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(...

Täydet tiedot

Tallennettuna:
Bibliografiset tiedot
Julkaisussa:eLife
Päätekijät: Damond, Nicolas, Thorel, Fabrizio, Moyers, Julie S, Charron, Maureen J, Vuguin, Patricia M, Powers, Alvin C, Herrera, Pedro L
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: eLife Sciences Publications, Ltd 2016
Aiheet:
Human Biology and Medicine
Linkit:https://ncbi.nlm.nih.gov/pmc/articles/PMC4871705/
https://ncbi.nlm.nih.gov/pubmed/27092792
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.7554/eLife.13828
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