Communications biology · 2021
Advanced lipodystrophy reverses fatty liver in mice lacking adipocyte hormone-sensitive lipase.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Pajed Laura, Taschler Ulrike, Tilp Anna, Hofer Peter, Kotzbeck Petra, Kolleritsch Stephanie, Radner Franz P W, Pototschnig Isabella, Wagner Carina, Schratter Margarita, Eder Sandra, Huetter Sabrina, Schreiber Renate, Haemmerle Guenter, Eichmann Thomas O, Schweiger Martina, Hoefler Gerald, Kershaw Erin E, Lass Achim, Schoiswohl Gabriele
Аннотация
Modulation of adipocyte lipolysis represents an attractive approach to treat metabolic diseases. Lipolysis mainly depends on two enzymes: adipose triglyceride lipase and hormone-sensitive lipase (HSL). Here, we investigated the short- and long-term impact of adipocyte HSL on energy homeostasis using adipocyte-specific HSL knockout (AHKO) mice. AHKO mice fed high-fat-diet (HFD) progressively developed lipodystrophy accompanied by excessive hepatic lipid accumulation. The increased hepatic triglyceride deposition was due to induced de novo lipogenesis driven by increased fatty acid release from adipose tissue during refeeding related to defective insulin signaling in adipose tissue. Remarkably, the fatty liver of HFD-fed AHKO mice reversed with advanced age. The reversal of fatty liver coincided with a pronounced lipodystrophic phenotype leading to blunted lipolytic activity in adipose tissue. Overall, we demonstrate that impaired adipocyte HSL-mediated lipolysis affects systemic energy homeostasis in AHKO mice, whereby with older age, these mice reverse their fatty liver despite advanced lipodystrophy.