Adipocyte-specific ablation of plakoglobin in mice does not affect adiposity but results in sexual-dimorphic effects on weight gain.

The main transcriptional coactivator of the WNT pathway, β-catenin, is a well-established regulator of adipogenesis and fat expansion, but our knowledge of how other members of the catenin family participate in adipogenesis remains incomplete. Previous studies have elucidated a role for the β-catenin homolog, plakoglobin, in the regulation of adipogenesis in vitro, as its depletion impaired lipid accumulation. Moreover, plakoglobin overexpression in murine cardiomyocytes has been reported to enhance adipogenesis within the heart, further implicating its role as a key regulator of differentiation. In the present study, we investigated the adipocyte-specific contributions of plakoglobin to adipogenesis and metabolism. Although deletion of plakoglobin in mature adipocytes had sex-specific effects on body weight gain, whereby only chow-fed knockout females weighed more than controls, no differences in adiposity or adipocyte size were observed. Moreover, no differences in glucose tolerance or insulin sensitivity were noted. Challenging mice with a high-fat diet revealed diet-induced metabolic disturbances only in male mice, but had no impact on adiposity or body weight. Together, our data demonstrate that plakoglobin in mature adipocytes is not required for adipogenesis or the expansion of adipose tissue mass.