Blockade of glucagon signaling prevents or reverses diabetes onset only if residual β-cells persist

Glucagon secretion dysregulation in diabetes fosters hyperglycemia. Recent studies report that mice lacking glucagon receptor (Gcgr-/-) do not develop diabetes following streptozotocin (STZ)-mediated ablation of insulin-producing β-cells. Here, we show that diabetes prevention in STZ-treated Gcgr-/-...

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Bibliographic Details
Main Authors: Nicolas Damond, Fabrizio Thorel, Julie S Moyers, Maureen J Charron, Patricia M Vuguin, Alvin C Powers, Pedro L Herrera
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2016-04-01
Series:eLife
Subjects:
Online Access:https://elifesciences.org/articles/13828