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The Roles of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists in Health and Disease

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 25 December 2026 | Viewed by 6528

Editor

Dr. Katarzyna Kaczyńska

E-Mail Website
Guest Editor
Department of Respiration Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5, 02-106 Warsaw, Poland
Interests: obesity- related asthma - mechanisms and contributing factors; GLP-1 in asthma; respiratory disorders in neurodegenerative diseases; neuropeptides and opioids in regulation of breathing; reversal of post-opioid respiratory depression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

GLP-1 is a key endocrine hormone that plays an integral role in regulating blood glucose levels, lipid metabolism, and improving metabolic syndrome. In recent years, GLP-1 therapeutics have attracted the attention of the medical community for their innovative mechanisms of action, remarkable therapeutic efficacy, and great potential for development. I am pleased to invite you to participate in the Special Issue, “The Roles of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists in Health and Disease”. This Special Issue is devoted to the application of GLP-1 receptor agonists (GLP-1RAs) in various physiological and pathophysiological conditions and their effects on multiple body systems, such as the nervous, cardiovascular, musculoskeletal, endocrine, and digestive systems, among others. The role of the GLP-1 receptor in alleviating inflammation, diabetes, and obesity, in neuroprotection and enhancing cardiovascular function, as well as other areas, is welcomed. This Special Issue will collect full articles, communication articles, and review articles covering various aspects of the GLP-1 molecule, such as pathogenesis, molecular pathways, and the beneficial effects of therapy using GLP-1 agonists.

I look forward to receiving your contributions.

Dr. Katarzyna Kaczyńska
Guest Editor

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Keywords

  • GLP-1
  • GLP-1 receptor
  • GLP-1 signaling pathway
  • mechanism of action
  • GLP-1 agonists
  • human diseases
  • adverse effects

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Published Papers (3 papers)

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Research

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20 pages, 2321 KB  
Article
Combination GLP-1RA and Low-Dose IL-2 Modulates Peripheral Immune Activation and Attenuates CNS Inflammatory Transcript Signatures In Vivo
by Aaron D. Thome, Jinghong Wang, Alireza Faridar, Weihua Zhao, Valerie Saetzler, David R. Beers and Stanley H. Appel
Int. J. Mol. Sci. 2026, 27(17), 7855; https://doi.org/10.3390/ijms27177855 - 2 Sep 2026
Viewed by 185
Abstract
Immune dysregulation characterized by persistent myeloid activation and associated impairment of regulatory T cell (Treg) function contributes to inflammatory signaling across peripheral and central compartments in neurodegenerative diseases. We evaluated whether combining a glucagon-like peptide-1 receptor agonist (GLP-1RA; semaglutide) with low-dose interleukin-2 (LD-IL2) [...] Read more.
Immune dysregulation characterized by persistent myeloid activation and associated impairment of regulatory T cell (Treg) function contributes to inflammatory signaling across peripheral and central compartments in neurodegenerative diseases. We evaluated whether combining a glucagon-like peptide-1 receptor agonist (GLP-1RA; semaglutide) with low-dose interleukin-2 (LD-IL2) could modulate myeloid-associated transcript expression and enhance Treg-associated regulatory transcripts in a subacute lipopolysaccharide (LPS)-induced model of systemic and CNS inflammation. Mice received LPS once daily for 5 days, while GLP-1RA, LD-IL2, or combination treatment was initiated 24 h after LPS onset and continued daily. Splenic immune populations were quantified, and transcript expressions were assessed in magnetically enriched CD11b+ myeloid cells and CD4+CD25+ Tregs, as well as in cortex and hippocampus. As monotherapies, GLP-1RA reduced myeloid expansion with modest modulation of pro-inflammatory and anti-inflammatory myeloid transcripts, whereas LD-IL2 selectively enhanced Treg numbers and increased transcripts associated with Treg stability and suppressive regulation, including Il2ra (CD25), Foxp3, Ctla4, Ikzf2 (HELIOS), Entpd1 (CD39), and Nt5e (CD73). Combination treatment significantly reduced LPS-induced myeloid Il6, Il1b, and Tnf expression and increased Arg1 expression. Combination treatment further enhanced Treg-associated Il2ra (CD25), Tgfb1, and Ctla4 expression relative to monotherapies. In cortical and hippocampal tissues, combination treatment produced more robust modulation of inflammatory transcripts compared with effects observed with monotherapies, including reductions in Il6 and Il1b and increases in Cd163 and Mrc1 (CD206) expression. Together, these findings demonstrate coordinated and complementary changes in peripheral immune-cell populations and myeloid inflammatory and Treg-associated regulatory transcripts and warrant further evaluation of this combination in inflammation-driven neurodegenerative disease. Full article
(This article belongs to the Special Issue The Roles of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists in Health and Disease)
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Review

