Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity
Purpose: Obesity is thought to arise, in part, from deficits in the inhibitory control over appetitive behavior. Such motivational processes are regulated by neuromodulators, specifically acetylcholine (ACh), via α4β2* nicotinic ACh receptors (nAChR). These nAChR are highly enriched in the thalamus...
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MDPI AG
2022-12-01
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author | Eva Schweickert de Palma Tilman Günnewig Michael Rullmann Julia Luthardt Mohammed K. Hankir Philipp M. Meyer Georg-Alexander Becker Marianne Patt Sarah Martin Anja Hilbert Matthias Blüher Osama Sabri Swen Hesse |
author_facet | Eva Schweickert de Palma Tilman Günnewig Michael Rullmann Julia Luthardt Mohammed K. Hankir Philipp M. Meyer Georg-Alexander Becker Marianne Patt Sarah Martin Anja Hilbert Matthias Blüher Osama Sabri Swen Hesse |
author_sort | Eva Schweickert de Palma |
collection | DOAJ |
description | Purpose: Obesity is thought to arise, in part, from deficits in the inhibitory control over appetitive behavior. Such motivational processes are regulated by neuromodulators, specifically acetylcholine (ACh), via α4β2* nicotinic ACh receptors (nAChR). These nAChR are highly enriched in the thalamus and contribute to the thalamic gating of cortico-striatal signaling, but also act on the mesoaccumbal reward system. The changes in α4β2* nAChR availability, however, have not been demonstrated in human obesity thus far. The aim of our study was, thus, to investigate whether there is altered brain α4β2* nAChR availability in individuals with obesity compared to normal-weight healthy controls. Methods: We studied 15 non-smoking individuals with obesity (body mass index, BMI: 37.8 ± 3.1 kg/m<sup>2</sup>; age: 39 ± 14 years, 9 females) and 16 normal-weight controls (non-smokers, BMI: 21.9 ± 1.7 kg/m<sup>2</sup>; age: 28 ± 7 years, 13 females) by using PET and the α4β2* nAChR selective (−)-[<sup>18</sup>F]flubatine, which was applied within a bolus-infusion protocol (294 ± 16 MBq). Volume-of-interest (VOI) analysis was performed in order to calculate the regional total distribution volume (V<sub>T</sub>). Results: No overall significant difference in V<sub>T</sub> between the individuals with obesity and the normal-weight volunteers was found, while the V<sub>T</sub> in the nucleus basalis of Meynert tended to be lower in the individuals with obesity (10.1 ± 2.1 versus 11.9 ± 2.2; <i>p</i> = 0.10), and the V<sub>T</sub> in the thalamus showed a tendency towards higher values in the individuals with obesity (26.5 ± 2.5 versus 25.9 ± 4.2; <i>p</i> = 0.09). Conclusion: While these first data do not show greater brain α4β2* nAChR availability in human obesity overall, the findings of potentially aberrant α4β2* nAChR availability in the key brain regions that regulate feeding behavior merit further exploration. |
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spelling | doaj.art-259b9b4dd35145d8812af1d0427790372023-11-24T13:39:20ZengMDPI AGBrain Sciences2076-34252022-12-011212164810.3390/brainsci12121648Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human ObesityEva Schweickert de Palma0Tilman Günnewig1Michael Rullmann2Julia Luthardt3Mohammed K. Hankir4Philipp M. Meyer5Georg-Alexander Becker6Marianne Patt7Sarah Martin8Anja Hilbert9Matthias Blüher10Osama Sabri11Swen Hesse12Department of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of General, Visceral, Transplantation, Vascular and Pediatric Surgery, University Hospital Wuerzburg, 97080 Wuerzburg, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyIntegrated Research and Treatment Center Adiposity Diseases, Leipzig University Medical Centre, 04103 Leipzig, GermanyDepartment of Psychosomatic Medicine and Psychotherapy, Integrated Research and Treatment Center Adiposity Diseases, Behavioral Medicine Research Unit, University of Leipzig Medical Center, 04103 Leipzig, GermanyHelmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, 04103 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyDepartment of Nuclear Medicine, University of Leipzig, 04013 Leipzig, GermanyPurpose: Obesity is thought to arise, in part, from deficits in the inhibitory control over appetitive behavior. Such motivational processes are regulated by neuromodulators, specifically acetylcholine (ACh), via α4β2* nicotinic ACh receptors (nAChR). These nAChR are highly enriched in the thalamus and contribute to the thalamic gating of cortico-striatal signaling, but also act on the mesoaccumbal reward system. The changes in α4β2* nAChR availability, however, have not been demonstrated in human obesity thus far. The aim of our study was, thus, to investigate whether there is altered brain α4β2* nAChR availability in individuals with obesity compared to normal-weight healthy controls. Methods: We studied 15 non-smoking individuals with obesity (body mass index, BMI: 37.8 ± 3.1 kg/m<sup>2</sup>; age: 39 ± 14 years, 9 females) and 16 normal-weight controls (non-smokers, BMI: 21.9 ± 1.7 kg/m<sup>2</sup>; age: 28 ± 7 years, 13 females) by using PET and the α4β2* nAChR selective (−)-[<sup>18</sup>F]flubatine, which was applied within a bolus-infusion protocol (294 ± 16 MBq). Volume-of-interest (VOI) analysis was performed in order to calculate the regional total distribution volume (V<sub>T</sub>). Results: No overall significant difference in V<sub>T</sub> between the individuals with obesity and the normal-weight volunteers was found, while the V<sub>T</sub> in the nucleus basalis of Meynert tended to be lower in the individuals with obesity (10.1 ± 2.1 versus 11.9 ± 2.2; <i>p</i> = 0.10), and the V<sub>T</sub> in the thalamus showed a tendency towards higher values in the individuals with obesity (26.5 ± 2.5 versus 25.9 ± 4.2; <i>p</i> = 0.09). Conclusion: While these first data do not show greater brain α4β2* nAChR availability in human obesity overall, the findings of potentially aberrant α4β2* nAChR availability in the key brain regions that regulate feeding behavior merit further exploration.https://www.mdpi.com/2076-3425/12/12/1648obesityPETacetylcholinenicotinic receptors(−)-[<sup>18</sup>F]flubatinenucleus basalis of Meynert |
spellingShingle | Eva Schweickert de Palma Tilman Günnewig Michael Rullmann Julia Luthardt Mohammed K. Hankir Philipp M. Meyer Georg-Alexander Becker Marianne Patt Sarah Martin Anja Hilbert Matthias Blüher Osama Sabri Swen Hesse Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity Brain Sciences obesity PET acetylcholine nicotinic receptors (−)-[<sup>18</sup>F]flubatine nucleus basalis of Meynert |
title | Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity |
title_full | Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity |
title_fullStr | Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity |
title_full_unstemmed | Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity |
title_short | Availability of Central α4β2* Nicotinic Acetylcholine Receptors in Human Obesity |
title_sort | availability of central α4β2 nicotinic acetylcholine receptors in human obesity |
topic | obesity PET acetylcholine nicotinic receptors (−)-[<sup>18</sup>F]flubatine nucleus basalis of Meynert |
url | https://www.mdpi.com/2076-3425/12/12/1648 |
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