English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Meeting Abstract

Changes of serotonin transporter (SERT) availability in human obesity prior and 6 month after an integrative treatment approach

MPS-Authors
/persons/resource/persons19531

Arélin,  Katrin
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Vettermann, F., Rullmann, M., Becker, G., Luthardt, J., Zientek, F., Meyer, P., et al. (2015). Changes of serotonin transporter (SERT) availability in human obesity prior and 6 month after an integrative treatment approach. Journal of Nuclear Medicine, 56(Suppl. 3): 528.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0029-7C5E-8
Abstract
Objectives: Central serotonergic systems comprise important neuromodulatory capacity and participate in regulating appetite and satiety, thus contributing to obesogenic mechanism. Especially presynaptic SERT are target structures for modern antidepressants and interventions aiming to reduce weight. The aim of our study was to quantitatively assess SERT availability in obese, non-depressed humans at baseline and following a 6 months integrative treatment program. SERT was compared with changes in body mass index (BMI) as the outcome parameter. This study investigates SERT levels in obese individuals(OB) and normal-weight, healthy control subjects (NW). Methods: Twenty-two OB (BMI 41±5kg/m2, age 38±11yrs, 14♀) and 15 NW (BMI 23±2 kg/m2, age 36±7yrs, 10♀) were investigated prior and after a 6 month of treatment program including diet, physical and psychological intervention by using C-11-DASB and PET. Parametric images of binding potential BPND (MRTM2) were generated from atlas-based analysis of VOI after coregistration with individual 3D MRI data. Results: In OB, BPND and BMI were negatively associated (P<0.05) in the left medial prefrontal cortex (PFC) (R=-0.37), the left dorso-lateral PFC (R=-0.38), the right hippocampus (R=-0.37) and the left amygdala (R=-0.39, p=0.037). All of these regions showed a significant BPND increase after the OB lost weight (delta BMI -1.02±2.1kg/m2). No significant BPND changes over time were found in the NW. Conclusions: Changes of SERT availability in obese are evident in regions thought to be relevant of eating control. Furthermore, correlation between losing weight and higher SERT mainly in the PFC after the 6 month program suggest that the PFC likely has an essential role in feeding behavior modulated by the serotonin system and SERT availability in those brain areas may serve as a predictor for treatment response.