Adipose Tissue; Brain; Energy Metabolism; Fatty Liver
Our lab is interested in understanding how hormones and nutrients are detected by the brain and how these metabolic signals are integrated in the CNS. Our research especially focuses on hormonal feedback mechanisms (i.e. insulin and leptin) that affect energy metabolism via modulation of autonomic nervous system outputs to organs, such as the liver, muscle, white and brown adipose tissue. Since the brain is able to communicate with several metabolic organs simultaneously via its neuronal connections, we are interested in elucidating novel neuronal regulatory pathways necessary to orchestrate glucose and lipid metabolism in selective metabolic states, such as high calorie feeding, insulin resistance, obesity and diabetes. New insights into the inter-organ crosstalk between the brain and the periphery under physiologic conditions and during disease likely provide novel drug targets to fight obesity and obesity-related comorbidities, like diabetes, non-alcoholic fatty liver disease and cardiovascular disease. Furthermore, we strive to translate our findings from basic research into the clinics in order to advance patient care in human metabolic disease.
Techniques, methods & infrastructure
Metabolic phenotyping in rodents (including clamp studies); stereotaxic infusion experiments; tracer dilution techniques, protein chemistry; qPCR; immunoassays; lipid profiling; translational studies in humans
- The role of lepTin in regulating HepAtic Lipid metAbolisM (2019)
Source of Funding: FWF (Austrian Science Fund), Programme Clinical Research (KLIF), Projekt KLI 782
- The role of intranasal insulin in regulating hepatic lipid and amino acid metabolism in humans (2016)
Source of Funding: Medical Scientific Fund of the Mayor of the City of Vienna, Grant # 15228
- The role of brain insulin and leptin action in modulating hepatic triglyceride secretion (2014)
Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
- Hackl, M.T. et al., 2019. Brain leptin reduces liver lipids by increasing hepatic triglyceride secretion and lowering lipogenesis. Nature Communications, 10(1). Available at: http://dx.doi.org/10.1038/s41467-019-10684-1.
- Scherer, T. et al., 2017. Chronic Intranasal Insulin Does Not Affect Hepatic Lipids but Lowers Circulating BCAAs in Healthy Male Subjects. The Journal of Clinical Endocrinology & Metabolism, 102(4), pp.1325–1332. Available at: http://dx.doi.org/10.1210/jc.2016-3623.
- Scherer, T. et al., 2016. Insulin Regulates Hepatic Triglyceride Secretion and Lipid Content via Signaling in the Brain. Diabetes, 65(6), pp.1511–1520. Available at: http://dx.doi.org/10.2337/db15-1552.
- Scherer, T. et al., 2012. Short Term Voluntary Overfeeding Disrupts Brain Insulin Control of Adipose Tissue Lipolysis. Journal of Biological Chemistry, 287(39), pp.33061–33069. Available at: http://dx.doi.org/10.1074/jbc.M111.307348.
- Scherer, T. et al., 2011. Brain Insulin Controls Adipose Tissue Lipolysis and Lipogenesis. Cell Metabolism, 13(2), pp.183–194. Available at: http://dx.doi.org/10.1016/j.cmet.2011.01.008.