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<p>The aquaporin-7 (AQP7) channel mediates glycerol release from adipocytes. Genetic variants decreasing AQP7 expression are associated with adiposity and metabolic complications in humans. Using human data, mouse models, and cellular systems, we investigated how AQP7 influences adipose tissue maturation and homeostasis. Negative correlations between methylation on the <i>AQP7</i> locus, expression of <i>AQP7</i> in the adipose tissue and BMI were observed in humans. Mice lacking <i>Aqp7</i> had increased body weight and visceral fat accumulation, due to adipocyte hypertrophy and chronic inflammation, impairing transport across the peritoneal membrane. These changes were further intensified by a high-glucose diet. Mechanistically, AQP7 deficiency disrupted the expression of genes related to adipogenesis and adipocyte function, resulting in a shift toward fibrosis and inflammation, while secreted factors from AQP7-null adipocytes promoted fibroblast activation. These findings establish AQP7 as a key regulator of adipose tissue homeostasis, metabolic dysregulation, and inflammation/fibrosis, exacerbated by glucose-induced obesity.</p>

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AQP7 deficiency drives adipose tissue remodeling and disrupts homeostasis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月7日

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  • Ines PD Costa,
  • Guglielmo Schiano,
  • Juan Manuel Sacnun,
  • Rebecca Herzog,
  • Alastair Kerr,
  • Ingrid Dahlman,
  • Christine Delporte,
  • Klaus Kratochwill,
  • Olivier Devuyst

摘要

The aquaporin-7 (AQP7) channel mediates glycerol release from adipocytes. Genetic variants decreasing AQP7 expression are associated with adiposity and metabolic complications in humans. Using human data, mouse models, and cellular systems, we investigated how AQP7 influences adipose tissue maturation and homeostasis. Negative correlations between methylation on the AQP7 locus, expression of AQP7 in the adipose tissue and BMI were observed in humans. Mice lacking Aqp7 had increased body weight and visceral fat accumulation, due to adipocyte hypertrophy and chronic inflammation, impairing transport across the peritoneal membrane. These changes were further intensified by a high-glucose diet. Mechanistically, AQP7 deficiency disrupted the expression of genes related to adipogenesis and adipocyte function, resulting in a shift toward fibrosis and inflammation, while secreted factors from AQP7-null adipocytes promoted fibroblast activation. These findings establish AQP7 as a key regulator of adipose tissue homeostasis, metabolic dysregulation, and inflammation/fibrosis, exacerbated by glucose-induced obesity.