Tissues with known high energy consumption such as heart, skeletal muscle, kidney and liver displayed increased expression of OXPHOS genes compared to tissues with lower energy demand such as skin and lung.
These mice were sensitive to CCl4-induced liver injury and displayed increased levels of hepatic necrosis (Fig. 5H K) with significant morbidity occurring within 2 weeks (Fig. 5L).
The livers of aged rats displayed increased levels of the premature form of IL-1β as well as increased levels of the activated form of IL-1β (Fig. 3C).
Vdr −/− mice subjected to bile duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice.
GhrR KO mice fed a HFD also showed a modest, but significant decrease in conversion of pyruvate to glucose, as would be anticipated if these mice displayed increased liver insulin sensitivity.
To a lesser degree, the livers of EAF2−/− and VHL+/− alone mice also displayed increased microvessel density which was consistent with previous reports [ 10, 14].
Mutant mice displayed increased mitochondrial numbers in the brain and liver, expected with a defect in mitophagy, and morphologically abnormal mitochondria.
However, in response to insulin stimulation, BACE1 −/− and BACE1 +/− mice displayed increased phospho-PKB levels in skeletal muscle and liver compared with their WT littermates.
Interestingly, when normalized to actin loading control, livers from P2 3 Smn +/−;SMN2 heterozygotes that lack any overt neurological phenotype displayed increased CREB levels and, subsequently, increased p-CREB levels relative to wild-type (Smn +/+;SMN2) littermates.
Mice expressing human CSF-1 displayed increased frequency and more efficient differentiation of human fetal liver-derived HSCs into monocytes/macrophages in various organs and increased functional properties, such as migration, phagocytosis and activation, and response to LPS.
