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The brain's supply and demand in obesity
During psychosocial stress, the brain demands extra energy from the body to satisfy its increased needs. For that purpose it uses a mechanism referred to as “cerebral insulin suppression” (CIS). Specifically, activation of the stress system suppresses insulin secretion from pancreatic beta-cells, an...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297086/ https://www.ncbi.nlm.nih.gov/pubmed/22408618 http://dx.doi.org/10.3389/fnene.2012.00004 |
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author | Kubera, Britta Hubold, Christian Zug, Sophia Wischnath, Hannah Wilhelm, Ines Hallschmid, Manfred Entringer, Sonja Langemann, Dirk Peters, Achim |
author_facet | Kubera, Britta Hubold, Christian Zug, Sophia Wischnath, Hannah Wilhelm, Ines Hallschmid, Manfred Entringer, Sonja Langemann, Dirk Peters, Achim |
author_sort | Kubera, Britta |
collection | PubMed |
description | During psychosocial stress, the brain demands extra energy from the body to satisfy its increased needs. For that purpose it uses a mechanism referred to as “cerebral insulin suppression” (CIS). Specifically, activation of the stress system suppresses insulin secretion from pancreatic beta-cells, and in this way energy—particularly glucose—is allocated to the brain rather than the periphery. It is unknown, however, how the brain of obese humans organizes its supply and demand during psychosocial stress. To answer this question, we examined 20 obese and 20 normal weight men in two sessions (Trier Social Stress Test and non-stress control condition followed by either a rich buffet or a meager salad). Blood samples were continuously taken and subjects rated their vigilance and mood by standard questionnaires. First, we found a low reactive stress system in obesity. While obese subjects showed a marked hormonal response to the psychosocial challenge, the cortisol response to the subsequent meal was absent. Whereas the brains of normal weight subjects demanded for extra energy from the body by using CIS, CIS was not detectable in obese subjects. Our findings suggest that the absence of CIS in obese subjects is due to the absence of their meal-related cortisol peak. Second, normal weight men were high reactive during psychosocial stress in changing their vigilance, thereby increasing their cerebral energy need, whereas obese men were low reactive in this respect. Third, normal weight subjects preferred carbohydrates after stress to supply their brain, while obese men preferred fat and protein instead. We conclude that the brain of obese people organizes its need, supply, and demand in a low reactive manner. |
format | Online Article Text |
id | pubmed-3297086 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-32970862012-03-09 The brain's supply and demand in obesity Kubera, Britta Hubold, Christian Zug, Sophia Wischnath, Hannah Wilhelm, Ines Hallschmid, Manfred Entringer, Sonja Langemann, Dirk Peters, Achim Front Neuroenergetics Neuroscience During psychosocial stress, the brain demands extra energy from the body to satisfy its increased needs. For that purpose it uses a mechanism referred to as “cerebral insulin suppression” (CIS). Specifically, activation of the stress system suppresses insulin secretion from pancreatic beta-cells, and in this way energy—particularly glucose—is allocated to the brain rather than the periphery. It is unknown, however, how the brain of obese humans organizes its supply and demand during psychosocial stress. To answer this question, we examined 20 obese and 20 normal weight men in two sessions (Trier Social Stress Test and non-stress control condition followed by either a rich buffet or a meager salad). Blood samples were continuously taken and subjects rated their vigilance and mood by standard questionnaires. First, we found a low reactive stress system in obesity. While obese subjects showed a marked hormonal response to the psychosocial challenge, the cortisol response to the subsequent meal was absent. Whereas the brains of normal weight subjects demanded for extra energy from the body by using CIS, CIS was not detectable in obese subjects. Our findings suggest that the absence of CIS in obese subjects is due to the absence of their meal-related cortisol peak. Second, normal weight men were high reactive during psychosocial stress in changing their vigilance, thereby increasing their cerebral energy need, whereas obese men were low reactive in this respect. Third, normal weight subjects preferred carbohydrates after stress to supply their brain, while obese men preferred fat and protein instead. We conclude that the brain of obese people organizes its need, supply, and demand in a low reactive manner. Frontiers Media S.A. 2012-03-08 /pmc/articles/PMC3297086/ /pubmed/22408618 http://dx.doi.org/10.3389/fnene.2012.00004 Text en Copyright © 2012 Kubera, Hubold, Zug, Wischnath, Wilhelm, Hallschmid, Entringer, Langemann and Peters. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
spellingShingle | Neuroscience Kubera, Britta Hubold, Christian Zug, Sophia Wischnath, Hannah Wilhelm, Ines Hallschmid, Manfred Entringer, Sonja Langemann, Dirk Peters, Achim The brain's supply and demand in obesity |
title | The brain's supply and demand in obesity |
title_full | The brain's supply and demand in obesity |
title_fullStr | The brain's supply and demand in obesity |
title_full_unstemmed | The brain's supply and demand in obesity |
title_short | The brain's supply and demand in obesity |
title_sort | brain's supply and demand in obesity |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297086/ https://www.ncbi.nlm.nih.gov/pubmed/22408618 http://dx.doi.org/10.3389/fnene.2012.00004 |
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