Carrière Frédéric, Grandval Philippe, Renou Christophe, Palomba Aurélie, Priéri Florence, Giallo Jacqueline, Henniges Friederike, Sander-Struckmeier Suntje, Laugier René
Laboratoire d'Enzymologie Interfaciale et de Physiologie de la Lipolyse, IBSM-CNRS, 31 Chemin Joseph Aiguier, 13402 Marseille Cedex 20, France.
Clin Gastroenterol Hepatol. 2005 Jan;3(1):28-38. doi: 10.1016/s1542-3565(04)00601-9.
BACKGROUND & AIMS: The contribution of human gastric lipase (HGL) to the overall lipolysis process in chronic pancreatitis (CP), as well as the relative pancreatic enzyme levels, rarely are addressed. This study was designed to quantify pancreatic and extrapancreatic enzyme output, activity, and stability in CP patients vs. healthy volunteers.
Healthy volunteers (n = 6), mild CP patients (n = 5), and severe (n = 7) CP patients were intubated with gastric and duodenal tubes before the administration of a test meal. HGL, human pancreatic lipase (HPL), chymotrypsin, and amylase concentrations were assessed in gastric and duodenal samples by measuring the respective enzymatic activities. Intragastric and overall lipolysis levels at the angle of Treitz were estimated based on quantitative analysis of lipolysis products. Similar analyses were performed on duodenal contents incubated ex vivo for studying enzyme stability and evolution of lipolysis.
Although HPL, chymotrypsin, and amylase outputs all were extremely low, HGL outputs in patients with severe CP (46.8 +/- 31.0 mg) were 3-4-fold higher than in healthy controls (13.3 +/- 13.8 mg). Intragastric lipolysis did not increase, however, in patients with severe CP, probably because of the rapid decrease in the pH level of the gastric contents caused by a higher gastric acid secretion. HGL remains active and highly stable in the acidic duodenal contents of CP patients, and, overall, can achieve a significant lipolysis of the dietary triglycerides (30% of the control values) in the absence of HPL.
Although all pancreatic enzyme secretions are simultaneously reduced in severe CP, gastric lipase can compensate partly for the loss of pancreatic lipase but not normalize overall lipolytic activity.
人类胃脂肪酶（HGL）对慢性胰腺炎（CP）整体脂肪分解过程的贡献以及相对的胰腺酶水平很少被提及。本研究旨在量化CP患者与健康志愿者的胰腺和胰腺外酶输出、活性及稳定性。
在给予试验餐之前，对健康志愿者（n = 6）、轻度CP患者（n = 5）和重度（n = 7）CP患者插入胃管和十二指肠管。通过测量各自的酶活性来评估胃和十二指肠样本中HGL、人类胰腺脂肪酶（HPL）、胰凝乳蛋白酶和淀粉酶的浓度。基于脂肪分解产物的定量分析估计Treitz角处的胃内和整体脂肪分解水平。对十二指肠内容物进行体外孵育以研究酶稳定性和脂肪分解的演变，并进行类似分析。
尽管HPL、胰凝乳蛋白酶和淀粉酶的输出量都极低，但重度CP患者的HGL输出量（46.8±31.0毫克）比健康对照组（13.3±13.8毫克）高3至4倍。然而，重度CP患者的胃内脂肪分解并未增加，这可能是由于胃酸分泌增加导致胃内容物pH值迅速下降。HGL在CP患者的酸性十二指肠内容物中仍保持活性且高度稳定，总体而言，在没有HPL的情况下，它能够对膳食甘油三酯进行显著的脂肪分解（达到对照值的30%）。
尽管重度CP患者所有胰腺酶分泌同时减少，但胃脂肪酶可部分补偿胰腺脂肪酶的损失，但无法使整体脂肪分解活性恢复正常。
