Cantor P, Petronijevic L, Worning H
Pancreas. 1986;1(6):488-93. doi: 10.1097/00006676-198611000-00004.
Plasma concentrations of cholecystokinin (CCK) have been reported to be elevated in patients with chronic pancreatitis. The elevations are suggested to be due to increased release of CCK from the upper small intestine secondary to the absence of protease activity (trypsin and chymotrypsin) in the intestinal lumen. We have studied plasma CCK levels before and after liquid as well as solid meals in eight patients with pancreatic insufficiency due to advanced chronic pancreatitis and in eight healthy controls. CCK concentrations were measured with a sensitive and specific radioimmunoassay using an antibody directed against the sulfated tyrosyl region of CCK. No differences in basal or maximal postprandial plasma CCK levels between patients and controls were observed. In the liquid meal study, basal CCK concentrations in patients and controls were 2.2 +/- 0.7 and 2.5 +/- 0.4 pM, respectively, with maximal postprandial concentrations of 9.6 +/- 2.2 and 11.2 +/- 1.4 pM. In the solid meal study, basal CCK concentrations in patients and controls were 2.5 +/- 0.6 and 2.6 +/- 0.4 pM, respectively, with maximal postprandial concentrations of 9.4 +/- 1.6 and 8.6 +/- 1.4 pM. The only difference observed was a significantly longer time interval to maximal plasma CCK levels in patients as compared with controls after the liquid meal. Two patients with no detectable trypsin activity in the small intestinal lumen during a Lundh test meal had basal CCK levels of 1.3 and 1.8 pM. Thus, the present study does not support the hypothesis that trypsin is involved in the regulation of CCK release.(ABSTRACT TRUNCATED AT 250 WORDS)
据报道,慢性胰腺炎患者的血浆胆囊收缩素(CCK)浓度会升高。这种升高被认为是由于肠腔中缺乏蛋白酶活性(胰蛋白酶和糜蛋白酶),导致上段小肠CCK释放增加所致。我们研究了8例晚期慢性胰腺炎导致胰腺功能不全的患者和8例健康对照者在进食流食和固体食物前后的血浆CCK水平。使用针对CCK硫酸化酪氨酰区域的抗体,通过灵敏且特异的放射免疫测定法测量CCK浓度。未观察到患者与对照者之间基础或餐后血浆CCK水平的差异。在流食研究中,患者和对照者的基础CCK浓度分别为2.2±0.7和2.5±0.4 pM,餐后最高浓度分别为9.6±2.2和11.2±1.4 pM。在固体食物研究中,患者和对照者的基础CCK浓度分别为2.5±0.6和2.6±0.4 pM,餐后最高浓度分别为9.4±1.6和8.6±1.4 pM。观察到的唯一差异是,与对照者相比,患者在进食流食后达到血浆CCK最高水平的时间间隔明显更长。在伦德试验餐期间,两名小肠腔中未检测到胰蛋白酶活性的患者的基础CCK水平分别为1.3和1.8 pM。因此,本研究不支持胰蛋白酶参与CCK释放调节的假说。(摘要截短于250字)