Field F Jeffrey, Born Ella, Mathur Satya N
Department of Veterans Affairs and Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA.
J Lipid Res. 2003 Jun;44(6):1199-208. doi: 10.1194/jlr.M300013-JLR200. Epub 2003 Mar 16.
Hamsters were fed a control diet or diets containing palm, olive, safflower, or fish oil for 2 weeks. In villus cell populations from duodenum, jejunum, and ileum, rates of intestinal fatty acid and cholesterol synthesis were estimated, as were sterol regulatory element-binding protein (SREBP)-1a, SREBP-1c, SREBP-2, HMG-CoA synthase, fatty acid synthase, ATP citrate lyase, acetyl-CoA carboxylase mRNA levels, and SREBP-1 and SREBP-2 mass. Plasma cholesterol and triacylglcerol levels were increased in animals ingesting palm oil and decreased in animals ingesting fish oil. Fatty acid synthesis and fatty acid synthase activity were decreased in the proximal intestine of animals ingesting all the fat-containing diets. Intestinal cholesterol synthesis was unaltered. In animals fed fat, SREBP-1c gene expression was modestly increased in the duodenum of hamsters fed palm oil or olive oil, and decreased in animals ingesting safflower oil or fish oil. Fatty acid synthase, acetyl-CoA carboxylase, ATP citrate lyase, SREBP-2, and HMG-CoA synthase mRNA levels were not altered, nor were SREBP-1 or SREBP-2 mass. In the intestine, dietary polyunsaturated fatty acids suppress SREBP-1c mRNA without altering expression of its target genes, fatty acid synthase, acetyl-CoA carboxylase, or ATP citrate lyase. Fatty acid influx decreases intestinal fatty acid synthesis by a posttranscriptional mechanism independent of the SREBP pathway.
给仓鼠喂食对照饮食或含棕榈油、橄榄油、红花油或鱼油的饮食，持续2周。在十二指肠、空肠和回肠的绒毛细胞群体中，估计肠道脂肪酸和胆固醇的合成速率，以及固醇调节元件结合蛋白（SREBP）-1a、SREBP-1c、SREBP-2、HMG-CoA合酶、脂肪酸合酶、ATP柠檬酸裂解酶、乙酰辅酶A羧化酶的mRNA水平和SREBP-1及SREBP-2的量。摄入棕榈油的动物血浆胆固醇和三酰甘油水平升高，而摄入鱼油的动物则降低。摄入所有含脂肪饮食的动物近端肠道中脂肪酸合成和脂肪酸合酶活性降低。肠道胆固醇合成未改变。在喂食脂肪的动物中，喂食棕榈油或橄榄油的仓鼠十二指肠中SREBP-1c基因表达略有增加，而摄入红花油或鱼油的动物中则降低。脂肪酸合酶、乙酰辅酶A羧化酶、ATP柠檬酸裂解酶、SREBP-2和HMG-CoA合酶的mRNA水平未改变，SREBP-1或SREBP-2的量也未改变。在肠道中，膳食多不饱和脂肪酸抑制SREBP-1c mRNA，而不改变其靶基因脂肪酸合酶、乙酰辅酶A羧化酶或ATP柠檬酸裂解酶的表达。脂肪酸流入通过一种独立于SREBP途径的转录后机制降低肠道脂肪酸合成。
