Reilly J M, Thompson M P
Department of Biochemistry, University of Otago, Dunedin, New Zealand.
Biochem Biophys Res Commun. 2000 Nov 2;277(3):541-5. doi: 10.1006/bbrc.2000.3705.
States characterised by elevated plasma fatty acid levels are accompanied by increased UCP2 expression but the physiological regulation of UCP2 expression in white adipose tissue is not fully understood. We used 3T3-L1 preadipocytes to determine whether various dietary fatty acids (20:5, 18:3, 18:2, 18:1, 18:0) directly regulate UCP2 expression. Physiological concentrations of each class of polyunsaturated fatty acid and the monounsaturated fatty acid dramatically up-regulated UCP2 mRNA levels 5- to 8-fold, but the saturated fatty acid was not so effective (1.5-fold). The up-regulation occurred in a time- and dose-dependent manner, was evident by 4 h and maximum between 18 and 24 h, and was prevented by actinomycin D. Synthetic ligands selective for each PPAR isoform did not induce UCP2 expression, which suggests that fatty acids might not be acting solely via PPAR transcription factors. In conclusion, dietary unsaturated fatty acids may be physiological signals to alter energy balance by direct induction of UCP2.
血浆脂肪酸水平升高的状态伴随着UCP2表达的增加，但白色脂肪组织中UCP2表达的生理调节尚未完全了解。我们使用3T3-L1前脂肪细胞来确定各种膳食脂肪酸（20:5、18:3、18:2、18:1、18:0）是否直接调节UCP2表达。每类多不饱和脂肪酸和单不饱和脂肪酸的生理浓度显著上调UCP2 mRNA水平5至8倍，但饱和脂肪酸的效果不明显（1.5倍）。上调以时间和剂量依赖性方式发生，4小时时明显，18至24小时达到最大值，并被放线菌素D阻止。对每种PPAR亚型具有选择性的合成配体不会诱导UCP2表达，这表明脂肪酸可能并非仅通过PPAR转录因子起作用。总之，膳食不饱和脂肪酸可能是通过直接诱导UCP2来改变能量平衡的生理信号。
