Figure 4: Glucose homeostasis and pancreas morphology in mice with genetic reconstitution of mTORC1 downstream targets.
From: Loss of mTORC1 signalling impairs β-cell homeostasis and insulin processing

(a) Random fed blood glucose levels in control (raptorf/f), βraKO and βraKO mice crossed to 4E-BP1−/− (βraKO; Eif4ebp1−/−) and 4E-BP2−/− mice (βraKO; Eif4ebp2−/−). (b) Random fed glucose levels over time in control (raptorf/f), βraKO, βraKO mice crossed to mice overexpressing a constitutively active S6K (βraKO; cas6K) and βraKO mice crossed to cas6K and 4E-BP2−/− mice (βraKO; caS6K; Eif4ebp2−/−). Same glucose values for control and βraKO mice are included in a and b. (c) Insulin tolerance test at 90 days in the same group of mice. (d) Fasting glucose in 150 days of age. (e–g) Assessments of β-cell mass, β-cell proliferation and TUNEL at 150 days of age. (h) Measurement of cell size expressed as a fold change (n=6; a–h). Data are shown as means±s.e.m., n=6 per group. *P<0.05 versus raptorf/f (control) mice and #P<0.05 versus βraKO mice; nonparametric U-test (Mann–Whitney).