Meyer J H, Elashoff J D, Domeck M, Levy A, Jehn D, Hlinka M, Lake R, Graham L S, Gu Y G
Department of Medicine, Veterans Affairs Medical Center, Sepulveda 91343.
Am J Physiol. 1994 Jun;266(6 Pt 1):G1017-35. doi: 10.1152/ajpgi.1994.266.6.G1017.
Dietary fat is ingested in three forms: 1) in solid food, 2) as aqueous emulsions, and 3) as unemulsified, liquid oil. On the basis of a scant previous literature, we postulated that liquid fat (emulsions or oils) would empty from the stomach at speeds that varied with the amounts ingested but that this dynamic would be modulated by feedback inhibition from lipolytic products. To test these ideas, we used a gamma camera to track gastric emptying of 123I-labeled fat in dogs with chronic pancreatic fistulas by which lipase was excluded from or replenished in the duodenum in varied amounts after dogs were fed 15-, 30-, and 60-g loads of liquid fat given with solid foods or as emulsions. We also tracked concurrent gastric emptying of 113mIn, which marked the solid food phase or the water phase of emulsions. In some studies, we used a potent and specific inhibitor (orlistat) of pancreatic and gastric lipases to assess how lipolytic products modulated emptying of liquid fat. In the absence of pancreatic enzymes, both oils and emulsions emptied initially at high speeds that varied with fat loads, but emptying slowed 20 min after ingestion of emulsions and 60 min after ingestion of unemulsified oil. Studies with orlistat indicated that these changes in rates resulted from liberation of gastric lipolytic products. Emptying of oil emulsions was not altered by duodenal replenishment with pancreatic enzymes, but emptying of unemulsified oil was inhibited in a dose-related fashion, such that maximal inhibition was achieved when pancreatic enzymes were replenished at > or = 40% of normal amounts. Studies with orlistat confirmed that this dose-dependent slowing was due specifically to lipase. Emptying of solid food was much more sensitive to replenishment with enzymes, so that a 10% replenishment maximally inhibited solid emptying.
1)存在于固体食物中;2)以水性乳剂的形式;3)以未乳化的液态油的形式。基于以往极少的文献,我们推测液态脂肪(乳剂或油)从胃中排空的速度会随摄入量的不同而变化,但这种动态变化会受到脂解产物反馈抑制的调节。为了验证这些想法,我们使用γ相机追踪患有慢性胰瘘的狗摄入123I标记脂肪后的胃排空情况,在给狗喂食15克、30克和60克与固体食物一起或作为乳剂的液态脂肪后,通过慢性胰瘘以不同量排除或补充十二指肠中的脂肪酶。我们还追踪了同时摄入的113mIn的胃排空情况,113mIn标记了固体食物阶段或乳剂的水相。在一些研究中,我们使用一种强效且特异的胰腺和胃脂肪酶抑制剂(奥利司他)来评估脂解产物如何调节液态脂肪的排空。在没有胰腺酶的情况下,油和乳剂最初都以随脂肪负荷变化的高速排空,但摄入乳剂后20分钟和摄入未乳化油后60分钟排空速度减缓。使用奥利司他的研究表明,这些速率变化是由胃脂解产物的释放引起的。十二指肠补充胰腺酶不会改变油乳剂的排空,但未乳化油的排空以剂量相关的方式受到抑制,以至于当胰腺酶以正常量的≥40%补充时达到最大抑制。使用奥利司他的研究证实,这种剂量依赖性减缓具体是由脂肪酶引起的。固体食物的排空对酶的补充更为敏感,以至于10%的补充就能最大程度地抑制固体排空。