College of Animal Sciences, Zhejiang University, Key Laboratory of Animal Nutrition & Feed Sciences, Ministry of Agriculture, Zhejiang Provincial Laboratory of Feed and Animal Nutrition, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, PR China.
College of Animal Sciences, Zhejiang University, Key Laboratory of Animal Nutrition & Feed Sciences, Ministry of Agriculture, Zhejiang Provincial Laboratory of Feed and Animal Nutrition, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, PR China.
Biochim Biophys Acta Mol Cell Biol Lipids. 2019 Dec;1864(12):158508. doi: 10.1016/j.bbalip.2019.08.004. Epub 2019 Aug 22.
Family with Sequence Similarity 134, Member B (FAM134B) is a protein that known to be necessary for the long-term survival of nociceptive and autonomic ganglion neurons. Recent work has exhibited that FAM134B plays a pivotal role in autophagy-mediated turnover of endoplasmic reticulum (ER) membranes, tumor inhibition and lipid homeostasis. In this study, we provide mechanistic links between FAM134B and adipocyte differentiation. Here, we found that adipocyte-specific FAM134B overexpression mice are obese and have increased white adipose tissue (WAT) mass. Serum tests showed that they developed high glucose level and severe insulin resistance. In addition, they also exhibited enhanced autophagy and reduced mitochondria amount, suggesting the function of FAM134B to promote autophagy in adipocytes. Overexpression of FAM134B in 3 T3-L1 preadipocytes promoted autophagy and differentiation, while the effect could be inhibited after treatment with autophagyinhibitors, 3-methyladenine (3-MA). Overexpressioncells also showed an early reduction of mitochondria number, while its autophagy flux level increased fast from differentiation day 2. These findings indicate that FAM134B improves adipocytes differentiation through enhancing mitophagy.
家族性蛋白 134B（FAM134B）是一种已知对伤害性和自主神经节神经元的长期存活所必需的蛋白。最近的研究表明，FAM134B 在自噬介导的内质网（ER）膜周转、肿瘤抑制和脂质动态平衡中发挥着关键作用。在本研究中，我们提供了 FAM134B 与脂肪细胞分化之间的机制联系。我们发现，脂肪细胞特异性过表达 FAM134B 的小鼠肥胖，且白色脂肪组织（WAT）质量增加。血清检测表明它们的血糖水平升高，胰岛素抵抗严重。此外，它们还表现出增强的自噬和减少的线粒体数量，表明 FAM134B 在脂肪细胞中促进自噬的功能。在 3T3-L1 前体脂肪细胞中过表达 FAM134B 可促进自噬和分化，而在用自噬抑制剂 3-甲基腺嘌呤（3-MA）处理后，这种作用可以被抑制。过表达细胞的线粒体数量也较早减少，而其自噬通量水平从分化第 2 天开始快速增加。这些发现表明，FAM134B 通过增强线粒体自噬来改善脂肪细胞分化。
