Silva E L, Maranhão R C, Curi R, Guimarães A P, Hirata R D, Fernandes L C, Hirata M H
Heart Institute of the Medical School Hospital (Instituto do Coração do HC-FMUSP), Faculty of Pharmaceutical Sciences, University of São Paulo, Brazil.
J Am Coll Nutr. 1994 Aug;13(4):376-82. doi: 10.1080/07315724.1994.10718425.
Defects in lipid metabolism secondary to development of cancer are frequently observed and, in experimental animals, manipulation of the lipid content of the diet can significantly influence tumor growth. The effects of a high polyunsaturated fat vs a high saturated fat diet upon the chylomicron metabolism of rats bearing Walker 256 tumor were examined.
Chylomicron-like emulsions labeled with radioactive lipids were injected into rats bearing the tumor and control rats. The two groups were previously given a high polyunsaturated (n-6) (15% fat) or a high saturated fat diet (15% fat) for 6 weeks. Following injection, plasma samples were collected at 8 time intervals in 60 minutes and tissue fragments were excised after the animals were killed, for determination of the plasma fractional clearance rate (FCR, min-1) and organ uptake of radioactive lipids.
FCR of the emulsion triacylglycerols (TG) and cholesteryl oleate ether (CE) decreased in the tumor-bearing rats fed the polyunsaturated fat-rich diet (FCR-TG control = 0.26 +/- 0.09, tumor = 0.11 +/- 0.04; FCR-CE controls = 0.18 +/- 0.05, tumor = 0.10 +/- 0.02), as did activity of the lipoprotein and hepatic lipases (p < 0.05). This indicates that in this group, the presence of the tumor elicited defective lipolysis and delayed removal of the emulsion from the plasma. In the group fed the saturated fatty acid-rich diet, however, these alterations were not observed (FCR-TG control = 0.21 +/- 0.11, tumor = 0.20 +/- 0.08; FCR-CE control = 0.13 +/- 0.06, tumor = 0.10 +/- 0.05). The uptake by several tissues of the emulsion CE was similar in all rat groups.
The saturated fat-rich diet avoids the deficiency in chylomicron lipolysis elicited by the implanted Walker 256 tumor.
癌症发展继发的脂质代谢缺陷经常被观察到，并且在实验动物中，饮食中脂质含量的操控可显著影响肿瘤生长。研究了高多不饱和脂肪饮食与高饱和脂肪饮食对荷Walker 256肿瘤大鼠乳糜微粒代谢的影响。
将用放射性脂质标记的乳糜微粒样乳剂注入荷瘤大鼠和对照大鼠体内。两组大鼠此前分别给予高多不饱和（n-6）（15%脂肪）或高饱和脂肪饮食（15%脂肪）6周。注射后，在60分钟内分8个时间间隔采集血浆样本，并在处死动物后切除组织碎片，以测定血浆分数清除率（FCR，分钟-1）和放射性脂质的器官摄取量。
喂食富含多不饱和脂肪饮食的荷瘤大鼠中，乳剂三酰甘油（TG）和胆固醇油酸酯醚（CE）的FCR降低（FCR-TG对照组 = 0.26 ± 0.09，肿瘤组 = 0.11 ± 0.04；FCR-CE对照组 = 0.18 ± 0.05，肿瘤组 = 0.10 ± 0.02），脂蛋白脂肪酶和肝脂肪酶的活性也降低（p < 0.05）。这表明在该组中，肿瘤的存在引发了脂解缺陷并延迟了乳剂从血浆中的清除。然而，在喂食富含饱和脂肪酸饮食的组中，未观察到这些改变（FCR-TG对照组 = 0.21 ± 0.11，肿瘤组 = 0.20 ± 0.08；FCR-CE对照组 = 0.13 ± 0.06，肿瘤组 = 0.10 ± 0.05）。所有大鼠组中，乳剂CE在几种组织中的摄取相似。
富含饱和脂肪的饮食可避免植入的Walker 256肿瘤引发的乳糜微粒脂解缺陷。
