Abstract
[Extract] Recently Haase et al [1] reported that maternal low-protein diet in rats was associated with decreased beta cell mass and decreased expression of growth arrest specific protein 6 (GAS6) in islets of Langerhans, and that incubation of neonatal islets with GAS6 enhanced beta cell proliferation. Low beta cell mass early in life is associated with increased future risk of type 2 diabetes. Consistent with a protective effect of GAS6, the c.834+7G>A polymorphism is associated with type 2 diabetes risk in humans [2]. The AA phenotype is associated with higher levels of GAS6, lower glucose levels, and decreased diabetes risk. Currently used drugs affecting the incretin axis have stimulated interest in therapeutic approaches that either preserve or enhance beta cell mass or function, and GAS6 (secreted by alpha cells) is, therefore, an attractive therapeutic target.
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