Abstract
In August 2016, several leaders in glucagon biology gathered for the European Association for the Study of Diabetes Hagedorn Workshop in Oxford, England. A key point of discussion focused on the need for basal insulin to allow for the therapeutic benefit of glucagon blockade in the treatment of diabetes. Among the most enlightening experimental results presented were findings from studies in which glucagon receptor-deficient mice were administered streptozotocin to destroy pancreatic β cells or had undergone diphtheria toxin-induced β cell ablation. This article summarizes key features of the discussion as a consensus was reached. Agents that antagonize glucagon may be of great benefit for the treatment of diabetes; however, sufficient levels of basal insulin are required for their therapeutic efficacy.
Highlights
Jens Juul Holst,1 William Holland,2 Jesper Gromada,3 Young Lee,2 Roger H
We review much of the seminal work in glucagon biology and highlight recent mechanistic studies that elegantly use the glucagon receptor–deficient mouse model to further assess the ability of blocked glucagon signaling to counteract insulin deficiency
Studies of fasting patients with type 1 diabetes who were maintained at near euglycemia with insulin infusions demonstrated that plasma glucose and ketone levels increased rapidly after termination of the insulin infusion; importantly, this was paralleled by increases of plasma glucagon concentrations [9]
Summary
Jens Juul Holst,1 William Holland,2 Jesper Gromada,3 Young Lee,2 Roger H. In agreement with effects of the glucagonneutralizing antibodies, Gcgr null mice or normal animals administered the glucagon receptor ASOs did not develop hypoglycemia; only a mild lowering of fasted and fed plasma glucose concentrations was observed.
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