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LXRα and LXRβ are nuclear oxysterol receptors with established roles in cholesterol, lipid, and carbohydrate metabolism [23], [24], and have recently been shown to play an important role in maintaining beta cell function [25], [26].
Interstitial GABA may also have a role in maintaining beta cell mass [ 9, 10].
These results reveal a hitherto unknown essential role for mTORC2 in maintaining beta cell function and viability.
Another interesting finding is that repression of the gene aristaless-related homeobox (Arx) caused by DNA methylation is critical for maintaining beta cell phenotype [ 22].
As a result of the growing interest in beta cell preservation as a potential cure for diabetes, a number of different treatments aimed at protecting the beta cell and maintaining beta cell mass have been evaluated.
This report provides evidence that rapamycin toxicity is mediated by the inactivation of mTORC2 and the inhibition of PKB and thus reveals the molecular basis of rapamycin toxicity and the essential role of mTORC2 in maintaining beta cell function and survival.
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PKB integrates upstream survival signals to maintain beta cell viability.
Finally, the factors that maintain beta cell function will be reviewed in relation to age.
GLP1 amplifies glucose-induced insulin secretion and maintains beta cell mass by suppressing apoptosis and stimulating proliferation.
There is also evidence from animal studies that lixisenatide can maintain beta cell mass and function through stimulation of islet cell proliferation and neogenesis, and inhibition of islet cell apoptosis.
Although metformin is associated with beta cell decline, studies suggest that it is not as marked as with sulfonylureas [ 9, 12, 32].Accumulating data suggest that thiazolidinediones, GLP-1 agonists and DPP-IV inhibitors may help to maintain beta cell mass and function [ 9, 68].
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