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22 pages, 1453 KB  
Review
Therapeutic Potential of Glucagon-like Peptide-1 Receptor Agonists in Respiratory Disorders
by Ewelina Russjan, Dominika Zając and Katarzyna Kaczyńska
Int. J. Mol. Sci. 2026, 27(13), 5803; https://doi.org/10.3390/ijms27135803 - 26 Jun 2026
Viewed by 604
Abstract
Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted in response to food intake that acts biologically by binding to GLP-1 receptors. The primary function of GLP-1 is to stimulate insulin secretion and inhibit glucagon secretion, which helps limit after-meal spikes in blood glucose. [...] Read more.
Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted in response to food intake that acts biologically by binding to GLP-1 receptors. The primary function of GLP-1 is to stimulate insulin secretion and inhibit glucagon secretion, which helps limit after-meal spikes in blood glucose. GLP-1 reduces intestinal contractility, slows down gastrointestinal motility and emptying, and also acts directly on the hypothalamus, thereby regulating appetite and food intake. Due to its metabolic effects, GLP-1 forms the basis of medications currently used to treat type 2 diabetes (T2DM) and obesity. However, it has also been observed that the use of GLP-1 agonists in the treatment of obesity or diabetes has a beneficial effect on comorbid respiratory conditions. This narrative review analyzes the scientific literature and describes the most recent information on the impact of GLP-1 receptor agonist (GLP-1 RA) therapies on the most common respiratory disorders—both the beneficial and undesirable effects. We discuss evidence that acute lung injury, COVID-19, pulmonary fibrosis, asthma, chronic obstructive pulmonary disease (COPD), and obstructive sleep apnea can benefit from therapies with various GLP-1 RAs. They can complement existing lung-targeted treatments, but as research progresses, they are likely to play an ever more important role in the treatment of respiratory diseases. Full article
(This article belongs to the Special Issue The Roles of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists in Health and Disease)
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21 pages, 1369 KB  
Review
GLP-1 Receptor Agonists at the Crossroads of Circadian Biology, Sleep, and Metabolic Disease
by Ayush Gandhi, Ei Moe Phyu, Kwame Koom-Dadzie, Kodwo Bosomefi Dickson and Josiah Halm
Int. J. Mol. Sci. 2026, 27(6), 2853; https://doi.org/10.3390/ijms27062853 - 21 Mar 2026
Cited by 2 | Viewed by 5103
Abstract
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have transformed the management of type 2 diabetes and obesity, yet their actions extend beyond glycemic control and weight loss. This narrative review synthesizes current preclinical and clinical evidence examining the bidirectional relationship between glucagon-like peptide-1 (GLP-1) receptor [...] Read more.
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have transformed the management of type 2 diabetes and obesity, yet their actions extend beyond glycemic control and weight loss. This narrative review synthesizes current preclinical and clinical evidence examining the bidirectional relationship between glucagon-like peptide-1 (GLP-1) receptor agonists and circadian biology. A structured literature search was conducted in PubMed using combinations of the terms ‘GLP-1,’ ‘circadian,’ ‘chronobiology,’ ‘sleep,’ ‘obesity,’ and ‘type 2 diabetes’ through January 2026. Accumulating evidence indicates that GLP-1 physiology is closely coupled to circadian timing systems and sleep–wake regulation. In this narrative review, we synthesize emerging data that reframe GLP-1RAs as chronometabolic modulators, acting at the intersection of metabolism, circadian biology, and sleep. We review circadian control of GLP-1 secretion by intestinal L-cells, emphasizing the role of core clock genes and the vulnerability of incretin rhythms to circadian misalignment from shift work, nocturnal light exposure, and sleep loss. We then examine GLP-1 receptor signaling within central and peripheral clock networks, including feedback effects on hypothalamic and hepatic circadian regulation. Emerging data suggest that GLP-1 signaling is under circadian regulation and may, in turn, influence central and peripheral clock systems. Comparative discussion of semaglutide, liraglutide, and tirzepatide highlights agent-specific pharmacokinetics and emerging clinical data linking GLP-1RA therapy to sleep outcomes, particularly obstructive sleep apnea. Finally, we outline translational opportunities for chronotherapy and precision medicine, positioning GLP-1RAs as integrative tools for metabolic and sleep-related disease rather than purely weight-centric therapies. We propose that GLP-1 receptor agonists may function as chronometabolic modulators, with potential implications for personalized chronopharmacological strategies in metabolic disease. Full article
(This article belongs to the Special Issue The Roles of Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists in Health and Disease)
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