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Metabolism and inflammation related neural plasticity of the obese human brain induced by bariatric surgery

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Pleger,  Burkhard
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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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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Preusser,  Sven
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Heba,  Stefanie
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Hoyer,  Jana
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Rullmann,  Michael
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Pleger, B., Mueller, K., Poppitz, S., Preusser, S., Schütz, T., Dietrich, A., et al. (2019). Metabolism and inflammation related neural plasticity of the obese human brain induced by bariatric surgery. Clinical Neurophysiology, 130(8): e142. doi:10.1016/j.clinph.2019.04.651.


Cite as: https://hdl.handle.net/21.11116/0000-0005-C645-E
Abstract
Recent MRI findings suggest structural brain plasticity, one year after gastric-bypass surgery, comprising the cortex of all brain lobes, subcortical structures and the cerebellum. Changes in gray/white matter density (GMD/WMD) were closely related to elevated regional homogeneity of spontaneous neural activity suggesting widespread structural–functional plasticity. In the present study, we re-visited the same data to investigate brain plasticity specifically related to surgery-induced individual improvements in metabolism and inflammation. We found no relationship between markers of brain plasticity and improvements in inflammation. Improvements in metabolism correlated with GMD/WMD changes, but not with any functional plasticity markers. Six months after surgery, loss of body mass index (BMI) overlapped with decreased GMD in the hypothalamus, as the main homeostatic control center, and the dorsal striatum, assumed to guide everyday eating behavior. Reductions of HbA1c, indexing improved glucose metabolism, correlated with increased GMD in bilateral cuneus. After twelve months, BMI-loss correlated with increased GMD in the right cerebellar lobule VII/left medial temporal gyrus, and increased WMD in the vicinity of the right putamen/right fusiform gyrus. Together, these findings suggest metabolism-related plasticity in brain structures involved in sensory/cognitive integration processes, memory encoding, and the control of eating behavior.