Abstract
We evaluated the potential for a monoclonal antibody antagonist of the glucagon receptor (Ab-4) to maintain glucose homeostasis in type 1 diabetic rodents. We noted durable and sustained improvements in glycemia which persist long after treatment withdrawal. Ab-4 promoted β-cell survival and enhanced the recovery of insulin+ islet mass with concomitant increases in circulating insulin and C peptide. In PANIC-ATTAC mice, an inducible model of β-cell apoptosis which allows for robust assessment of β-cell regeneration following caspase-8-induced diabetes, Ab-4 drove a 6.7-fold increase in β-cell mass. Lineage tracing suggests that this restoration of functional insulin-producing cells was at least partially driven by α-cell-to-β-cell conversion. Following hyperglycemic onset in nonobese diabetic (NOD) mice, Ab-4 treatment promoted improvements in C-peptide levels and insulin+ islet mass was dramatically increased. Lastly, diabetic mice receiving human islet xenografts showed stable improvements in glycemic control and increased human insulin secretion.
Keywords:
diabetes; glucagon; insulin; islet; regeneration.
Copyright © 2021 the Author(s). Published by PNAS.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology*
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Blood Glucose / metabolism
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C-Peptide / metabolism
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Cell Lineage / drug effects
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Cell Transdifferentiation / drug effects
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Diabetes Mellitus, Experimental / genetics
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Diabetes Mellitus, Experimental / immunology
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Diabetes Mellitus, Experimental / pathology
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Diabetes Mellitus, Experimental / therapy*
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Diabetes Mellitus, Type 1 / genetics
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Diabetes Mellitus, Type 1 / immunology
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Diabetes Mellitus, Type 1 / pathology
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Diabetes Mellitus, Type 1 / therapy
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Gene Expression
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Glucagon / antagonists & inhibitors
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Glucagon / metabolism
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Glucagon-Secreting Cells / drug effects*
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Glucagon-Secreting Cells / metabolism
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Glucagon-Secreting Cells / pathology
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Humans
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Hypoglycemic Agents / pharmacology*
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Insulin / metabolism
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Insulin-Secreting Cells / drug effects*
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Insulin-Secreting Cells / metabolism
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Insulin-Secreting Cells / pathology
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Islets of Langerhans / metabolism
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Islets of Langerhans / physiology
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Islets of Langerhans Transplantation
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Mice
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Mice, Inbred NOD
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Organ Size / drug effects
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Receptors, Glucagon / antagonists & inhibitors*
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Receptors, Glucagon / genetics
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Receptors, Glucagon / metabolism
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Treatment Outcome
Substances
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Antibodies, Monoclonal
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Blood Glucose
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C-Peptide
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Hypoglycemic Agents
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Insulin
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Receptors, Glucagon
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Glucagon