[eyerxu]

A new study in Nature Genetics* shows, for the first time, that a loss-of-function mutation may be beneficial in preventing type 2 diabetes (T2D). This study included analyzing the genotype of ~150,000 individuals from diverse ancestry groups and found that carriers with rare protein-truncating variants in SLC30A8, which encodes islet zinc transporter (ZnT8), have a 65% reduction in type 2 diabetes risk.

The implication from this study uncovers a target and a pathway of treating T2D: selective inhibitors of ZnT8 may alleviate glucose intolerance with potentially minimal or no side effects. There are a number of ways to pursue antagonists for ZnT8, and GenScript can provide relevant services to explore them!

? Single domain antibodies (sdAb)
? Peptide library screening followed by peptibody construction to extend half-life in serum
? Cell therapy via genome editing technology such as CRISPR
? Assay development for small-molecule library screening

Common mouse models are unsuitable for in-vivo evaluation of therapeutic leads or candidates, because of the difference in physiology between mouse and human pancreatic tissue. Via collaboration, GenScript is open to collaborations of investigating humanized mouse carrying human pancreas tissue as a potentially efficacy model.

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aritcle source :* Flannick J. et al. Loss-of-function mutations in SLC30A8 protect against type 2 diabetes. Nat. Gen. 2014.