Dietary fatty acids: Friends or foes?
Dietary fatty acids: Friends or foes?
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膳食脂肪酸：是友还是敌？
DOI：
10.1002/oby.21141
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Rane,SushilG
中科院分区：
文献类型：
--
作者：
Yadav,Hariom;Rane,SushilG
不受控制的能量摄入，沿着能量消耗的减少，被认为是肥胖和糖尿病流行的主要驱动力。摄入过量的饱和脂肪酸与肥胖和胰岛素抵抗增加有关。另一方面，不饱和脂肪酸被认为危害较小，在某些情况下，甚至显示出代谢益处（1）。全身性炎症被认为是代谢功能障碍的一个强有力的促进因素，尽管其因果关系仍存在争议。同样，已知肠道环境的变化会对代谢状态产生积极或消极的影响（2）。因此，肠道菌群的变化以及肠道激素水平的变化在促进或避免代谢功能障碍方面的作用受到了广泛关注。在代谢性疾病中观察到肠道通透性的变化，认为“漏肠”会促进代谢功能障碍（3）。虽然这些不同的机制似乎都在疾病进展过程中发挥作用，但它们之间的相互关系尚不清楚。在这个问题上，使用高脂饮食小鼠模型，Lam和同事提供了重要的见解，了解肠道上皮通透性，肠道微生物适应，炎症和代谢状态之间的相互作用，以响应饮食脂肪酸摄入量的变化（4）。膳食脂肪酸（dFA）与代谢综合征的发病有关（1），尽管与特定类型的dFA相关的潜在益处或风险尚不清楚。使用高脂饮食小鼠模型，Lam等人（4）证明了补充n-3 dFA或其代谢物Resolvin D1的有益代谢作用。通过改善肠道完整性、降低炎症状态、减少肥胖和降低胰岛素抵抗，实现代谢益处（图1）。重要的是，作者发现在喂食饱和脂肪的小鼠中产生H2S的细菌丰度增加，而这些细菌的水平在补充n-3 dFA后显着降低。他们表明，H2S细菌丰度的改变与肠道屏障完整性的改善和炎症的减少有关，但与肥胖或胰岛素抵抗无关。
Uncontrolled energy intake, along with reduced energy expenditure, is considered a prime driver of the obesity and diabetes epidemics. Intake of excess saturated fatty acids is correlated with increased adiposity and insulin resistance. On the other hand, unsaturated fatty acids are considered to be less harmful, and, in some instances, even shown to impart metabolic benefits (1). Systemic inflammation is regarded as a strong promoter of metabolic dysfunction although its causative or consequential role is debated. Similarly, changes to the gut environment are known to either positively or negatively influence the metabolic state (2). Thus, the role of changes to the gut microflora, and that of the levels of gut hormones, has received widespread attention with regards to either promoting or warding off metabolic dysfunction. Changes to gut permeability are observed in metabolic disease, with “a leaky gut” considered to promote metabolic dysfunction (3). While these various mechanisms all seem to be at play during disease progression, the inter-relationships amongst them are less clear.In this issue, using a high-fat diet mouse model, Lam and colleagues provide important insight into the interactions amongst gut epithelial permeability, gut microflora adaptations, inflammation and the metabolic state in response to variations in dietary fatty acid intake (4). Dietary fatty acids (dFAs) are implicated in the onset of metabolic syndrome (1), although the underlying benefits or risks associated with specific types of dFAs are unclear. Using a high-fat diet mouse model, Lam et al (4) demonstrate beneficial metabolic effects of supplementing n-3 dFA or its metabolite Resolvin D1. The metabolic benefits occur via improved gut integrity, reduced inflammatory state, decreased adiposity and reduced insulin resistance (Figure 1). Importantly, the authors find increased abundance of H2S producing bacteria in mice fed with saturated fats, while the levels of those bacteria is significantly reduced upon n-3 dFA supplementation. They show that alteration to the H2S bacterial abundance is associated with improvement in gut barrier integrity and reduced inflammation, but not with obesity or insulin resistance.