The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Glucagon receptor knockout mice are resistant to diet-induced obesity and streptozotocin-mediated beta cell loss and hyperglycaemia
Open accessAbstract
Aims/hypothesis Under normal physiological conditions, glucagon signalling is important in glucose homeostasis. Hyperglucagonaemia or altered insulin:glucagon ratio plays a role in maintaining hyperglycaemia in subjects with type 2 diabetes. It has been reported that glucagon receptor knockout (Gcgr (-/-)) mice develop normally and have lower plasma glucose on a normal diet. The goal of the current research was to further investigate the role of glucagon signalling in metabolic control and glucose homeostasis.Methods Gcgr (-/-) mice were challenged with a high-fat diet (HFD) and with streptozotocin, which induces beta cell damage. They were then analysed for whole-body and serum metabolic phenotypes as well as pancreatic islet morphology.Results In comparison with wild-type mice, Gcgr (-/-) mice exhibited decreased body weight and food intake, reduced plasma glucose levels, and improved oral and intraperitoneal glucose tolerance. Elevated glucagon-like peptide-1 levels and reduced gastric emptying were also observed in Gcgr (-/-) mice, which also had reduced HFD-induced hyperinsulinaemia and hyperleptinaemia, and were resistant to the development of hepatic steatosis. In addition, Gcgr (-/-) mice were resistant to STZ-induced hyperglycaemia and pancreatic beta cell destruction.Conclusions/interpretation This study demonstrates that blocking glucagon signalling by targeted Gcgr gene deletion leads to an improvement in metabolic control in this mouse model.
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“While lack of GCGR signaling can normalize glycemia under insulin-deficient conditions15,16, this effect is contingent on the presence of residual insulin17.”
From Transforming obesity: The advancement of multi-receptor drugs (2024) · cites this paper as [15]
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Glucagon and regulation of glucose metabolism
Jiang, G., & Zhang, B. B. (2003) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00492.2002 · Cited by 905
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Self-citationMinireview: The Glucagon-Like Peptides
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EFFECT OF EPINEPHRINE ON RAT DIAPHRAGM
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Mice lacking dipeptidyl peptidase IV are protected against obesity and insulin resistance
Conarello, S., Li, Z., Ronan, J., Roy, R. S., Zhu, L., Jiang, G., Liu, F., Woods, J. W., Zycband, E., Moller, D. E., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0631828100 · Cited by 348
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Sloop, K. W., Cao, J. X. C., Siesky, A. M., Zhang, H. Y., Bodenmiller, D. M., Cox, A. L., Jacobs, S. J., Moyers, J. S., Owens, R. A., Showalter, A. D., et al. (2004) · Journal of Clinical Investigation · doi:10.1172/jci20911 · Cited by 219
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The metabolic actions of glucagon revisited
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Metadata
- Authors
- Conarello, S. L., Jiang, G., Mu, J., Li, Z., Woods, J., Zycband, E., Ronan, J., Liu, F., Roy, R. S., Zhu, L., Charron, M. J., & Zhang, B. B.
- Affiliations
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Zhang, B. B.
- Venue
- Diabetologia
- Published
- 2006-11-28
- Volume
- 50
- Issue
- 1
- Pages
- 142-150
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1988784323
- Cited by
- 224
- References
- 38
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 12 · 2023: 7 · 2022: 16 · 2021: 15 · 2020: 10 · 2019: 17 · 2018: 17 · 2017: 10 · 2016: 16 · 2015: 17 · 2014: 17 · 2013: 9 · 2012: 14
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- glucagon receptor, glucose homeostasis, diet-induced obesity, high-fat diet, beta cell destruction, hyperglycemia, insulin/glucagon ratio, glucagon-like peptide-1, gastric emptying, hepatic steatosis, hyperinsulinemia, leptin, type 2 diabetes
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Dietary Fats, Disease Models, Animal, Glucose, Homeostasis, Hyperglycemia, Male, Mice, Inbred C57BL, Obesity, Streptozocin, Apoptosis, Gene Deletion, Receptors, Glucagon, Mice, Knockout, Insulin-Secreting Cells, Mice
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