Cargando…

Brain–gut–adipose-tissue communication pathways at a glance

One of the ‘side effects’ of our modern lifestyle is a range of metabolic diseases: the incidence of obesity, type 2 diabetes and associated cardiovascular diseases has grown to pandemic proportions. This increase, which shows no sign of reversing course, has occurred despite education and new treat...

Descripción completa

Detalles Bibliográficos
Autores principales: Yi, Chun-Xia, Tschöp, Matthias H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Company of Biologists Limited 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3424454/
https://www.ncbi.nlm.nih.gov/pubmed/22915019
http://dx.doi.org/10.1242/dmm.009902
_version_ 1782241215332220928
author Yi, Chun-Xia
Tschöp, Matthias H.
author_facet Yi, Chun-Xia
Tschöp, Matthias H.
author_sort Yi, Chun-Xia
collection PubMed
description One of the ‘side effects’ of our modern lifestyle is a range of metabolic diseases: the incidence of obesity, type 2 diabetes and associated cardiovascular diseases has grown to pandemic proportions. This increase, which shows no sign of reversing course, has occurred despite education and new treatment options, and is largely due to a lack of knowledge about the precise pathology and etiology of metabolic disorders. Accumulating evidence suggests that the communication pathways linking the brain, gut and adipose tissue might be promising intervention points for metabolic disorders. To maintain energy homeostasis, the brain must tightly monitor the peripheral energy state. This monitoring is also extremely important for the brain’s survival, because the brain does not store energy but depends solely on a continuous supply of nutrients from the general circulation. Two major groups of metabolic inputs inform the brain about the peripheral energy state: short-term signals produced by the gut system and long-term signals produced by adipose tissue. After central integration of these inputs, the brain generates neuronal and hormonal outputs to balance energy intake with expenditure. Miscommunication between the gut, brain and adipose tissue, or the degradation of input signals once inside the brain, lead to the brain misunderstanding the peripheral energy state. Under certain circumstances, the brain responds to this miscommunication by increasing energy intake and production, eventually causing metabolic disorders. This poster article overviews current knowledge about communication pathways between the brain, gut and adipose tissue, and discusses potential research directions that might lead to a better understanding of the mechanisms underlying metabolic disorders.
format Online
Article
Text
id pubmed-3424454
institution National Center for Biotechnology Information
language English
publishDate 2012
publisher The Company of Biologists Limited
record_format MEDLINE/PubMed
spelling pubmed-34244542012-09-01 Brain–gut–adipose-tissue communication pathways at a glance Yi, Chun-Xia Tschöp, Matthias H. Dis Model Mech At a Glance One of the ‘side effects’ of our modern lifestyle is a range of metabolic diseases: the incidence of obesity, type 2 diabetes and associated cardiovascular diseases has grown to pandemic proportions. This increase, which shows no sign of reversing course, has occurred despite education and new treatment options, and is largely due to a lack of knowledge about the precise pathology and etiology of metabolic disorders. Accumulating evidence suggests that the communication pathways linking the brain, gut and adipose tissue might be promising intervention points for metabolic disorders. To maintain energy homeostasis, the brain must tightly monitor the peripheral energy state. This monitoring is also extremely important for the brain’s survival, because the brain does not store energy but depends solely on a continuous supply of nutrients from the general circulation. Two major groups of metabolic inputs inform the brain about the peripheral energy state: short-term signals produced by the gut system and long-term signals produced by adipose tissue. After central integration of these inputs, the brain generates neuronal and hormonal outputs to balance energy intake with expenditure. Miscommunication between the gut, brain and adipose tissue, or the degradation of input signals once inside the brain, lead to the brain misunderstanding the peripheral energy state. Under certain circumstances, the brain responds to this miscommunication by increasing energy intake and production, eventually causing metabolic disorders. This poster article overviews current knowledge about communication pathways between the brain, gut and adipose tissue, and discusses potential research directions that might lead to a better understanding of the mechanisms underlying metabolic disorders. The Company of Biologists Limited 2012-09 /pmc/articles/PMC3424454/ /pubmed/22915019 http://dx.doi.org/10.1242/dmm.009902 Text en © 2012. Published by The Company of Biologists Ltd This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
spellingShingle At a Glance
Yi, Chun-Xia
Tschöp, Matthias H.
Brain–gut–adipose-tissue communication pathways at a glance
title Brain–gut–adipose-tissue communication pathways at a glance
title_full Brain–gut–adipose-tissue communication pathways at a glance
title_fullStr Brain–gut–adipose-tissue communication pathways at a glance
title_full_unstemmed Brain–gut–adipose-tissue communication pathways at a glance
title_short Brain–gut–adipose-tissue communication pathways at a glance
title_sort brain–gut–adipose-tissue communication pathways at a glance
topic At a Glance
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3424454/
https://www.ncbi.nlm.nih.gov/pubmed/22915019
http://dx.doi.org/10.1242/dmm.009902
work_keys_str_mv AT yichunxia braingutadiposetissuecommunicationpathwaysataglance
AT tschopmatthiash braingutadiposetissuecommunicationpathwaysataglance