DIDO is necessary for the adipogenesis that promotes diet-induced obesity.
Ontology highlight
ABSTRACT: The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). Dido1 is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are f
SUBMITTER: Garcia-Lopez MA
PROVIDER: S-EPMC10801893 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA