Division of Gastroenterology and Liver Diseases, School of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, United States.
Digestive Health Research Institute, School of Medicine, Case Western Reserve University, Cleveland, OH, United States.
Front Immunol. 2021 Feb 2;11:604989. doi: 10.3389/fimmu.2020.604989. eCollection 2020.
With the epidemic of human obesity, dietary fats have increasingly become a focal point of biomedical research. Epidemiological studies indicate that high-fat diets (HFDs), especially those rich in long-chain saturated fatty acids (e.g., Western Diet, National Health Examination survey; NHANES 'What We Eat in America' report) have multi-organ pro-inflammatory effects. Experimental studies have confirmed some of these disease associations, and have begun to elaborate mechanisms of disease induction. However, many of the observed effects from epidemiological studies appear to be an over-simplification of the mechanistic complexity that depends on dynamic interactions between the host, the particular fatty acid, and the rather personalized genetics and variability of the gut microbiota. Of interest, experimental studies have shown that certain saturated fats (e.g., lauric and myristic fatty acid-rich coconut oil) could exert the opposite effect; that is, desirable anti-inflammatory and protective mechanisms promoting gut health by unanticipated pathways. Owing to the experimental advantages of laboratory animals for the study of mechanisms under well-controlled dietary settings, we focus this review on the current understanding of how dietary fatty acids impact intestinal biology. We center this discussion on studies from mice and rats, with validation in cell culture systems or human studies. We provide a scoping overview of the most studied diseases mechanisms associated with the induction or prevention of Inflammatory Bowel Disease in rodent models relevant to Crohn's Disease and Ulcerative Colitis after feeding either high-fat diet (HFD) or feed containing specific fatty acid or other target dietary molecule. Finally, we provide a general outlook on areas that have been largely or scarcely studied, and assess the effects of HFDs on acute and chronic forms of intestinal inflammation.
随着人类肥胖症的流行，膳食脂肪越来越成为生物医学研究的焦点。流行病学研究表明，高脂肪饮食（HFD），特别是富含长链饱和脂肪酸的饮食（如西方饮食、国家健康检查调查；NHANES《我们在美国吃什么》报告）对多器官具有促炎作用。实验研究证实了其中一些疾病相关性，并开始详细阐述疾病诱发的机制。然而，许多流行病学研究观察到的效应似乎过于简化了依赖于宿主、特定脂肪酸以及肠道微生物群相当个性化的遗传和变异性之间动态相互作用的机制复杂性。有趣的是，实验研究表明某些饱和脂肪（例如富含月桂酸和肉豆蔻酸的椰子油）可能产生相反的效果；也就是说，通过意想不到的途径促进肠道健康的理想抗炎和保护机制。由于实验室动物在研究受严格饮食控制的机制方面具有实验优势，我们将重点放在目前对饮食脂肪酸如何影响肠道生物学的理解上。我们将这一讨论集中在关于饮食脂肪酸影响肠道生物学的研究上。我们以小鼠和大鼠的研究为中心，并在细胞培养系统或人类研究中进行验证。我们对与克罗恩病和溃疡性结肠炎相关的啮齿动物模型中诱导或预防炎症性肠病的最相关疾病机制进行了广泛的概述，这些机制涉及高脂肪饮食（HFD）或含有特定脂肪酸或其他目标饮食分子的饲料喂养。最后，我们对研究较少或尚未研究的领域进行了一般性展望，并评估了 HFD 对急性和慢性肠道炎症的影响。
