of Alzheimer)
• PPS ‘LipidInflammaGenes’ (Norwegian Food Sector Consortium to investigate beneficial and detrimental effects of plant and animal derived consumer fats)

PhD supervision

My collaborations with academic partners and several University Medical Centers in the Netherlands (e.g. WUR, MUmc, AmsterdamUMC, Radboud UMC) also involve the supervision of PhD students that conduct their research at TNO. At the moment three PhD students work at TNO-MHR/Leiden:

• E. Gart (adjacent to the TKI-LSH/Agri-Food project Proliver)
• F. Seidel (ERP Body Brain Interactions with Radboud UMC)
• J. de Jong (TKI-LSH with Wageningen University)

And the contribution to 5 other PhDs PhD trajectories at WUR, AMC-VUmc, Radboudmc and MUmc. Supervisor of TNO PhDs.

Top publications

• O.Laurentya, J.van Diepen, I.Bobeldijk-Pastorova et al. SCD1, FADS1, and FADS2 activities as candidate biomarkers of early life growth and adiposity. Lancet eBioMedicine, 2021
• A.M. van den Hoek, G.C.M. Zondag, L.Verschuren et al. A novel nutritional supplement prevents muscle loss and accelerates muscle mass recovery in caloric-restricted mice. Metabolism, 2019.
• M.C. Morrison; L. Verschuren; K. Salic et al. OCA modulates serum metabolites and gene signatures characteristic for human NASH and attenuates inflammation and fibrosis progression in Ldlr-/-.Leiden mice. Hepatol.Commun., 2018