DBP transports Vitamin D metabolites in the circulation. It is highly expressed in liver and alpha cells, where it is a selective marker (encoded by the gene GC).
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DBP is also a major actin scavenger, perhaps amongst the most potent in the body.
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We see that alpha cells are smaller and hyperplastic in islets of DBP KO mice. They also display abnormal conductances and are less responsive to glucose. Glucagon granules are also distributed more diffusely. The end result is reduced rates of glucagon secretion.
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We did not see any changes in alpha cell transcription factor expression (Arx etc) in DBP KO islets. However, we observed large increases in F-actin abundance. When these changes are reversed using chemical F-actin inhibitors, alpha cell function is restored.
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We then wondered whether DBP was altered in T1D, since alpha cells are dysregulated in this condition. Using immunohistochemistry, we see that DBP expression is lower in late onset or longstanding T1D donors. DBP is co-localised to glucagon granules in humans.
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Together, these data show that DBP likely plays a major role in the regulation of alpha cell function. It's a really interesting protein and we are looking forward to understanding more about it.
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Some days I generate a piece of data that looks great and makes me feel like a scientist again; and then some days I look at manuscripts like yours,
@daveyboyhod and wonder what’s the point! Beautiful study, mate, tour de force
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Kind words as always Rob! The credit belongs to the guys in the lab, as well as the host of brilliant collaborators!
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