Clarke S D, Jump D B
Department of Human Ecology, University of Texas-Austin 78712-1907, USA.
Lipids. 1996 Mar;31 Suppl:S7-11. doi: 10.1007/BF02637044.
Polyunsaturated fatty acids (PUFA) of the n-6 and n-3 families inhibit transcription of a number of hepatic lipogenic and glycolytic genes, e.g. fatty acid synthase. In contrast, saturated and monounsaturated fatty acids exert no suppressive action on lipogenic gene expression. The unique PUFA regulation of gene expression extends beyond the liver to include genes such as adipocyte glucose transporter-4, lymphocyte stearoyl-CoA desaturase 2, and interleukins. Some of the transcriptional effects of PUFA appear to be mediated by eicosanoids, but PUFA suppression of lipogenic and glycolytic genes is independent of eicosanoid synthesis and appears to involve a nuclear mechanism directly modified by PUFA. With the recent cloning of a fatty acid-activated nuclear factor termed peroxisome-proliferator-activated receptor (PPAR) has come the suggestion that PPAR may be the PUFA response factor. This review, however, presents several lines of evidence that indicate that the PPAR and n-6 and n-3 PUFA regulation of lipogenic and glycolytic gene transcription involve separate and independent mechanisms. Thus PPAR appears not to be the PUFA response factor.
n-6和n-3族的多不饱和脂肪酸（PUFA）可抑制许多肝脏生脂和糖酵解基因的转录，如脂肪酸合酶。相反，饱和脂肪酸和单不饱和脂肪酸对生脂基因表达没有抑制作用。PUFA对基因表达的独特调控作用不仅限于肝脏，还包括脂肪细胞葡萄糖转运蛋白4、淋巴细胞硬脂酰辅酶A去饱和酶2和白细胞介素等基因。PUFA的一些转录作用似乎是由类二十烷酸介导的，但PUFA对生脂和糖酵解基因的抑制作用独立于类二十烷酸的合成，似乎涉及一种直接由PUFA修饰的核机制。随着一种名为过氧化物酶体增殖物激活受体（PPAR）的脂肪酸激活核因子的克隆，有人提出PPAR可能是PUFA反应因子。然而，这篇综述提供了几条证据，表明PPAR以及n-6和n-3 PUFA对生脂和糖酵解基因转录的调控涉及不同且独立的机制。因此，PPAR似乎不是PUFA反应因子。
