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Anti-inflammatory Effects of Glucagon-Like Peptide-1
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Anti-inflammatory Effects of Glucagon-Like Peptide-1

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Macromolecules".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 27743

Special Issue Editors

Dr. Alessandra Puddu

E-Mail Website
Guest Editor
Department of Internal Medicine and Medical Specialties, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy
Interests: diabetes; retinopathy; VEGF-A; IGF-1; advanced glycation end-products
Special Issues, Collections and Topics in MDPI journals
Dr. Davide Maggi

E-Mail Website
Guest Editor
Department of Internal Medicine and Medical Specialties, University of Genova, 16132 Genova, Italy
Interests: the role of caveoles in the insulin and IGF1 signal; new technologies in the treatment of diabetes mellitus; role of bariatric surgery in the regulation of metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glucagon-like peptide-1 (GLP-1) is an incretin hormone which regulates glucose homeostasis and is mainly produced by intestinal epithelial endocrine L cells. The use of GLP-1 analogous, GLP-1 receptor (GLP-1R) agonists, as well as dipeptidyl peptidase-IV (DPP-IV) inhibitors, is well established in the treatment of type 2 diabetes. GLP-1R is widely expressed in several tissues, and therapies based on GLP-1 are of great clinical interest not only regarding its effects at the level of the beta cells, but also the biological actions exerted in other tissues. Among them, anti-inflammatory activity seems to be a common mechanism through which these therapies achieve beneficial effects.

The focus of this Special Issue is any aspect of pancreatic and extra-pancreatic anti-inflammatory effects of GLP-1. The implication not only for diabetes, but also for other diseases is of particular interest.

Dr. Alessandra Puddu
Dr. Davide Maggi
Guest Editors

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Keywords

  • GLP-1
  • diabetes
  • inflammation
  • diabetic complications
  • extra-pancreatic effects of GLP-1
  • molecular mechanisms

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Published Papers (6 papers)

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Editorial

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4 pages, 181 KiB  
Editorial
Special Issue: “Anti-inflammatory Effects of Glucagon-like Peptide-1”
by Alessandra Puddu and Davide Maggi
Int. J. Mol. Sci. 2024, 25(4), 1997; https://doi.org/10.3390/ijms25041997 - 7 Feb 2024
Viewed by 1522
Abstract
From the failure of gut extracts in diabetic patients’ therapy to the effective action in cardiovascular outcomes [...] Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)

