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Cited by 113Pancreatic function and diabetesDiabetes Management and ResearchDiabetes and associated disorders

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

Glucagon receptor antibody completely suppresses type 1 diabetes phenotype without insulin by disrupting a novel diabetogenic pathway

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Wang, May-Yun, Yan, Hai, Shi, Zhiqing, Evans, Matthew R., Yu, Xinxin, Lee, Young, Chen, Shiuhwei, Williams, Annie, Philippe, Jacques, Roth, Michael G., Unger, Roger H.·2015·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1424934112PMC PMC4345619
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Abstract

Significance: Subcutaneous injections of insulin sustain life in mammals unable to produce insulin (type 1 diabetes) but do not prevent hyperglycemic and hypoglycemic swings or decrease hemoglobin A1c levels to normal amounts. In mice treated with insulin alone, repeated episodes of transient elevated blood glucose cause long-term damage. We show that in mice with type 1 diabetes treated with insulin, the transient high blood glucose levels require production of glucagon, a hormone that will cause the liver to produce more glucose. Blocking the action of glucagon with an antibody to the glucagon receptor completely normalizes blood glucose and hemoglobin A1c in the complete absence of insulin therapy. Suppressing glucagon action in combination with low-dose insulin would be a superior treatment for type 1 diabetes.

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Metadata

Authors
Wang, M.-Y., Yan, H., Shi, Z., Evans, M. R., Yu, X., Lee, Y., Chen, S., Williams, A., Philippe, J., Roth, M. G., & Unger, R. H.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • REMD Biotherapeutics, Inc., Camarillo, CA 93012;
  • Department of Biochemistry and
  • University of Notre Dame (US)
  • University of Geneva School of Medicine, 1211 Geneva, Switzerland; and
  • VA North Texas Health Care System (US)
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2015-02-09
Volume
112
Issue
8
Pages
2503-2508
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.1424934112
PMC
PMC4345619
OpenAlex
W1964812502
Cited by
112
References
36
Citations by year
2026: 3 · 2025: 8 · 2024: 11 · 2023: 6 · 2022: 9 · 2021: 11 · 2020: 6 · 2019: 8 · 2018: 10 · 2017: 15 · 2016: 15 · 2015: 9
FWCI
16.44
Type
journal article
Language
en
Update notices
correction (2015-07-01)
Open access
Licence
www.pnas.org/site/misc/userlicense.xhtml (vor, 181 d)
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders
  • REMD Therapeutic INC (OTD-107432)
  • Veterans Affairs Merit Review Award (N/A)
  • Bristol-Myer Squibb (Contract 101563)
  • Diane and Hal Brierley Chair in Biomedical Research (endowment)
  • HHS | NIH | National Center for Research Resources (CO6-RR15437)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
type 1 diabetes, glucagon receptor, hyperglycemia, glucagon secretion, insulin deficiency, HbA1c, phosphoenolpyruvate carboxykinase, beta-cell dysfunction, glucose homeostasis
MeSH terms
Animals, Antibodies, Monoclonal, Blood Glucose, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 1, Female, Glucagon, Humans, Insulin, Rats, Zucker, Mice, Inbred NOD, Receptors, Glucagon, Paracrine Communication, Mice, Rats

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