Journal
DIABETES
Volume 70, Issue 1, Pages 182-195Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db19-1239
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Funding
- National Research Foundation of Korea - Korean government (Ministry of Science and ICT) [NRF-2020R1A3B2078617, 2018R1A2A1A05022746, 2020R1A4A1019063, 2019R1I1A 01058338]
- Brain Korea 21 PLUS Project for Medical Science
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This study demonstrates that adipocyte-specific deficiency of Becn1 results in severe lipodystrophy, adipose tissue inflammation, hepatic steatosis, and insulin resistance, suggesting that Becn1 plays a crucial role in adipocyte survival and adipose tissue homeostasis.
Becn1/Beclin-1 is a core component of the class III phosphatidylinositol 3-kinase required for autophagosome formation and vesicular trafficking. Although Becn1 has been implicated in numerous diseases such as cancer, aging, and neurodegenerative disease, the role of Becn1 in white adipose tissue and related metabolic diseases remains elusive. In this study, we show that adipocyte-specific Becn1 knockout mice develop severe lipodystrophy, leading to adipose tissue inflammation, hepatic steatosis, and insulin resistance. Ablation of Becn1 in adipocytes stimulates programmed cell death in a cell-autonomous manner, accompanied by elevated endoplasmic reticulum (ER) stress gene expression. Furthermore, we observed that Becn1 depletion sensitized mature adipocytes to ER stress, leading to accelerated cell death. Taken together, these data suggest that adipocyte Becn1 would serve as a crucial player for adipocyte survival and adipose tissue homeostasis.
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