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. Author manuscript; available in PMC: 2018 Apr 9.
Published in final edited form as: Drug Discov Today Dis Models. 2013 Summer;10(2):e101–e109. doi: 10.1016/j.ddmod.2013.02.001

Figure 3. Mouse models of β-cell KATP channel insulin secretory disorders.

Figure 3

An increase in basal KATP channel activity reduces insulin secretion and leads to neonatal diabetes. Mouse models of increased KATP channel activity display hyperglycaemia and hypoinsulinaemia: they include those with Kir6.2-V59M, Kir6.2-ΔN30, and Kir6.2-ΔN30,K185Q mutations. Reduced basal KATP channel activity results in congenital hyperinsulinism. Mouse models with partial deletion (Kir6.2+/-, SUR+/-) or ablated channel expression / function (Kir6.2-/-, SUR-/-, Kir6.2-Y12X, Kir6.2-AAA) have been generated but do not fully recapitulate the human disease.