Type 2 diabetes is an extremely common chronic condition characterized by high levels of sugar in the blood as a result of either insufficient production of the hormone insulin or an inability of cells to respond to insulin. A combination of genetic and environmental factors causes an individual to develop type 2 diabetes. Among the most reproducible genetic variations associated with type 2 diabetes in different ethnic populations are those in the CDKAL1 gene. However, the mechanisms underlying these associations have not yet been determined. But now, a team of researchers, led by Kazuhito Tomizawa, at Kumamoto University, Japan, has generated evidence in mice that could potentially explain why individuals carrying certain variants of the CDKAL1 gene are at increased risk of developing type 2 diabetes. Specifically, the team found that lack of the Cdkal1 protein led to misreading of certain parts of the gene that produces insulin, a process known as decoding infidelity, and thereby to both decreased insulin production and impaired functioning of insulin-producing cells.
TITLE: Deficit of tRNALys modification by Cdkal1 causes the development of type 2 diabetes in mice
Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
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