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Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes
Glucagon is historically described as the counterregulatory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through action mediated in the liver. However, it is becoming clear that the biology of glucagon is much more complex and extends beyond hepatic actions to exert con...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Diabetes Association
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7085250/ https://www.ncbi.nlm.nih.gov/pubmed/31178432 http://dx.doi.org/10.2337/dbi19-0004 |
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author | Finan, Brian Capozzi, Megan E. Campbell, Jonathan E. |
author_facet | Finan, Brian Capozzi, Megan E. Campbell, Jonathan E. |
author_sort | Finan, Brian |
collection | PubMed |
description | Glucagon is historically described as the counterregulatory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through action mediated in the liver. However, it is becoming clear that the biology of glucagon is much more complex and extends beyond hepatic actions to exert control on glucose metabolism. We discuss the inconsistencies with the canonical view that glucagon is primarily a hyperglycemic agent driven by fasting/hypoglycemia and highlight the recent advances that have reshaped the metabolic role of glucagon. These concepts are placed within the context of both normal physiology and the pathophysiology of disease and then extended to discuss emerging strategies that incorporate glucagon agonism in the pharmacology of treating diabetes. |
format | Online Article Text |
id | pubmed-7085250 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | American Diabetes Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-70852502021-04-01 Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes Finan, Brian Capozzi, Megan E. Campbell, Jonathan E. Diabetes Diabetes Symposium Glucagon is historically described as the counterregulatory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through action mediated in the liver. However, it is becoming clear that the biology of glucagon is much more complex and extends beyond hepatic actions to exert control on glucose metabolism. We discuss the inconsistencies with the canonical view that glucagon is primarily a hyperglycemic agent driven by fasting/hypoglycemia and highlight the recent advances that have reshaped the metabolic role of glucagon. These concepts are placed within the context of both normal physiology and the pathophysiology of disease and then extended to discuss emerging strategies that incorporate glucagon agonism in the pharmacology of treating diabetes. American Diabetes Association 2020-04 2019-06-09 /pmc/articles/PMC7085250/ /pubmed/31178432 http://dx.doi.org/10.2337/dbi19-0004 Text en © 2019 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at https://www.diabetesjournals.org/content/license. |
spellingShingle | Diabetes Symposium Finan, Brian Capozzi, Megan E. Campbell, Jonathan E. Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title | Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title_full | Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title_fullStr | Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title_full_unstemmed | Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title_short | Repositioning Glucagon Action in the Physiology and Pharmacology of Diabetes |
title_sort | repositioning glucagon action in the physiology and pharmacology of diabetes |
topic | Diabetes Symposium |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7085250/ https://www.ncbi.nlm.nih.gov/pubmed/31178432 http://dx.doi.org/10.2337/dbi19-0004 |
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