Feeding supression after a lipid meal in normal and obese rats

我们测试了大鼠十二指肠内输注甘油三酯（含或不含普朗尼克L-81（L-81））后的饱腹感，以评估脂肪餐后饱腹感的吸收后因素。L-81通过阻止乳糜微粒的形成来抑制脂质转运到肠系膜淋巴中。在不受限制的条件下，将脂肪乳剂注入禁食24小时的大鼠体内，持续8小时。输注后，测量前30分钟内的摄食量和血样。与仅输注溶剂的大鼠相比，8小时脂质输注后的摄食量显著降低。由于L-81处理，脂质的饱足效应丧失，但摄食量仍显著降低。通过喂食脂质加L-81而失去的摄食抑制作用通过停止L-81插管而完全逆转。在输注脂肪乳剂的大鼠中，血浆甘油三酯和载脂蛋白A-IV水平显著升高。这种增加被脂质输注液中L-81的存在所消除。本研究表明，吸收后因素是重要的厌食症后观察到的脂肪餐除了吸收前的因素。这种厌食作用在Zucker肥胖大鼠中减弱，表明Zucker肥胖大鼠对吸收后因子的敏感性丧失导致其肥胖的发展。这项研究进一步支持了我们以前的结论，载脂蛋白A-IV是一个重要的吸收后因素饱后脂肪餐。

We tested the satiation after intraduodenal infusion of triglyceride with or without Pluronic L-81 (L-81) in rats to evaluate postabsorptive factors for satiation after a lipid meal. L-81 suppresses lipid transport into mesenteric lymph by preventing the formation of chylomicrons. Under unrestrained condition, a lipid emulsion was infused into 24h fasted rats intraduodenally for 8h. Following the infusion, food intake during the first 30 min and blood samples were measured. Food intake after the 8-h lipid infusion decreased significantly compared to that of rats infused with vehicle only. The satiation effect of the lipid was lost as a result of L-81 treatment but food intake was still significantly decreased. The loss of inhibition of food intake by the feeding of lipid plus L-81 was totally reversed by the cessation of L-81 intusion. In rats infused with the lipid emulsion, plasma level of triglyceride and apolipoprotein A-IV increased significantly. This increase was abolished by the presence of L-81 in the lipid infusate. The present study indicates that postabsorptive factors are important for anorexia observed after a lipid meal in addition to preabsorptive factors. This anorectic effect was attenuated in Zucker obese rats, indicating that loss of sensitivity to post-absorptive factors in Zucker obese rats contributed to the development of their obesity. This study further supports our previous conclusion that apolipoprotein A-IV is an important postabsorptive factor for satiation after a lipid meal.