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The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets

Joshua Reed, Steve Bain Orcid Logo, Venkat Kanamarlapudi Orcid Logo

Diabetes, Metabolic Syndrome and Obesity, Volume: 17, Pages: 2419 - 2456

Swansea University Authors: Steve Bain Orcid Logo, Venkat Kanamarlapudi Orcid Logo

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DOI (Published version): 10.2147/dmso.s415934

Abstract

In healthy humans, the complex biochemical interplay between organs maintains metabolic homeostasis and pathological alterations in this process result in impaired metabolic homeostasis, causing metabolic diseases such as diabetes and obesity, which are major global healthcare burdens. The great adv...

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Published in: Diabetes, Metabolic Syndrome and Obesity
ISSN: 1178-7007
Published: Informa UK Limited 2024
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URI: https://cronfa.swan.ac.uk/Record/cronfa66737
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The great advancements made during the last century in understanding both metabolic disease phenotypes and the regulation of metabolic homeostasis in healthy individuals have yielded new therapeutic options for diseases like type 2 diabetes (T2D). However, it is unlikely that highly desirable more efficacious treatments will be developed for metabolic disorders until the complex systemic regulation of metabolic homeostasis becomes more intricately understood. Hormones produced by pancreatic islet beta-cells (insulin) and alpha-cells (glucagon) are pivotal for maintaining metabolic homeostasis; the activity of insulin and glucagon are reciprocally correlated to achieve strict control of glucose levels (normoglycaemia). Metabolic hormones produced by other pancreatic islet cells and incretins produced by the gut are also crucial for maintaining metabolic homeostasis. Recent studies highlighted the incomplete understanding of metabolic hormonal synergism and, therefore, further elucidation of this will likely lead to more efficacious treatments for diseases such as T2D. 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spelling v2 66737 2024-06-14 The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets 5399f4c6e6a70f3608a084ddb938511a 0000-0001-8519-4964 Steve Bain Steve Bain true false 63741801137148abfa4c00cd547dcdfa 0000-0002-8739-1483 Venkat Kanamarlapudi Venkat Kanamarlapudi true false 2024-06-14 MEDS In healthy humans, the complex biochemical interplay between organs maintains metabolic homeostasis and pathological alterations in this process result in impaired metabolic homeostasis, causing metabolic diseases such as diabetes and obesity, which are major global healthcare burdens. The great advancements made during the last century in understanding both metabolic disease phenotypes and the regulation of metabolic homeostasis in healthy individuals have yielded new therapeutic options for diseases like type 2 diabetes (T2D). However, it is unlikely that highly desirable more efficacious treatments will be developed for metabolic disorders until the complex systemic regulation of metabolic homeostasis becomes more intricately understood. Hormones produced by pancreatic islet beta-cells (insulin) and alpha-cells (glucagon) are pivotal for maintaining metabolic homeostasis; the activity of insulin and glucagon are reciprocally correlated to achieve strict control of glucose levels (normoglycaemia). Metabolic hormones produced by other pancreatic islet cells and incretins produced by the gut are also crucial for maintaining metabolic homeostasis. Recent studies highlighted the incomplete understanding of metabolic hormonal synergism and, therefore, further elucidation of this will likely lead to more efficacious treatments for diseases such as T2D. The objective of this review is to summarise the systemic actions of the incretins and the metabolic hormones produced by the pancreatic islets and their interactions with their respective receptors. Journal Article Diabetes, Metabolic Syndrome and Obesity 17 2419 2456 Informa UK Limited 1178-7007 type 2 diabetes, obesity, insulin, glucagon, GLP-1, GLP-1R, incretin, metabolism 13 6 2024 2024-06-13 10.2147/dmso.s415934 COLLEGE NANME Medical School COLLEGE CODE MEDS Swansea University External research funder(s) paid the OA fee (includes OA grants disbursed by the Library) The work in VK’s laboratory was supported by a grant from the Biotechnology and Biological Sciences Research Council (BBSRC) UK (BB/S019588/1). JR was a recipient of the Knowledge Economy Skills Scholarship (KESS) II UK PhD studentship. We thank the members of the VK laboratory. 2024-11-04T11:49:28.4329547 2024-06-14T17:23:46.3906945 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Joshua Reed 1 Steve Bain 0000-0001-8519-4964 2 Venkat Kanamarlapudi 0000-0002-8739-1483 3 66737__30948__dc4aeb022a4a46b894e5392d55da0ee0.pdf 66737.VoR.pdf 2024-07-23T14:17:50.4774449 Output 10317151 application/pdf Version of Record true © 2024 Reed et al. This work is published by Dove Medical Press Limited, and licensed under a Creative Commons Attribution License. true eng http://creativecommons.org/licenses/by/4.0/
title The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
spellingShingle The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
Steve Bain
Venkat Kanamarlapudi
title_short The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
title_full The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
title_fullStr The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
title_full_unstemmed The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
title_sort The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets
author_id_str_mv 5399f4c6e6a70f3608a084ddb938511a
63741801137148abfa4c00cd547dcdfa
author_id_fullname_str_mv 5399f4c6e6a70f3608a084ddb938511a_***_Steve Bain
63741801137148abfa4c00cd547dcdfa_***_Venkat Kanamarlapudi
author Steve Bain
Venkat Kanamarlapudi
author2 Joshua Reed
Steve Bain
Venkat Kanamarlapudi
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container_title Diabetes, Metabolic Syndrome and Obesity
container_volume 17
container_start_page 2419
publishDate 2024
institution Swansea University
issn 1178-7007
doi_str_mv 10.2147/dmso.s415934
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department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
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description In healthy humans, the complex biochemical interplay between organs maintains metabolic homeostasis and pathological alterations in this process result in impaired metabolic homeostasis, causing metabolic diseases such as diabetes and obesity, which are major global healthcare burdens. The great advancements made during the last century in understanding both metabolic disease phenotypes and the regulation of metabolic homeostasis in healthy individuals have yielded new therapeutic options for diseases like type 2 diabetes (T2D). However, it is unlikely that highly desirable more efficacious treatments will be developed for metabolic disorders until the complex systemic regulation of metabolic homeostasis becomes more intricately understood. Hormones produced by pancreatic islet beta-cells (insulin) and alpha-cells (glucagon) are pivotal for maintaining metabolic homeostasis; the activity of insulin and glucagon are reciprocally correlated to achieve strict control of glucose levels (normoglycaemia). Metabolic hormones produced by other pancreatic islet cells and incretins produced by the gut are also crucial for maintaining metabolic homeostasis. Recent studies highlighted the incomplete understanding of metabolic hormonal synergism and, therefore, further elucidation of this will likely lead to more efficacious treatments for diseases such as T2D. The objective of this review is to summarise the systemic actions of the incretins and the metabolic hormones produced by the pancreatic islets and their interactions with their respective receptors.
published_date 2024-06-13T11:49:27Z
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