Adipocyte-specific deletion of Dbc1 does not recapitulate healthy obesity phenotype but suggests regulation of inflammation signaling
The protein Deleted in Breast Cancer 1 (Dbc1) is crucial for regulating metabolism, obesity, and aging-related processes. Knockout mice for Dbc1 develop obesity but are protected against liver steatosis, insulin resistance, and atherosclerosis, likely due to adipose tissue expansion. To explore Dbc1's role in adipocytes during obesity, we generated conditional Dbc1 knockout mice (cAT-Dbc1) by crossing them with CRE-AdipoQ transgenic mice, effectively knocking out Dbc1 in mature adipocytes. We then performed mRNA sequencing on adipocytes isolated from obese mice. Transcriptomic analysis revealed an mRNA expression profile indicating increased inflammation in Dbc1 KO adipocytes.