Research

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10 pages, 1781 KiB  
Article
Effects of Semaglutide and Empagliflozin on Inflammatory Markers in Patients with Type 2 Diabetes
by Ingrid Reppo, Maili Jakobson and Vallo Volke
Int. J. Mol. Sci. 2023, 24(6), 5714; https://doi.org/10.3390/ijms24065714 - 16 Mar 2023
Cited by 6 | Viewed by 3358
Abstract
Low-grade inflammation is associated with complications of type 2 diabetes. Glucagon-like peptide-1 receptor agonists and sodium-glucose transporter-2 inhibitors have shown cardioprotective effects that are independent of their glucose-lowering effects. Cardio-protection could be mediated by the anti-inflammatory effects of these medications, but there is [...] Read more.
Low-grade inflammation is associated with complications of type 2 diabetes. Glucagon-like peptide-1 receptor agonists and sodium-glucose transporter-2 inhibitors have shown cardioprotective effects that are independent of their glucose-lowering effects. Cardio-protection could be mediated by the anti-inflammatory effects of these medications, but there is currently limited evidence to support this hypothesis. We conducted a prospective clinical study in patients with type 2 diabetes requiring treatment intensification. Ten patients were assigned to receive empagliflozin 10 mg and 10 patients to receive s/c semaglutide (titrated to 1 mg once a week) in a non-randomised manner. All parameters were measured at baseline and after 3 months. Fasting plasma glucose and glycated haemoglobin improved significantly in both treatment groups, with no between-group differences. Body weight and body mass index reduced significantly more in the semaglutide group, whereas waist circumference decreased only in the empagliflozin group. There was a trend for high-sensitivity CRP reduction in both treatment groups that did not reach statistical significance. Interleukin-6 and the neutrophil-to-lymphocyte ratio did not change in either group. Ferritin and uric acid decreased significantly only in the empagliflozin group, and ceruloplasmin decreased significantly only in the semaglutide group. Though there were clinically meaningful improvements in diabetes control in both treatment arms, we could detect only minor changes in some inflammatory markers. Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)
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12 pages, 2087 KiB  
Article
Isosinensetin Stimulates Glucagon-like Peptide-1 Secretion via Activation of hTAS2R50 and the Gβγ-Mediated Signaling Pathway
by Seung-Hyeon Lee, Hyun Min Ko, Wona Jee, Hyungsuk Kim, Won-Seok Chung and Hyeung-Jin Jang
Int. J. Mol. Sci. 2023, 24(4), 3682; https://doi.org/10.3390/ijms24043682 - 12 Feb 2023
Cited by 4 | Viewed by 3027
Abstract
Bitter taste receptors (TAS2Rs) are G protein-coupled receptors localized in the taste buds of the tongue. They may also be present in non-lingual organs, including the brain, lung, kidney, and gastrointestinal (GI) tract. Recent studies on bitter taste receptor functions have suggested TAS2Rs [...] Read more.
Bitter taste receptors (TAS2Rs) are G protein-coupled receptors localized in the taste buds of the tongue. They may also be present in non-lingual organs, including the brain, lung, kidney, and gastrointestinal (GI) tract. Recent studies on bitter taste receptor functions have suggested TAS2Rs as potential therapeutic targets. The human bitter taste receptor subtype hTAS2R50 responds to its agonist isosinensetin (ISS). Here, we demonstrated that, unlike other TAS2R agonists, isosinensetin activated hTAS2R50 as well as increased Glucagon-like peptide 1 (GLP-1) secretion through the Gβγ-mediated pathway in NCI-H716 cells. To confirm this mechanism, we showed that ISS increased intracellular Ca2+ and was suppressed by the IP3R inhibitor 2-APB as well as the PLC inhibitor U73122, suggesting that TAS2Rs alters the physiological state of enteroendocrine L cells in a PLC-dependent manner. Furthermore, we demonstrated that ISS upregulated proglucagon mRNA and stimulated GLP-1 secretion. ISS-mediated GLP-1 secretion was suppressed in response to small interfering RNA-mediated silencing of Gα-gust and hTAS2R50 as well as 2-APB and U73122. Our findings improved the understanding of how ISS modulates GLP-1 secretion and indicates the possibility of using ISS as a therapeutic agent in the treatment of diabetes mellitus. Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)
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Review

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19 pages, 504 KiB  
Review
Potential Role of Glucagon-like Peptide-1 Receptor Agonists in the Treatment of Cognitive Decline and Dementia in Diabetes Mellitus
by Maria Chiara Pelle, Isabella Zaffina, Federica Giofrè, Roberta Pujia and Franco Arturi
Int. J. Mol. Sci. 2023, 24(14), 11301; https://doi.org/10.3390/ijms241411301 - 11 Jul 2023
Cited by 16 | Viewed by 3843
Abstract
Dementia is a permanent illness characterized by mental instability, memory loss, and cognitive decline. Many studies have demonstrated an association between diabetes and cognitive dysfunction that proceeds in three steps, namely, diabetes-associated cognitive decrements, mild cognitive impairment (MCI; both non-amnesic MCI and amnesic [...] Read more.
Dementia is a permanent illness characterized by mental instability, memory loss, and cognitive decline. Many studies have demonstrated an association between diabetes and cognitive dysfunction that proceeds in three steps, namely, diabetes-associated cognitive decrements, mild cognitive impairment (MCI; both non-amnesic MCI and amnesic MCI), and dementia [both vascular dementia and Alzheimer’s disease (AD)]. Based on this association, this disease has been designated as type 3 diabetes mellitus. The underlying mechanisms comprise insulin resistance, inflammation, lipid abnormalities, oxidative stress, mitochondrial dysfunction, glycated end-products and autophagy. Moreover, insulin and insulin-like growth factor-1 (IGF-1) have been demonstrated to be involved. Insulin in the brain has a neuroprotective role that alters cognitive skills and alteration of insulin signaling determines beta-amyloid (Aβ) accumulation, in turn promoting brain insulin resistance. In this complex mechanism, other triggers include hyperglycemia-induced overproduction of reactive oxygen species (ROS) and inflammatory cytokines, which result in neuroinflammation, suggesting that antidiabetic drugs may be potential treatments to protect against AD. Among these, glucagon-like peptide-1 receptor agonists (GLP-1RAs) are the most attractive antidiabetic drugs due to their actions on synaptic plasticity, cognition and cell survival. The present review summarizes the significant data concerning the underlying pathophysiological and pharmacological mechanisms between diabetes and dementia. Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)
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13 pages, 567 KiB  
Review
Anti-Inflammatory Effects of GLP-1R Activation in the Retina
by Alessandra Puddu and Davide Maggi
Int. J. Mol. Sci. 2022, 23(20), 12428; https://doi.org/10.3390/ijms232012428 - 17 Oct 2022
Cited by 5 | Viewed by 2987
Abstract
Glucagon-like peptide-1 (GLP-1) is an incretin hormone, mainly produced by enteroendocrine L cells, which participates in the regulation of glucose homeostasis, and in reduction in body weight by promoting satiety. Actions of GLP-1 are mediated by activation of its receptor GLP-1R, which is [...] Read more.
Glucagon-like peptide-1 (GLP-1) is an incretin hormone, mainly produced by enteroendocrine L cells, which participates in the regulation of glucose homeostasis, and in reduction in body weight by promoting satiety. Actions of GLP-1 are mediated by activation of its receptor GLP-1R, which is widely expressed in several tissues including the retina. The effects of GLP-1R activation are useful in the management of type 2 diabetes mellitus (T2DM). In addition, the activation of GLP-1R has anti-inflammatory effects in several organs, suggesting that it may be also useful in the treatment of inflammatory diseases. Inflammation is a common element in the pathogenesis of several ocular diseases, and the protective effects of treatment with GLP-1 emerged also in retinal diseases. In this review we highlight the anti-inflammatory effects of GLP-1R activation in the retina. Firstly, we summarized the pathogenic role of inflammation in ocular diseases. Then, we described the pleiotropic effects of GLP-1R activation on the cellular components of the retina which are mainly involved in the pathogenesis of inflammatory retinal diseases: the retinal ganglion cells, retinal pigment epithelial cells and endothelial cells. Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)
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24 pages, 1689 KiB  
Review
Anti-Inflammatory Effects of GLP-1 Receptor Activation in the Brain in Neurodegenerative Diseases
by Yolanda Diz-Chaves, Zainab Mastoor, Carlos Spuch, Lucas C. González-Matías and Federico Mallo
Int. J. Mol. Sci. 2022, 23(17), 9583; https://doi.org/10.3390/ijms23179583 - 24 Aug 2022
Cited by 27 | Viewed by 12149
Abstract
The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. However, GLP-1 is also produced in the brain and displays a critical role in neuroprotection and inflammation by activating the GLP-1 receptor [...] Read more.
The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. However, GLP-1 is also produced in the brain and displays a critical role in neuroprotection and inflammation by activating the GLP-1 receptor signaling pathways. Several studies in vivo and in vitro using preclinical models of neurodegenerative diseases show that GLP-1R activation has anti-inflammatory properties. This review explores the molecular mechanistic action of GLP-1 RAS in relation to inflammation in the brain. These findings update our knowledge of the potential benefits of GLP-1RAS actions in reducing the inflammatory response. These molecules emerge as a potential therapeutic tool in treating neurodegenerative diseases and neuroinflammatory pathologies. Full article
(This article belongs to the Special Issue Anti-inflammatory Effects of Glucagon-Like Peptide-1)
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