Sexually dimorphic leanness and hypermobility in p16^Ink4a/CDKN2A-deficient mice coincides with phenotypic changes in the cerebellum.

ABSTRACT: p16^Ink4a/CDKN2A is a tumor suppressor that critically regulates the cell cycle. Indeed, p16^Ink4a deficiency promotes tumor formation in various tissues. We now report that p16^Ink4a deficiency in female mice, but not male mice, induces leanness especially in old age, as indicated by lower body weight and smaller white adipose tissue, although other major organs are unaffected. Unexpectedly, the integrity, number, and sizes of adipocytes in white adipose tissue were unaffected, as was macrophage infiltration. Hence, hypermobility appeared to be accountable for the phenotype, since food consumption was not altered. Histological analysis of the cerebellum and deep cerebellar nuclei, a vital sensorimotor control center, revealed increased proliferation of neuron

SUBMITTER: Kim KH 

PROVIDER: S-EPMC6671985 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature