Backed by cutting edge technology, an uncompromising focus on ease-of-use and dedicated customer service, Indica Labs’ software and services are being used to make vital discoveries in pathology labs and research organizations around the world.

Mice harboring the human SLC30A8 R138X loss-of-function mutation have increased insulin secretory capacity

SLC30A8 encodes a zinc transporter that is primarily expressed in the pancreatic islets of Langerhans. In β-cells it transports zinc into insulin-containing secretory granules. Loss-of-function (LOF) mutations in SLC30A8 protect against type 2 diabetes in humans. In this study, we generated a knockin mouse model carrying one of the most common human LOF mutations for SLC30A8, R138X. The R138X mice had normal body weight, glucose tolerance, and pancreatic β-cell mass. Interestingly, in hyperglycemic conditions induced by the insulin receptor antagonist S961, the R138X mice showed a 50% increase in insulin secretion. This effect was not associated with enhanced β-cell proliferation or mass. Our data suggest that the SLC30A8 R138X LOF mutation may exert beneficial effects on glucose metabolism by increasing the capacity of β-cells to secrete insulin under hyperglycemic conditions.


Click here to access full article.


Sandra KleinerDaniel GomezBezawit MegraErqian NaRamandeep BhavsarKatie CavinoYurong XinJose RojasGiselle Dominguez-GutierrezBrian ZambrowiczGaelle CarratPauline ChabosseauMing HuAndrew J. MurphyGeorge D. YancopoulosGuy A. Rutter, and Jesper Gromada


PNAS | Published July 23rd, 2018 | DOI