Gilham Dean, Labonté Eric D, Rojas Juan C, Jandacek Ronald J, Howles Philip N, Hui David Y
Department of Pathology and Laboratory Medicine, Genome Research Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio 45237, USA.
J Biol Chem. 2007 Aug 24;282(34):24642-9. doi: 10.1074/jbc.M702530200. Epub 2007 Jun 29.
This study evaluated the contributions of carboxyl ester lipase (CEL) and pancreatic triglyceride lipase (PTL) in lipid nutrient absorption. Results showed PTL deficiency has minimal effect on triacylglycerol (TAG) absorption under low fat dietary conditions. Interestingly, PTL(-)(/)(-) mice displayed significantly reduced TAG absorption compared with wild type mice under high fat/high cholesterol dietary conditions (80.1 +/- 3.7 versus 91.5 +/- 0.7%, p < 0.05). Net TAG absorption was reduced further to 61.1 +/- 3.8% in mice lacking both PTL and CEL. Cholesterol absorption was 41% lower in PTL(-/-) mice compared with control mice (p < 0.05), but this difference was not exaggerated in PTL(-/-), CEL(-/-) mice. Retinyl palmitate absorption was reduced by 45 and 60% in PTL(-/-) mice (p < 0.05) and PTL(-/-), CEL(-/-) mice (p < 0.01), respectively. After 15 weeks of feeding, the high fat/high cholesterol diet, wild type, and CEL(-/-) mice gained approximately 24 g of body weight. However, body weight gain was 6.2 and 8.6 g less (p < 0.01) in PTL(-/-) and PTL(-/-), CEL(-/-) mice, respectively, despite their consumption of comparable amounts of the high fat/high cholesterol diet. The decrease body weight gain in PTL(-/-) and PTL(-/-), CEL(-/-) mice was attributed to their absorption of fewer calories from the high fat/high cholesterol diet, thereby resulting in less fat mass accumulation than that observed in wild type and CEL(-/-) mice. Thus, this study documents that PTL and CEL serve complementary functions, working together to mediate the absorption of a major portion of dietary fat and fat-soluble vitamin esters. The reduced lipid absorption efficiency due to PTL and CEL inactivation also resulted in protection against diet-induced obesity.
本研究评估了羧基酯脂肪酶（CEL）和胰腺甘油三酯脂肪酶（PTL）在脂质营养吸收中的作用。结果显示，在低脂饮食条件下，PTL缺乏对三酰甘油（TAG）吸收的影响极小。有趣的是，在高脂/高胆固醇饮食条件下，与野生型小鼠相比，PTL(-)(/)(-)小鼠的TAG吸收显著降低（80.1±3.7%对91.5±0.7%，p<0.05）。在同时缺乏PTL和CEL的小鼠中，净TAG吸收进一步降至61.1±3.8%。与对照小鼠相比，PTL(-/-)小鼠的胆固醇吸收降低了41%（p<0.05），但在PTL(-/-)、CEL(-/-)小鼠中这种差异并未扩大。在PTL(-/-)小鼠（p<0.05）和PTL(-/-)、CEL(-/-)小鼠（p<0.01）中，棕榈酸视黄酯吸收分别降低了45%和60%。喂食高脂/高胆固醇饮食15周后，野生型和CEL(-/-)小鼠体重增加约24克。然而，尽管PTL(-/-)和PTL(-/-)、CEL(-/-)小鼠摄入了等量的高脂/高胆固醇饮食，但它们的体重增加分别比野生型小鼠少6.2克和8.6克（p<0.01）。PTL(-/-)和PTL(-/-)、CEL(-/-)小鼠体重增加减少归因于它们从高脂/高胆固醇饮食中吸收的热量较少，从而导致脂肪量积累比野生型和CEL(-/-)小鼠少。因此，本研究证明PTL和CEL发挥互补功能，共同介导大部分膳食脂肪和脂溶性维生素酯的吸收。由于PTL和CEL失活导致的脂质吸收效率降低也对饮食诱导的肥胖起到了保护作用。
