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- W1566883741 abstract "Type 1 diabetes (T1D) occurs when β-cell death causes insufficient β-cell mass to maintain normoglycemia. Although select T1D patients are candidates for transplantation, no pharmaceutical cure for T1D exists. Such cures would augment the residual β-cell mass had by most, if not all, T1D patients. We showed the α subunit of the heterotrimeric Gz protein, Gαz, inhibits production of cAMP, a second messenger proposed to potentiate β-cell function and mass. In an obesity-linked T2D model, we demonstrated islets from Gαz-null mice have constitutively increased β-cell cAMP production, insulin secretion, and replicative capacity. We hypothesized Gαz-null mice subjected to chemical induction of T1D would have improved β-cell replication, survival, and, ultimately, mass, especially when treated with drugs known to stimulate cAMP production. To test our hypothesis, we induced diabetes in mice with streptozotocin. The Gαz-null mutation partially protected against hyperglycemia, as did treatment with the known cAMP potentiator, exendin-4. Combining the Gαz-null mutation with exendin-4 treatment was completely protective. These pancreas sections had both increased β-cell replication and decreased apoptosis. In vitro assays with novel Gαz variants are pinpointing critical downstream signaling pathways. Overall, our results support targeting Gαz signaling to preserve and regenerate functional β-cell mass. Grant Funding Source: Supported by the Juvenile Diabetes Research Foundation" @default.
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- W1566883741 date "2014-04-01" @default.
- W1566883741 modified "2023-09-23" @default.
- W1566883741 title "Elucidating the role of inhibitory G‐protein, Gz, in β‐cell preservation and regeneration (1062.3)" @default.
- W1566883741 doi "https://doi.org/10.1096/fasebj.28.1_supplement.1062.3" @default.
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