Impairment of lysophospholipid metabolism in obesity: altered plasma profile and desensitization to the modulatory properties of n-3 polyunsaturated fatty acids in a randomized controlled trial
Impairment of lysophospholipid metabolism in obesity: altered plasma profile and desensitization to the modulatory properties of n-3 polyunsaturated fatty acids in a randomized controlled trial
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DOI：
10.3945/ajcn.116.130872
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发表时间：
2016-08-01
影响因子：
7.1
通讯作者：
Calder, Philip C.
中科院分区：
文献类型：
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作者：
del Bas, Josep M.;Caimari, Antoni;Calder, Philip C.
背景资料：血浆溶血磷脂已成为对炎症、胰岛素抵抗和脂肪肝疾病具有重要影响的信号分子，其中每一种都与肥胖密切相关。膳食n-3（omega-3）多不饱和脂肪酸（PUFAs）可能能够改善这些conditions.Objective：本研究的目的是评估血浆溶血磷脂对肥胖、n-3 PUFA消耗和高脂餐挑战的反应，以更好地了解溶血磷脂代谢在肥胖相关疾病进展中的作用。设计：我们测定了34名正常体重和38名肥胖受试者血浆中8种溶血磷脂酰胆碱、11种溶血磷脂酰乙醇胺和7种溶血磷脂酰肌醇的浓度，这些受试者被随机分配食用玉米油（对照）或富含n-3多不饱和脂肪酸的鱼油（3 g/d; n = 15-19只/组）90 d。在研究的最后一天，在空腹条件下和高脂餐（1135 kcal，86 g脂肪）激发后6 h采集血样。分泌的溶血磷脂的配置文件进行了研究，在HepG 2细胞棕榈酸诱导的脂肪atosis.Results：肥胖和正常体重的受试者有不同的配置文件的血浆溶血磷脂。26种溶血磷脂的多变量组合可以区分正常体重和肥胖受试者，准确率为98%。高脂膳食挑战改变了血浆溶血磷脂酰胆碱的浓度在油治疗依赖性的方式在正常体重，但不肥胖的受试者，这表明肥胖损害溶血磷脂代谢的敏感性n-3多不饱和脂肪酸。HepG 2细胞中的非细胞毒性脂肪变性影响溶血磷脂的分泌模式，部分类似于在血浆中观察到的肥胖subjects.Conclusions的变化：肥胖对溶血磷脂代谢有重大影响，改变血浆溶血磷脂的配置文件，并取消其敏感性饮食n-3多不饱和脂肪酸。这些影响可能导致与肥胖相关的改变的发生或进展，如炎症，胰岛素抵抗和脂肪肝疾病。
Background: Plasma lysophospholipids have emerged as signaling molecules with important effects on inflammation, insulin resistance, and fatty liver disease, each of which is linked closely to obesity. Dietary n-3 (omega-3) polyunsaturated fatty acids (PUFAs) may be able to improve these conditions.Objective: The objective of this study was to assess the response of plasma lysophospholipids to obesity, n-3 PUFA consumption, and a high-fat meal challenge to better understand the role of lysophospholipid metabolism in the progression of obesity-related disorders.Design: We determined the concentrations of 8 lysophosphatidylcholines, 11 lysophosphatidylethanolamines, and 7 lysophosphatidylinositols in the plasma of 34 normal-weight and 38 obese subjects randomly assigned to consume corn oil (control) or n-3 PUFA-rich fish oil (3 g/d; n = 15-19/group) for 90 d. Blood samples were collected on the last day of the study under fasting conditions and 6 h after a high-fat meal (1135 kcal, 86 g fat) challenge. The profile of secreted lysophospholipids was studied in HepG2 cells under palmitate-induced steatosis.Results: Obese and normal-weight subjects had different profiles of plasma lysophospholipids. A multivariate combination of the 26 lysophospholipids could discriminate between normal-weight and obese subjects with an accuracy of 98%. The high-fat meal challenge altered the concentration of plasma lysophosphatidylcholines in an oil treatment-dependent manner in normal-weight but not obese subjects, suggesting that obesity impairs the sensitivity of lysophospholipid metabolism to n-3 PUFAs. Noncytotoxic steatosis in HepG2 cells affected the secretion pattern of lysophospholipids, partially resembling the changes observed in the plasma of obese subjects.Conclusions: Obesity has a substantial impact on lysophospholipid metabolism, altering the plasma lysophospholipid profile and abolishing its sensitivity to dietary n-3 PUFAs. These effects could contribute to the onset or progression of alterations associated with obesity, such as inflammation, insulin resistance, and fatty liver disease.