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Neurohumoral stimulation in type-2-diabetes as an emerging disease concept
Neurohumoral stimulation comprising both autonomic-nervous-system dysfunction and activation of hormonal systems including the renin-angiotensin-aldosterone system (RAAS) was found to be associated with Type-2-diabetes (T2D). Therapeutic strategies such as RAAS interference proved to be beneficial i...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2004
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC406517/ https://www.ncbi.nlm.nih.gov/pubmed/15028121 http://dx.doi.org/10.1186/1475-2840-3-4 |
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author | Pliquett, RU Fasshauer, M Blüher, M Paschke, R |
author_facet | Pliquett, RU Fasshauer, M Blüher, M Paschke, R |
author_sort | Pliquett, RU |
collection | PubMed |
description | Neurohumoral stimulation comprising both autonomic-nervous-system dysfunction and activation of hormonal systems including the renin-angiotensin-aldosterone system (RAAS) was found to be associated with Type-2-diabetes (T2D). Therapeutic strategies such as RAAS interference proved to be beneficial in both T2D treatment and prevention. In addition to an activated RAAS, hyperleptinemia in obesity, hyperinsulinemia in conditions of peripheral insulin resistance and overall oxidative stress in T2D represent known activators of the sympathetic component of the autonomic nervous system. Here, we hypothesize that sympathetic activation may cause peripheral insulin resistance defined as partial blocking of insulin effects on glucose uptake. Resulting hyperinsulinemia or hyperglycemia-related oxidative stress may further aggravate sympatho-excitation. This notion leads to a secondary hypothesis: sympathetic activation worsens from obesity towards insulin resistance, and further towards T2D. In this review, existing evidence relating to neurohumoral stimulation in T2D and consequences thereof, such as oxidative stress and inflammation, are discussed. The aim of this review is to provide a rationale for therapies, which are able to intercept neuroendocrine pathways in T2D and precursor states such as obesity. |
format | Text |
id | pubmed-406517 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2004 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-4065172004-05-13 Neurohumoral stimulation in type-2-diabetes as an emerging disease concept Pliquett, RU Fasshauer, M Blüher, M Paschke, R Cardiovasc Diabetol Hypothesis Neurohumoral stimulation comprising both autonomic-nervous-system dysfunction and activation of hormonal systems including the renin-angiotensin-aldosterone system (RAAS) was found to be associated with Type-2-diabetes (T2D). Therapeutic strategies such as RAAS interference proved to be beneficial in both T2D treatment and prevention. In addition to an activated RAAS, hyperleptinemia in obesity, hyperinsulinemia in conditions of peripheral insulin resistance and overall oxidative stress in T2D represent known activators of the sympathetic component of the autonomic nervous system. Here, we hypothesize that sympathetic activation may cause peripheral insulin resistance defined as partial blocking of insulin effects on glucose uptake. Resulting hyperinsulinemia or hyperglycemia-related oxidative stress may further aggravate sympatho-excitation. This notion leads to a secondary hypothesis: sympathetic activation worsens from obesity towards insulin resistance, and further towards T2D. In this review, existing evidence relating to neurohumoral stimulation in T2D and consequences thereof, such as oxidative stress and inflammation, are discussed. The aim of this review is to provide a rationale for therapies, which are able to intercept neuroendocrine pathways in T2D and precursor states such as obesity. BioMed Central 2004-03-17 /pmc/articles/PMC406517/ /pubmed/15028121 http://dx.doi.org/10.1186/1475-2840-3-4 Text en Copyright © 2004 Pliquett et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. |
spellingShingle | Hypothesis Pliquett, RU Fasshauer, M Blüher, M Paschke, R Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title | Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title_full | Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title_fullStr | Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title_full_unstemmed | Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title_short | Neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
title_sort | neurohumoral stimulation in type-2-diabetes as an emerging disease concept |
topic | Hypothesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC406517/ https://www.ncbi.nlm.nih.gov/pubmed/15028121 http://dx.doi.org/10.1186/1475-2840-3-4 |
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