ReviewFrontiers in endocrinology2022
Is Glucagon Receptor Activation the Thermogenic Solution for Treating Obesity?
Review in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07050134 (A Randomized, Double-Blind, Placebo-Controlled Clinical Trial to Evaluate the Efficacy and Safety of DR10624 in Patients With Hypertriglyceridemia and Carotid Atherosclerotic Plaque), which is not on this map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Randomized, Double-Blind, Placebo-Controlled Clinical Trial to Evaluate the Efficacy and Safety of DR10624 in Patients With Hypertriglyceridemia and Carotid Atherosclerotic Plaque
Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Improving incretin-mediated body weight loss via energy expenditure.Trends in endocrinology and metabolism: TEM · 2026Review
- Alternative Receptor Signaling for the Selective and Multifaceted Regulation of Human Brown Adipocytes.International journal of molecular sciences · 2026Review
- Obesity pharmacotherapy reimagined: The era of multi-receptor agonists and next-generation metabolic modulators, perspectives and controversies.Metabolism open · 2026Review
- Multi-omic profiling reveals Retatrutide alleviates adipose tissue fibrosis via metabolic reprogramming and tissue repair.Diabetology & metabolic syndrome · 2026Article
- Management of Obese Patients with Cardiovascular Disease with Emerging Weight-Lowering Drugs: A Narrative Review.Biomedicines · 2026Review
- IUPHAR review: From foe to friend: Repurposing glucagon to treat obesity and type 2 diabetes.Pharmacological research · 2026Review
- Adipose Tissue, at the Core of the Action of Incretin and Glucagon-Based Anti-Obesity Drugs.Current obesity reports · 2025Review
- Review Article: GLP-1 Receptor Agonists and Glucagon/GIP/GLP-1 Receptor Dual or Triple Agonists-Mechanism of Action and Emerging Therapeutic Landscape in MASLD.Alimentary pharmacology & therapeutics · 2025Review
- Pharmacotherapy for Obesity: Recent Updates.Clinical pharmacology : advances and applications · 2025Review
- Efficacy and safety of retatrutide, a novel GLP-1, GIP, and glucagon receptor agonist for obesity treatment: a systematic review and meta-analysis of randomized controlled trials.Proceedings (Baylor University. Medical Center) · 2025Review
- Review
- Incretin and glucagon receptor polypharmacology in chronic kidney disease.American journal of physiology. Endocrinology and metabolism · 2024Review
- Mechanisms of action of incretin receptor based dual- and tri-agonists in pancreatic islets.American journal of physiology. Endocrinology and metabolism · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major challenge of obesity therapy is to sustain clinically relevant weight loss over time. Achieving this goal likely requires both reducing daily caloric intake and increasing caloric expenditure. Over the past decade, advances in pharmaceutical engineering of ligands targeting G protein-coupled receptors have led to the development of highly effective anorectic agents. These include mono-agonists of the GLP-1R and dual GIPR/GLP-1R co-agonists that have demonstrated substantial weight loss in experimental models and in humans. By contrast, currently, there are no medicines available that effectively augment metabolic rate to promote weight loss. Here, we present evidence indicating that activation of the GCGR may provide a solution to this unmet therapeutic need. In adult humans, GCGR agonism increases energy expenditure to a magnitude sufficient for inducing a negative energy balance. In preclinical studies, the glucagon-GCGR system affects key metabolically relevant organs (including the liver and white and brown adipose tissue) to boost whole-body thermogenic capacity and protect from obesity. Further, activation of the GCGR has been shown to augment both the magnitude and duration of weight loss that is achieved by either selective GLP-1R or dual GIPR/GLP-1R agonism in rodents. Based on the accumulation of such findings, we propose that the thermogenic activity of GCGR agonism will also complement other anti-obesity agents that lower body weight by suppressing appetite.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.