ArticleCell reports. Medicine2022
Hypoaminoacidemia underpins glucagon-mediated energy expenditure and weight loss.
Article in Cell reports. Medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of Glucagon-Like Peptide-1 Receptor Agonists (Mono and Combination Therapy) on Energy Expenditure: A Scoping Review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Article
- Hepatic GCGR is required for the superior weight loss and metabolic effects of a structurally related analogue of the dual GCGR/GLP-1R agonist survodutide in mice.Diabetes, obesity & metabolism · 2026Article
- IUPHAR review: From foe to friend: Repurposing glucagon to treat obesity and type 2 diabetes.Pharmacological research · 2026Review
- Brain amino acid sensing for organismal amino acid homeostasis.Open biology · 2025Review
- What is the pipeline for future medications for obesity?International journal of obesity (2005) · 2025Review
- Female glucagon receptor knockout mice are prone to steatosis but resistant to weight gain when fed a MASH-promoting GAN diet and a high-fat diet.Physiological reports · 2025Article
- Clinical Data Mega-Collection of Obesity and Obesity-Related Trials: Primary Inclusion Criteria from All Studies and Highlights of Clinical Efficacy Analysis of GLP-1 Drugs.Journal of clinical medicine · 2025Article
- Triple Agonism Based Therapies for Obesity.Current cardiovascular risk reports · 2025Review
- Variable glucagon metabolic actions in diverse mouse models of obesity and type 2 diabetes.Molecular metabolism · 2024Article
- Class B1 GPCRs: insights into multireceptor pharmacology for the treatment of metabolic disease.American journal of physiology. Endocrinology and metabolism · 2024Review
- Phosphoproteomics-directed manipulation reveals SEC22B as a hepatocellular signaling node governing metabolic actions of glucagon.Nature communications · 2024Article
- ErbB3 is required for hyperaminoacidemia-induced pancreatic α cell hyperplasia.The Journal of biological chemistry · 2024Article
- Targeting the incretin system in obesity and type 2 diabetes mellitus.Nature reviews. Endocrinology · 2024Review
- Review
- Glucagon resistance and metabolic-associated steatotic liver disease: a review of the evidence.The Journal of endocrinology · 2024Review
- Incretin and glucagon receptor polypharmacology in chronic kidney disease.American journal of physiology. Endocrinology and metabolism · 2024Review
- From classical dualistic antagonism to hormone synergy: potential of overlapping action of glucagon, insulin and GLP-1 for the treatment of diabesity.Endocrine connections · 2024Review
- Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Glucagon analogs show promise as components of next-generation, multi-target, anti-obesity therapeutics. The biology of chronic glucagon treatment, in particular, its ability to induce energy expenditure and weight loss, remains poorly understood. Using a long-acting glucagon analog, G108, we demonstrate that glucagon-mediated body weight loss is intrinsically linked to the hypoaminoacidemia associated with its known amino acid catabolic action. Mechanistic studies reveal an energy-consuming response to low plasma amino acids in G108-treated mice, prevented by dietary amino acid supplementation and mimicked by a rationally designed low amino acid diet. Therefore, low plasma amino acids are a pre-requisite for G108-mediated energy expenditure and weight loss. However, preventing hypoaminoacidemia with additional dietary protein does not affect the ability of G108 to improve glycemia or hepatic steatosis in obese mice. These studies provide a mechanism for glucagon-mediated weight loss and confirm the hepatic glucagon receptor as an attractive molecular target for metabolic disease therapeutics.
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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 OpenQuestion graph.