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<p>White adipose tissue (WAT) dysfunction under nutrient excess is a central driver of obesity and its related metabolic disorders. Maintaining precise regulation of adipogenesis and lipid metabolism in WAT is essential for systemic energy balance and metabolic health. Here, we identify Ssu72 phosphatase as a critical regulator of adipogenesis required for WAT expansion. Ssu72 expression is elevated in obese WAT. Notably, adipocyte-specific deletion of Ssu72 in mice confers resistance to high-fat diet (HFD)-induced obesity, accompanied by improved insulin sensitivity and altered energy expenditure. Ssu72 deficiency diminishes HFD-induced adipocyte hypertrophy and inflammation in WAT. Mechanistically, loss of Ssu72 inhibits PPARγ-mediated adipogenesis and lipid storage by hyperphosphorylation of GSK3β, resulting in suppression of WAT expansion. In addition, metabolic alterations in Ssu72-deleted WAT are reversed by restoring Ssu72 expression. Taken together, our findings reveal a novel adipocyte Ssu72-GSK3β axis that regulates obesogenic adipogenesis in white adipocytes, suggesting that Ssu72 is a promising target for controlling diet-induced obesity and whole-body metabolic homeostasis.</p><p></p>

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Ssu72 phosphatase orchestrates obesogenic adipogenesis and metabolic homeostasis during nutrient excess

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月1日

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  • Si Chen,
  • Joon-Sup Yoon,
  • Eun-Ji Park,
  • Chong Li,
  • Rehna Paula Ginting,
  • Min-Woo Lee,
  • Gia Cac Chau,
  • Min-Hee Kim,
  • Myong-Joon Hahn,
  • Sung Hee Um,
  • Chang-Woo Lee

摘要

White adipose tissue (WAT) dysfunction under nutrient excess is a central driver of obesity and its related metabolic disorders. Maintaining precise regulation of adipogenesis and lipid metabolism in WAT is essential for systemic energy balance and metabolic health. Here, we identify Ssu72 phosphatase as a critical regulator of adipogenesis required for WAT expansion. Ssu72 expression is elevated in obese WAT. Notably, adipocyte-specific deletion of Ssu72 in mice confers resistance to high-fat diet (HFD)-induced obesity, accompanied by improved insulin sensitivity and altered energy expenditure. Ssu72 deficiency diminishes HFD-induced adipocyte hypertrophy and inflammation in WAT. Mechanistically, loss of Ssu72 inhibits PPARγ-mediated adipogenesis and lipid storage by hyperphosphorylation of GSK3β, resulting in suppression of WAT expansion. In addition, metabolic alterations in Ssu72-deleted WAT are reversed by restoring Ssu72 expression. Taken together, our findings reveal a novel adipocyte Ssu72-GSK3β axis that regulates obesogenic adipogenesis in white adipocytes, suggesting that Ssu72 is a promising target for controlling diet-induced obesity and whole-body metabolic homeostasis.