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Autophagy regulates inflammation in adipocytes
Authors:Yoshizaki Takeshi  Kusunoki Chisato  Kondo Motoyuki  Yasuda Mako  Kume Shinji  Morino Katsutaro  Sekine Osamu  Ugi Satoshi  Uzu Takashi  Nishio Yoshihiko  Kashiwagi Atsunori  Maegawa Hiroshi
Institution:Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Shiga, Japan. yosizaki@belle.shiga-med.ac.jp
Abstract:Autophagy is an essential process for both the maintenance and the survival of cells, with homeostatic low levels of autophagy being critical for intracellular organelles and proteins. In insulin resistant adipocytes, various dysfunctional/damaged molecules, organelles, proteins, and end-products accumulate. However, the role of autophagy (in particular, whether autophagy is activated or not) is poorly understood. In this study we found that in adipose tissue of insulin resistant mice and hypertrophic 3T3-L1 adipocytes autophagy was suppressed. Also in hypertrophic adipocytes, autophagy-related gene expression, such as LAMP1, LAMP2, and Atg5 was reduced, whereas gene expression in the inflammatory-related genes, such as MCP-1, IL-6, and IL-1β was increased. To find out whether suppressed autophagy was linked to inflammation we used the autophagy inhibitor, 3-methyladenine, to inhibit autophagy. Our results suggest that such inhibition leads to an increase in inflammatory gene expression and causes endoplasmic reticulum (ER) stress (which can be attenuated by treatment with the ER stress inhibitor, Tauroursodeoxycholic Acid). Conversely, the levels of inflammatory gene expression were reduced by the activation of autophagy or by the inhibition of ER stress. The results indicate that the suppression of autophagy increases inflammatory responses via ER stress, and also defines a novel role of autophagy as an important regulator of adipocyte inflammation in systemic insulin resistance.
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