Li Xue, Morita Masahiro, Kikuguchi Chisato, Takahashi Akinori, Suzuki Toru, Yamamoto Tadashi
Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.
Department of Biochemistry, Goodman Cancer Research Centre, McGill University, Montreal, Canada.
FEBS Lett. 2017 Jan;591(2):358-368. doi: 10.1002/1873-3468.12550. Epub 2017 Jan 12.
Lipodystrophy involves a loss of adipose tissue. In mice, disruption of adipose tissue Cnot3, a subunit of the CCR4-NOT deadenylase complex, causes adipose tissue anomalies. In Cnot3 mice, white adipose tissue (WAT) decreases concomitantly with enhanced inflammation, whereas brown adipose tissue increases and contains larger lipid droplets. Cnot3 mice show hyperinsulinemia, hyperglycemia, insulin resistance, and glucose intolerance, and cannot maintain body temperature during cold exposure. Increased expression of inflammatory genes and decreased leptin expression also occur in Cnot3 WAT, achieving levels similar to those in lipodystrophic aP2-nSrebp1c and Pparg mice; thus, Cnot3 mice exhibit lipodystrophy.
脂肪营养不良涉及脂肪组织的缺失。在小鼠中，破坏CCR4-NOT去腺苷酸化酶复合体的一个亚基——脂肪组织中的Cnot3，会导致脂肪组织异常。在Cnot3基因敲除小鼠中，白色脂肪组织（WAT）减少，同时炎症增强，而棕色脂肪组织增加且含有更大的脂滴。Cnot3基因敲除小鼠表现出高胰岛素血症、高血糖、胰岛素抵抗和葡萄糖不耐受，并且在冷暴露期间无法维持体温。Cnot3基因敲除小鼠的白色脂肪组织中炎症基因表达增加，瘦素表达减少，达到与脂肪营养不良的aP2-nSrebp1c和Pparg基因敲除小鼠相似的水平；因此，Cnot3基因敲除小鼠表现出脂肪营养不良。
