Alexander Aguilera Alfonso, Hernández Díaz Guillermo, Lara Barcelata Martín, Angulo Guerrero Ofelia, Oliart Ros Rosa M
Facultad de Bioanálisis, Universidad Veracruzana, Iturbide s/n Veracruz, Veracruzna, Col. Centro. 91879, Mexico.
J Nutr Biochem. 2006 Nov;17(11):760-5. doi: 10.1016/j.jnutbio.2005.12.007. Epub 2006 Feb 3.
Cd36 is an integral membrane glycoprotein expressed on the surface of cells active in fatty acid metabolism (adipocytes, muscle cells, platelets, monocytes, heart and intestine cells). This protein plays diverse functions including uptake of long-chain fatty acids and oxidized low-density lipoproteins. A recent report demonstrates that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridemia in spontaneously hypertensive rats (SHRs). Cd36 is a tightly regulated protein whose expression is modulated through peroxisome proliferator-activated receptor (PPAR) transcription factors, by conditions that alter lipid metabolism such as diabetes mellitus and high-fat feeding. The purpose of this study was to evaluate the effect of dietary fish oil, rich in n-3 polyunsaturated fatty acids (PUFAs), on metabolic parameters and on the expression levels of Cd36 in adipose tissue in the SHR. Spontaneously hypertensive rats showed lower Cd36 mRNA levels when compared to Kyoto-Wistar (KW) rats (control). After 6 weeks of fish oil (FO) administration, this group of SHRs (FO-SHR) presented increased levels of Cd36 mRNA, concomitantly with decreased insulin, free fatty acids (FFAs), triglycerides, cholesterol, LDL, HDL, total lipids and blood pressure, in comparison to control rats that received a corn-canola oil diet. The study confirmed the beneficial effects of fish oil administration on the metabolic syndrome, suggesting that the induction of Cd36 expression could be one of the molecular mechanisms elicited by fish oil PUFAs.
Cd36是一种整合膜糖蛋白，在参与脂肪酸代谢的细胞（脂肪细胞、肌肉细胞、血小板、单核细胞、心脏和肠道细胞）表面表达。这种蛋白质具有多种功能，包括摄取长链脂肪酸和氧化型低密度脂蛋白。最近的一份报告表明，Cd36缺乏是自发性高血压大鼠（SHR）胰岛素抵抗、脂肪酸代谢缺陷和高甘油三酯血症的基础。Cd36是一种受到严格调控的蛋白质，其表达通过过氧化物酶体增殖物激活受体（PPAR）转录因子，以及诸如糖尿病和高脂喂养等改变脂质代谢的条件进行调节。本研究的目的是评估富含n-3多不饱和脂肪酸（PUFA）的膳食鱼油对SHR代谢参数和脂肪组织中Cd36表达水平的影响。与京都-威斯塔大鼠（KW，对照）相比，自发性高血压大鼠的Cd36 mRNA水平较低。在给予鱼油（FO）6周后，与接受玉米油-菜籽油饮食的对照大鼠相比，这组SHR（FO-SHR）的Cd36 mRNA水平升高，同时胰岛素、游离脂肪酸（FFA）、甘油三酯、胆固醇、低密度脂蛋白、高密度脂蛋白、总脂质和血压降低。该研究证实了鱼油给药对代谢综合征的有益作用，表明Cd36表达的诱导可能是鱼油PUFA引发的分子机制之一。
