Levinson S, Bhasker M, Gibson T R, Morin R, Snape W J
Dig Dis Sci. 1985 Jan;30(1):33-9. doi: 10.1007/BF01318368.
Eating a 1000-kcal mixed meal stimulates an increase in distal colonic motility. Fat is the dietary component which is the major stimulant of colonic spike activity. In this study the colonic spike activity increased similarly after the mixed meal [19.1 +/- 2.4 spike potentials (SP)/30 min] and after the fat meal (19.4 +/- 5.4 SP/30 min). Fat stimulated a concentration-dependent increase in colonic motility only when in contact with the gastroduodenal mucosa. Intravenous administration of Liposyn (100 kcal/hr) did not stimulate an increase in colonic spike activity (3.3 +/- 1.3 SP/30 min) despite greater increase in plasma total fatty acid levels than after the oral ingestion of fat. In contrast both the oral ingestion and the intravenous administration of an amino acid mixture (Aminosyn) inhibited the gastrocolonic response after the 1000-kcal mixed meal. Thus, these studies demonstrate: (1) fat stimulates colonic motility only through direct mucosal contact, and (2) a mixture of amino acid inhibits colonic motility through either mucosal contact or by circulating in the plasma. The exact neurohumoral mechanisms involved in both of these effects is unknown at present.
进食一顿1000千卡的混合餐会刺激远端结肠蠕动增加。脂肪是饮食成分中刺激结肠峰电位活动的主要因素。在本研究中,混合餐后结肠峰电位活动(19.1±2.4个峰电位/30分钟)和脂肪餐后(19.4±5.4个峰电位/30分钟)的增加情况相似。脂肪仅在与胃十二指肠黏膜接触时才会刺激结肠蠕动呈浓度依赖性增加。静脉输注力补脂肪乳(100千卡/小时)尽管血浆总脂肪酸水平的升高幅度大于口服脂肪后,但并未刺激结肠峰电位活动增加(3.3±1.3个峰电位/30分钟)。相反,口服和静脉输注氨基酸混合物(复方氨基酸注射液)均抑制了1000千卡混合餐后的胃结肠反应。因此,这些研究表明:(1)脂肪仅通过直接黏膜接触刺激结肠蠕动,(2)氨基酸混合物通过黏膜接触或在血浆中循环来抑制结肠蠕动。目前尚不清楚这两种效应所涉及的确切神经体液机制。