Postprandial lysophospholipid suppresses hepatic fatty acid oxidation: the molecular link between group 1B phospholipase A2 and diet-induced obesity
Postprandial lysophospholipid suppresses hepatic fatty acid oxidation: the molecular link between group 1B phospholipase A2 and diet-induced obesity
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DOI：
10.1096/fj.09-144436
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发表时间：
2010-07-01
期刊：
影响因子：
4.8
通讯作者：
Hui, David Y.
中科院分区：
文献类型：
--
作者：
Labonte, Eric D.;Pfluger, Paul T.;Hui, David Y.
高脂饮食引起的脂肪分解代谢率降低会导致饮食诱导的肥胖。本研究使用对高血糖具有抵抗力的1B型磷脂酶A（2）（Pla 2g 1b）缺陷小鼠来验证Pla 2g 1b及其脂肪分解产物溶血磷脂抑制肝脏脂肪利用和能量代谢以促进饮食诱导的肥胖的假设。在Pla 2g 1b（+/+）和Pla 2g 1b（-/-）小鼠之间比较高热量饮食的代谢后果，包括体重增加、能量消耗和脂肪酸氧化。Pla 2g 1b（-/-）小鼠在喂食食物时表现出正常的能量平衡，但在高热量饮食下对肥胖有抵抗力。Pla 2g 1b（-/-）小鼠的肥胖抵抗是由于它们在高热量饮食时维持升高的能量消耗和核心体温的能力，这在Pla 2g 1b（-/-）小鼠中没有观察到。Pla 2g 1b（-/-）小鼠还显示出餐后肝脏脂肪利用增加，这是由于过氧化物酶体增殖物激活受体（PPAR-alpha）、PPAR-delta、PPAR-gamma、cd 36/Fat和Ucp 2的表达增加，这与餐后血浆溶血磷脂水平降低一致。通过Pla 2g 1b水解产生的溶血磷脂抑制肝脏脂肪利用并下调能量消耗，从而阻止代谢上有益的适应高脂饮食暴露，促进饮食诱导的肥胖和2型糖尿病。拉邦特，E. D.，Pfluger，P.T.，卡什，杰杰Kuhel，D.G.，罗哈斯，J.C.，Magness，D.P.，Jandacek，R.J.，Tschop，M.H.，Hui，D.Y.餐后溶血磷脂抑制肝脂肪酸氧化：1B型磷脂酶A与饮食诱导肥胖之间的分子联系FASEB J.24，2516-2524（2010）. www.fasebj.org
Decrease in fat catabolic rate on consuming a high-fat diet contributes to diet-induced obesity. This study used group 1B phospholipase A(2) (Pla2g1b)-deficient mice, which are resistant to hyperglycemia, to test the hypothesis that Pla2g1b and its lipolytic product lysophospholipid suppress hepatic fat utilization and energy metabolism in promoting diet-induced obesity. The metabolic consequences of hypercaloric diet, including body weight gain, energy expenditure, and fatty acid oxidation, were compared between Pla2g1b(+/+) and Pla2g1b(-/-) mice. The Pla2g1b(-/-) mice displayed normal energy balance when fed chow, but were resistant to obesity when challenged with a hypercaloric diet. Obesity resistance in Pla2g1b(-/-) mice is due to their ability to maintain elevated energy expenditure and core body temperature when subjected to hypercaloric diet, which was not observed in Pla2g1b(-/-) mice. The Pla2g1b(-/-) mice also displayed increased postprandial hepatic fat utilization due to increased expression of peroxisome proliferator-activated receptor (PPAR)-alpha, PPAR-delta, PPAR-gamma, cd36/Fat, and Ucp2, which coincided with reduced postprandial plasma lysophospholipid levels. Lysophospholipids produced by Pla2g1b hydrolysis suppress hepatic fat utilization and down-regulate energy expenditure, thereby preventing metabolically beneficial adaptation to a high-fat diet exposure in promoting diet-induced obesity and type 2 diabetes.-Labonte, E.D., Pfluger, P.T., Cash, J.G., Kuhel, D.G., Rojas, J.C., Magness, D.P., Jandacek, R.J., Tschop, M.H., Hui, D.Y. Postprandial lysophospholipid suppresses hepatic fatty acid oxidation: the molecular link between group 1B phospholipase A(2) and diet-induced obesity. FASEB J. 24, 2516-2524 (2010). www.fasebj.org