ArticleMolecular metabolism2019
The brown adipose tissue glucagon receptor is functional but not essential for control of energy homeostasis in mice.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 86 citations in OpenAlex.
- Brown Adipose Tissue: Molecular Mechanisms of Regulation, Physiological Functions, and Therapeutic Targets.MedComm · 2026Review
- Constitutively active glucagon receptor (GCGR) physiologically regulates body temperature in lizards.Science advances · 2026Article
- Review
- Improving incretin-mediated body weight loss via energy expenditure.Trends in endocrinology and metabolism: TEM · 2026Review
- The expanding landscape of the glucagon signaling network: mechanisms and outcomes.Endocrinology · 2026Review
- Incretin and Glucagon Signalling in MASLD and MASH: Integrating Metabolic Pathways With Disease Progression.Diabetes, obesity & metabolism · 2026Review
- Engineered nutrient-stimulated hormonal multi-agonists for precision targeting of obesity and metabolic disorders.Clinical and molecular hepatology · 2026Review
- Association of fasting plasma glucagon with osteopenia/osteoporosis in Chinese patients with type 2 diabetes.BMC endocrine disorders · 2026Article
- GCGR agonism requires GABAergic signaling in the medial basal hypothalamus to promote weight loss in obese mice.Molecular metabolism · 2026Article
- 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
- Brain amino acid sensing for organismal amino acid homeostasis.Open biology · 2025Review
- Emerging Insights into Brown Adipose Tissue Crosstalk With Pancreatic β-Cells in Metabolic Regulation.Endocrinology · 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
- GLP-1R/GCGR dual agonism dissipates hepatic steatosis to restore insulin sensitivity and rescue pancreatic β-cell function in obese male mice.Nature communications · 2025Article
- The homotherapy for heteropathy: GCGR/GLP1R pathway in fibrotic diseases.Acta pharmaceutica Sinica. B · 2025Article
- The dual GLP-1/glucagon receptor agonist G49 mimics bariatric surgery effects by inducing metabolic rewiring and inter-organ crosstalk.Nature communications · 2024Article
- Class B1 GPCRs: insights into multireceptor pharmacology for the treatment of metabolic disease.American journal of physiology. Endocrinology and metabolism · 2024Review
- Futile lipid cycling: from biochemistry to physiology.Nature metabolism · 2024Review
- Pharmacological Advances in Incretin-Based Polyagonism: What We Know and What We Don't.Physiology (Bethesda, Md.) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveAdministration of glucagon (GCG) or GCG-containing co-agonists reduces body weight and increases energy expenditure. These actions appear to be transduced by multiple direct and indirect GCG receptor (GCGR)-dependent mechanisms. Although the canonical GCGR is expressed in brown adipose tissue (BAT) the importance of BAT GCGR activity for the physiological control of body weight, or the response to GCG agonism, has not been defined.
methodsWe studied the mechanisms linking GCG action to acute increases in oxygen consumption using wildtype (WT), Ucp1
resultsAcute GCG administration induced lipolysis and increased the expression of thermogenic genes in BAT cells, whereas knockdown of Gcgr reduced expression of genes related to thermogenesis. GCG increased energy expenditure (measured by oxygen consumption) both in vivo in WT mice and ex vivo in BAT and liver explants. GCG also increased acute energy expenditure in Ucp1
conclusionsExogenous GCG increases oxygen consumption in mice, also evident both in liver and BAT explants ex vivo, through UCP1-independent, FGF21-dependent pathways. Nevertheless, GCGR signaling within BAT is not physiologically essential for control of body weight, whole body energy expenditure, glucose homeostasis, or the adaptive metabolic response to cold or prolonged exposure to an energy dense diet.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.