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Leptin substitution in patients with lipodystrophy: Neural correlates for long-term success in the normalization of eating behavior

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Mueller,  Karsten
Methods and Development Unit Nuclear Magnetic Resonance, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Horstmann,  Annette
Integrated Research and Treatment Center Adiposity Diseases, University of Leipzig, Germany;
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Villringer,  Arno
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Clinic for Cognitive Neurology, University of Leipzig, Germany;

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Pleger,  Burkhard
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Department of Neurology, University Hospital Bergmannsheil, Bochum, Germany;

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Citation

Schlögl, H., Mueller, K., Horstmann, A., Miehle, K., Püschel, J., Villringer, A., et al. (2016). Leptin substitution in patients with lipodystrophy: Neural correlates for long-term success in the normalization of eating behavior. Diabetes, 65(8), 2179-2186. doi:10.2337/db15-1550.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-6384-2
Abstract
Lipodystrophy (LD) is a rare disease with a paucity of subcutaneous adipocytes and leptin-deficiency. Patients often develop severe diabetes mellitus and show disturbed eating behavior with reduced satiety that can be restored by substitution with the leptin analogue metreleptin. However, long-term effects of metreleptin on resting-state brain connectivity in treatment-naïve LD patients have not been assessed. In this study, resting-state functional magnetic resonance imaging (fMRI) scans and extensive behavioral testing assessing changes in hunger/satiety regulation were performed during the first 52 weeks of metreleptin treatment in nine LD patients. Resting-state connectivity significantly increased over the course of metreleptin treatment in three brain areas, i.e. hypothalamus, insula/superior temporal gyrus, and medial prefrontal cortex. Behavioral tests demonstrated that perceived hunger, importance of eating, eating frequencies, and liking ratings of food pictures significantly decreased during metreleptin therapy. Taken together, leptin substitution was accompanied by long-term changes of hedonic and homeostatic central nervous networks regulating eating behavior, as well as decreased hunger feelings and diminished incentive value of food. It needs to be assessed in future studies whether metreleptin treatment in LD restores physiological processes important for the development of satiety.