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Dietary fat and fiber interactively modulate apoptosis and mitochondrial bioenergetic profiles in mouse colon in a site-specific manner

机译:膳食脂肪和纤维以位点特异性方式交互调节小鼠结肠的凋亡和线粒体生物能谱

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摘要

We have demonstrated that the combination of bioactive components generated by fish oil (containing n-3 polyunsaturated fatty acids) and fermentable fiber (leading to butyrate production) act coordinately to protect against colon cancer. This is the result, in part, to an enhancement of apoptosis at the base of the crypt throughout all stages (initiation, promotion and progression) of colon tumorigenesis. Since mitochondria are key organelles capable of regulating the intrinsic apoptotic pathway and mediating programmed cell death, we investigated the effects of diet on mitochondrial function by measuring mucosal cardiolipin composition, mitochondrial respiratory parameters and apoptosis in isolated crypts from the proximal and distal colon. C57BL/6 mice (n=15 per treatment) were fed one of two dietary fats (corn oil and fish oil) and two fibers (pectin and cellulose) for 4 wk in a 2 × 2 factorial design. In general, diet modulated apoptosis and the mucosal bioenergetic profiles in a site-specific manner. The fish/pectin diet promoted a more proapoptotic phenotype, e.g., increased proton leak (P-interaction = 0.002), compared to corn/cellulose (control) only in the proximal colon. With respect to the composition of cardiolipin, a unique phospholipid localized to the mitochondrial inner membrane where it mediates energy metabolism, fish oil feeding indirectly influenced its molecular species with a combined carbon number of C68 or greater, suggesting compensatory regulation. These data indicate that dietary fat and fiber can interactively modulate the mitochondrial metabolic profile and thereby potentially modulate apoptosis and subsequent colon cancer risk.
机译:我们已经证明,鱼油(包含n-3多不饱和脂肪酸)和可发酵纤维(导致丁酸的产生)产生的生物活性成分的组合可协同发挥作用,以预防结肠癌。这部分是由于结肠肿瘤发生的所有阶段(起始,促进和发展)在隐窝底部细胞凋亡增强的结果。由于线粒体是能够调节内在的凋亡途径和介导程序性细胞死亡的关键细胞器,我们通过测量粘膜心磷脂成分,线粒体呼吸参数和近端和远端结肠隐窝的凋亡来研究饮食对线粒体功能的影响。以2×2因子设计将C57BL / 6小鼠(每次处理n = 15)喂食两种膳食脂肪(玉米油​​和鱼油)和两种纤维(果胶和纤维素)之一,持续4周。通常,饮食以位点特异性方式调节细胞凋亡和粘膜生物能谱。与仅在近端结肠中的玉米/纤维素(对照)相比,鱼/果胶饮食促进了更多的凋亡表型,例如增加的质子泄漏(P-相互作用= 0.002)。关于心磷脂的组成,心磷脂是一种独特的磷脂,定位于线粒体内膜,介导能量代谢,鱼油的摄入间接影响了其分子种类,总碳数为C68或更高,表明存在补偿性调节作用。这些数据表明,膳食脂肪和纤维可以交互地调节线粒体的代谢谱,从而潜在地调节细胞凋亡和随后发生结肠癌的风险。

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