RESPONSE OF GASTRIC INHIBITORY POLYPEPTIDE (GIP) TO TEST MEAL IN CHRONIC-PANCREATITIS - RELATIONSHIP TO ENDOCRINE AND EXOCRINE INSUFFICIENCY

RESPONSE OF GASTRIC INHIBITORY POLYPEPTIDE (GIP) TO TEST MEAL IN CHRONIC-PANCREATITIS - RELATIONSHIP TO ENDOCRINE AND EXOCRINE INSUFFICIENCY
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DOI:
10.1007/bf01220638
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发表时间:
1976-01-01
期刊:
影响因子:
8.2
通讯作者:
ARNOLD, R
ARNOLD, R
中科院分区:
医学1区
文献类型:
--
作者:
EBERT, R;CREUTZFELDT, W;ARNOLD, R

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慢性胰腺炎患者 (29 名) 对测试餐的 IR-GIP [免疫反应性胃抑制肽] 反应明显高于 15 名对照者。这种增加的反应与脂肪泻或葡萄糖不耐受的程度无关。在 IRI(免疫反应性胰岛素)释放中度受损和中度脂肪泻的患者组中,这种情况最为明显。 IR-GIP 对测试餐的反应至少由两个因素决定:通过胰岛素分泌的反馈控制和脂肪的同化。在慢性胰腺炎中,内分泌功能不全可能会引起 GIP 反应过度,而严重的外分泌功能不全可能会阻止脂肪引起的 GIP 释放。胃泌素不参与慢性胰腺炎患者的不同 GIP 反应。
Patients with chronic pancreatitis (29) had a significantly greater IR-GIP [immunoreactive gastric inhibitory peptide] response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI [immunoreactive insulin] release and medium steatorrhea. IR-GIP response to a test meal is determined by at least 2 factors: feedback control via insulin secretion, and assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response, and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.