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首页> 外文期刊>Current opinion in lipidology >Intestinal phospholipid and lysophospholipid metabolism in cardiometabolic disease
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Intestinal phospholipid and lysophospholipid metabolism in cardiometabolic disease

机译：心脏代谢疾病中的肠道磷脂和溶血磷脂代谢

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Purpose of reviewPhospholipids are major constituents in the intestinal lumen after meal consumption. This article highlights current literature suggesting the contributory role of intestinal phospholipid metabolism toward cardiometabolic disease manifestation.Recent findingsGroup 1b phospholipase A(2) (PLA2g1b) catalyzes phospholipid hydrolysis in the intestinal lumen. The digestive product lysophospholipid, particularly lysophosphatidylcholine (LPC), has a direct role in mediating chylomicron assembly and secretion. The LPC in the digestive tract is further catabolized into lysophosphatidic acid and choline via autotaxin-mediated and autotaxin-independent mechanisms. The LPC and lysophosphatidic acid absorbed through the digestive tract and transported to the plasma directly promote systemic inflammation and cell dysfunction, leading to increased risk of cardiovascular disease and obesity/diabetes. The choline moiety generated in the digestive tract can also be used by gut bacteria to generate trimethylamine, which is subsequently transported to the liver and oxidized into trimethylamine-N-oxide that also enhances atherosclerosis and cardiovascular abnormalities.SummaryProducts of phospholipid metabolism in the intestine through PLA2g1b and autotaxin-mediated pathways directly contribute to cardiometabolic diseases through multiple mechanisms. The implication of these studies is that therapeutic inhibition of PLA2g1b and autotaxin in the digestive tract may be a viable approach for cardiovascular and metabolic disease intervention.
机译：审查目的磷脂是进餐后肠道内腔的主要成分。本文突出了当前的文献，提示肠道磷脂代谢对心脏代谢疾病表现的贡献作用。最新发现1b组磷脂酶A（2）（PLA2g1b）催化肠腔内磷脂的水解。消化产物溶血磷脂，尤其是溶血磷脂酰胆碱（LPC）在介导乳糜微粒的组装和分泌中具有直接作用。消化道中的LPC通过自分泌素介导的和自分泌素非依赖性机制进一步分解为溶血磷脂酸和胆碱。通过消化道吸收并转运至血浆的LPC和溶血磷脂酸直接促进全身性炎症和细胞功能障碍，导致心血管疾病和肥胖症/糖尿病的风险增加。消化道中产生的胆碱部分也可以被肠道细菌用来产生三甲胺，然后被运到肝脏并被氧化成三甲胺-N-氧化物，这也增强了动脉粥样硬化和心血管疾病的异常。 PLA2g1b和autotaxin介导的途径通过多种机制直接导致了心脏代谢疾病。这些研究的含义是，在消化道中抑制PLA2g1b和自分泌运动素可能是心血管和代谢疾病干预的可行方法。

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