Figure 5.
Overexpression of Ppp1r3b in liver enhances hepatic glycogen storage and delayed responses to fasting. A, 4-h fasted liver lysates were used for measurement of transcript levels of Ppp1r3b, Ppp1r3c (PTG), Ppp1r3a (GM), Gys2, and Pygl from C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b (n = 4/group). B, hepatic glycogen content in 4- and 8-h fasted liver lysates from C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b (n = 3–4/group). C, PAS staining of paraffin-embedded liver sections from 4- and 8-h fasted C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b, showing increased amount of glycogen (purple stain) in AAV-Ppp1r3b-overexpressing mice. D, protein expression of total GS, P-GS (Ser-641), total GP, and PP1 in liver lysates from 4-h fasted from C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b (n = 4/group). The ratio of total GS to β-actin is increased and P-GS to total GS is decreased in AAV-Ppp1r3b-overexpressing mice compared with the Null group (n = 4/genotype). E, blood glucose levels during a 36-h fasting period in C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b (n = 7–8/group). F, total ketone bodies in blood measured during ad libitum fed and 12-, 24-, and 36-h fasting conditions in C57BL/6J mice injected with AAV-null and AAV-Ppp1r3b (n = 7–8/group). The mice were injected at 9 weeks of age, and liver lysates were analyzed at 11–12 weeks post injection. The results were replicated in at least two independent experiments. The data are expressed as the means ± S.E. Significance was determined in all panels by unpaired Student's t test. *, p < 0.05; **, p < 0.005; ***, p < 0.0001. n.s, not significant.