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The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents
During type 1 diabetes, an autoimmune attack destroys pancreatic β-cells leading to the inability to maintain glucose homeostasis. These β-cells are neuroresponsive endocrine cells which normally secrete insulin partially in response to input from the vagus nerve. This neural pathway can be utilized...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10309008/ https://www.ncbi.nlm.nih.gov/pubmed/37397461 http://dx.doi.org/10.3389/fnins.2023.1179276 |
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author | Dirr, Elliott W. Patel, Yogi Johnson, Richard D. Otto, Kevin J. |
author_facet | Dirr, Elliott W. Patel, Yogi Johnson, Richard D. Otto, Kevin J. |
author_sort | Dirr, Elliott W. |
collection | PubMed |
description | During type 1 diabetes, an autoimmune attack destroys pancreatic β-cells leading to the inability to maintain glucose homeostasis. These β-cells are neuroresponsive endocrine cells which normally secrete insulin partially in response to input from the vagus nerve. This neural pathway can be utilized as a point of therapeutic intervention by delivering exogenous stimulation to drive increased insulin secretion. In this study, a cuff electrode was implanted on the pancreatic branch of the vagus nerve just prior to pancreatic insertion in rats, and a continuous glucose meter was implanted into the descending aorta. Streptozotocin (STZ) was used to induce a diabetic state, and changes in blood glucose were assessed using various stimulation parameters. Stimulation driven changes in hormone secretion, pancreatic blood flow, and islet cell populations were assessed. We found increased changes in the rate of blood glucose change during stimulation which subsided after stimulation ended paired with increased concentration of circulating insulin. We did not observe increased pancreatic perfusion, which suggests that the modulation of blood glucose was due to the activation of b-cells rather than changes in the extra-organ transport of insulin. Pancreatic neuromodulation showed potentially protective effects by reducing deficits in islet diameter, and ameliorating insulin loss after STZ treatment. |
format | Online Article Text |
id | pubmed-10309008 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103090082023-06-30 The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents Dirr, Elliott W. Patel, Yogi Johnson, Richard D. Otto, Kevin J. Front Neurosci Neuroscience During type 1 diabetes, an autoimmune attack destroys pancreatic β-cells leading to the inability to maintain glucose homeostasis. These β-cells are neuroresponsive endocrine cells which normally secrete insulin partially in response to input from the vagus nerve. This neural pathway can be utilized as a point of therapeutic intervention by delivering exogenous stimulation to drive increased insulin secretion. In this study, a cuff electrode was implanted on the pancreatic branch of the vagus nerve just prior to pancreatic insertion in rats, and a continuous glucose meter was implanted into the descending aorta. Streptozotocin (STZ) was used to induce a diabetic state, and changes in blood glucose were assessed using various stimulation parameters. Stimulation driven changes in hormone secretion, pancreatic blood flow, and islet cell populations were assessed. We found increased changes in the rate of blood glucose change during stimulation which subsided after stimulation ended paired with increased concentration of circulating insulin. We did not observe increased pancreatic perfusion, which suggests that the modulation of blood glucose was due to the activation of b-cells rather than changes in the extra-organ transport of insulin. Pancreatic neuromodulation showed potentially protective effects by reducing deficits in islet diameter, and ameliorating insulin loss after STZ treatment. Frontiers Media S.A. 2023-06-15 /pmc/articles/PMC10309008/ /pubmed/37397461 http://dx.doi.org/10.3389/fnins.2023.1179276 Text en Copyright © 2023 Dirr, Patel, Johnson and Otto. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Dirr, Elliott W. Patel, Yogi Johnson, Richard D. Otto, Kevin J. The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title | The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title_full | The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title_fullStr | The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title_full_unstemmed | The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title_short | The effects of targeted vagus nerve stimulation on glucose homeostasis in STZ-induced diabetic rodents |
title_sort | effects of targeted vagus nerve stimulation on glucose homeostasis in stz-induced diabetic rodents |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10309008/ https://www.ncbi.nlm.nih.gov/pubmed/37397461 http://dx.doi.org/10.3389/fnins.2023.1179276 |
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