Ledeboer M, Masclee A A, Biemond I, Lamers C B
Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands.
JPEN J Parenter Enteral Nutr. 1999 Jul-Aug;23(4):203-6. doi: 10.1177/0148607199023004203.
Fat is a potent stimulus of cholecystokinin (CCK) release. Apart from lipolysis, fatty acid chain length, and saturation, emulsification may also determine the magnitude of CCK release.
We have studied the effect of emulsification of soybean oil on CCK and pancreatic polypeptide (PP) release (radioimmunoassay [RIA]) and gallbladder motility (ultrasonography). Six healthy subjects were studied on three separate occasions in random order during (1) intraduodenal administration of emulsified long-chain triglycerides (LCT) (6 mmol/h for 120 minutes); (2) equimolar amounts of nonemulsified LCT with addition of emulsifier; and (3) saline with emulsifier (control).
Intraduodenal administration of both nonemulsified LCT and emulsified LCT induced significant (p < .05) increases in plasma CCK and PP levels and reductions in gallbladder volume. However, compared with nonemulsified LCT, emulsified LCT resulted in a readier and significantly stronger CCK release (212+/-62 pmol/L per 120 minutes vs 36+/-7 pmol/L per 120 minutes; p < .05); PP release (2034+/-461 pmol/L per 120 minutes vs 671+/-106 pmol/L per 120 minutes; p < .05); and gallbladder contraction (77%+/-2% vs 41%+/-7%; p < .05). No significant alterations were observed in plasma CCK or PP levels and gallbladder volume during administration of saline with emulsifier.
Intraduodenal administration of a low-dose emulsified LCT more potently stimulates CCK and PP release and gallbladder contraction in comparison to equimolar amounts of nonemulsified LCT. These findings point to an important role for solubilization of LCT in determining the magnitude of CCK release from the intestine.
脂肪是胆囊收缩素(CCK)释放的强效刺激物。除了脂解作用、脂肪酸链长度和饱和度外,乳化作用也可能决定CCK释放的程度。
我们研究了大豆油乳化对CCK和胰多肽(PP)释放(放射免疫分析法[RIA])以及胆囊运动(超声检查)的影响。在六个不同时间点,对六名健康受试者进行随机分组研究,分别为:(1)十二指肠内给予乳化长链甘油三酯(LCT)(6 mmol/h,持续120分钟);(2)等摩尔量的未乳化LCT并添加乳化剂;(3)添加乳化剂的生理盐水(对照)。
十二指肠内给予未乳化LCT和乳化LCT均显著(p <.05)提高了血浆CCK和PP水平,并减小了胆囊体积。然而,与未乳化LCT相比,乳化LCT导致CCK释放更快且显著更强(每120分钟212±62 pmol/L vs每120分钟36±7 pmol/L;p <.05);PP释放(每120分钟2034±461 pmol/L vs每120分钟671±106 pmol/L;p <.05);以及胆囊收缩(77%±2% vs 41%±7%;p <.05)。在给予添加乳化剂的生理盐水期间,血浆CCK或PP水平以及胆囊体积未观察到显著变化。
与等摩尔量的未乳化LCT相比,十二指肠内给予低剂量乳化LCT能更有效地刺激CCK和PP释放以及胆囊收缩。这些发现表明LCT的增溶作用在决定肠道CCK释放程度方面具有重要作用。