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Genetic Test for Type II Diabetes Moves Closer

Illumina's Infinium Human1 and Human Hap300 Beadarrays.

The study confirmed the association of mutated TCF7L2 genes with an increased risk of developing the disease, as well as identifying four other gene mutations that are also implicated in increased risk of disease development.

The most significant of the new genes identified was SLC30A8, which encodes a zinc transporter expressed solely by the secretory vesicles of beta-cells. This gene is implicated in the final stages of insulin biosynthesis, which involve the co-crystallisation with zinc. Notably, the over-expression of the SLC30A8 gene in insulinoma cells (pancreatic endocrine cancer cells) increases glucose-stimulated insulin secretion leading to hypoglyceamia.

Two significant mutations, rs1111875 and rs7923837, were located near the telomeric end of chromosome 10 which contains two genes of known biological significance, the insulin degrading enzyme (IDE) and the homeodomain protein HHEX as well as the kinesin-interacting factor 11(KIF11).

HHEX is essential for the development of the pancreas and liver and is a target of the Wnt signaling pathway, as is TCF7L2.

Two previous studies into the role of IDE in the onset of Type II diabetes indicated a weak association, which was not confirmed by a third study. Further mapping of the IDE-KIF11-HHEX loci in different populations as well as biological studies will be needed to identify the causative variant.

Two further loci were found in the study; the first located in the introns of exostosin 2 (EXT2), which modulates hedgehog signaling, early pancreatic development and insulin synthesis.

The second is located in chromosome 11, mapped to a linkage disequilibrium block that contains the hypothetical LOC387761 gene.

Professor David Balding, co-author of the study from Imperial's Division of Epidemiology, Public Health and Primary Care, said: "Until now, progress in unde
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