Experimental neuroendocrinology

Department of Internal Medicine I

Group Members

Hendrik Lehnert (Group leader)
Carla Schulz (Group leader)
Angela Oldörp (Technician)

Research Interests

Our focus of interest is on the central nervous action of adipokines in the context of homeostatic (based on energy balance) and hedonic (pleasure/reward related) regulation of energy homeostasis.

Within the frameworks of GRK 1957 “Adipocyte-brain crosstalk” and TR-SFB 137 “Ingestive behavior: homeostasis and reward” funded by the Deutsche Forschungsgemeinschaft, we currently address both homeostatic and hedonic aspects of one adipokine in particular, nesfatin-1, in rat and mouse animal models.

With regard to the hedonic regulation of food intake, we aim to dissect the effect of nesfatin-1 on liking and wanting and furthermore experimentally manipulate the central nervous dopaminergic system to affect reward related processes. To do this, we employ various operant conditioning paradigms and control dopaminergic output in selected central nervous target areas with the help of an optogenetic approach.

In the context of homeostatic regulation of energy homeostasis, we are mainly interested in the effects of nesfatin-1 on energy expenditure and to identify both the underlying central nervous and peripheral mechanisms. In-vivo microdialysis, direct calorimetry and thermography allow us to quantify energy expenditure and to pinpoint the structures involved.


  • Tamas Horvath, Yale School of Medicine, New Haven, CT, USA
  • Stephen Farmer, Boston University School of Medicine, Boston, MA, USA


  1. Dore R, Levata L, Lehnert H, Schulz C. Nesfatin-1: functions and physiology of a novel regulatory peptide. J Endocrinol. 2017 Jan;232(1):R45-R65
  2. Wernecke K, Lamprecht I, Jöhren O, Lehnert H, Schulz C. Nesfatin-1 increases energy expenditure and reduces food intake in rats. Obesity (Silver Spring). 2014 Jul;22(7):1662-8.
  3. Schulz C, Paulus K, Lobmann R, Dallman M, Lehnert H. Endogenous ACTH, not only alpha-melanocyte-stimulating hormone, reduces food intake mediated by hypothalamic mechanisms. Am J Physiol Endocrinol Metab. 2010 Feb;298(2):E237-44.