Skip to main content
. 2005 Jan 3;115(1):138–145. doi: 10.1172/JCI22232

Figure 7.

Figure 7

Effects of adenovirus-mediated restoration of PKCλ or HNF3β expression on insulin secretion in islets of βPKCλ–/– mice. (A–C) Islets isolated from control mice or βPKCλ–/– mice were infected with an adenovirus encoding either β-galactosidase (AxCALacZ) or wild-type PKCλ (AxCAλwt). The islets were then either subjected to immunoblot analysis with antibodies against PKCλ or β actin (A); assayed for insulin secretion in the presence of 2.8 or 16.8 mM glucose (white bars, control islets plus AxCALacZ; black bars, βPKCλ–/– islets plus AxCALacZ; gray bars, βPKCλ–/– islets plus AxCAλwt) (B); or subjected to real-time RT-PCR analysis of mRNAs for HNF3β, hexokinase 1, or Kir6.2 (C). (D and E) Islets isolated from control or βPKCλ–/– mice were infected with either AxCALacZ or an adenovirus encoding wild-type HNF3β (AxCAHNF3β). The islets were then either subjected to immunoblot analysis with antibodies against HNF3β or β actin (D) or assayed for insulin secretion in the presence of 2.8 or 16.8 mM glucose (E). Data are means ± SE of values from 6 mice (B and E) or of triplicates for pooled total RNA samples from 5 mice (C). *P < 0.05 (ANOVA) for the indicated comparisons.