饱和脂肪酸或可直接损伤个体心脏健康

  橄榄油被普遍认为是可以取代肉类脂肪的较为健康的饮食方式，植物油，比如橄榄油、菜籽油以及蔬菜油大部分是由不饱和脂肪酸组成的，然而动物脂肪则富含饱和脂肪酸；标准进餐后个体机体心脏的主要能量来源就是碳水化合物，在禁食情况下游离的脂肪酸会成为主要的能量产生着，饮食中的饱和脂肪酸被认为对机体心脏健康有害，但其度心肌的影响最近才被研究者们所研究。
  近日，一篇刊登在国际杂志Endoplasmic Reticulum Stress in Diseases上的研究论文中，来自加拿大蒙特利尔心脏研究所的科学家们就通过研究发现饱和脂肪酸或许可以直接损伤机体心脏的健康。
  有意思的是当饱和脂肪酸对细胞有毒害作用时，不饱和脂肪酸不仅不会对机体有害，反而会提供保护机体抵御饱和脂肪酸损伤的作用；对许多细胞系进行研究表明，饱和脂肪酸会促进细胞死亡，这其中就包括引发细胞内质网压力等，而该过程被认为参与到许多疾病的发病过程中。
  文章中研究者通过研究表明，心肌细胞在积累不饱和脂肪酸和饱和脂肪酸上存在明显的差异，而且饱和脂肪酸会通过引发细胞内质网的压力来诱发心肌细胞死亡，而跟踪对比研究结果却发现，不饱和脂肪酸恰巧可以保护机体细胞免于细胞的损伤。研究人员评估了棕榈酸盐和油酸盐对原代心肌细胞脂肪酸吸收、甘油三酯的合成、细胞内脂质分布、内质网压力以及细胞死亡的效应，该研究首次在来源于心脏的细胞中观察到了相应的现象，从而为揭示饱和脂肪酸在心脏疾病的发生过程中所扮演的角色提供了一定的研究基础。
  以脂质代谢在2型糖尿病发生中所扮演的角色为例，当前的研究发现揭示了饱和脂肪酸在糖尿病患者心脏疾病发生过程中所扮演的角色，相关研究为后期理解心肌细胞内脂质积累和糖尿病心肌病发病之间的关系提供了一定的基础，也为开发治疗糖尿病心肌病患者的靶向疗法提供了一定的希望。（转化医学网360zhyx.com）
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转化医学网推荐的原文摘要：

Saturated fatty acids induce endoplasmic reticulum stress in primary cardiomyocytes
Endoplasmic Reticulum Stress in Diseases    DOI: 10.1515/ersc-2015-0004
Taha Haffar12 / Félix-Antoine Bérubé-Simard1 / Jean-Claude Tardif12 / Nicolas Bousette13
Abstract: Introduction: Diabetes is a major contributor to cardiovascular disease. There is a growing body of evidence pointing towards intra-myocellular lipid accumulation as an integral etiological factor. Here we aimed to determine the effect of two common fatty acids on lipid accumulation and cellular stress in primary cardiomyocytes.

Methods: We evaluated lipid accumulation biochemically (by triacylglyceride assay and radiolabeled fatty acid uptake assay) as well as histologically (by BODIPY 493/503 staining) in mouse and rat neonatal cardiomyocytes treated with saturated (palmitate) or mono-unsaturated (oleate) fatty acids. Endoplasmic reticulum (ER) stress was evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability was assessed by propidium iodide staining.

Results: We found that both oleate and palmitate led to significant increases in intracellular lipid in cardiomyocytes; however there were distinct differences in the qualitative nature of BODIPY staining between oleate and palmitate treated cardiomyocytes. We also show that palmitate caused significant apoptotic cell death and this was associated with ER stress. Interestingly, co-administration of oleate with palmitate abolished cell death, and ER stress. Finally, palmitate treatment caused a significant increase in ubiquitination of Grp78, a key compensatory ER chaperone.

Conclusion: Palmitate causes ER stress and apoptotic cell death in primary cardiomyocytes and this is associated with apparent differences in BODIPY staining compared to oleate treated cardiomyocytes. Importantly, the lipotoxic effects of palmitate are abolished with the co-administration of oleate.