1978
DOI: 10.3109/00365527809181779
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Influence of Repeated Administration of Cholecystokinin and Secretin on the Pancreas of the Rat

Abstract: Repeated injections of cholecystokinin (CCK) during a period of up to 3 weeks significantly increased the weight of the pancreas in rats. This was associated with an increase in the amount of protein per unit weight of DNA, suggesting hypertrophy of the acinar cells, and with increase in the total amount of pancreatic DNA, indicating additional hyperplasia of the gland. CCK administration also increased the pancreatic content of amylase and trypsin, but the content of lipase remained unchanged. The rate of sec… Show more

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Cited by 146 publications
(58 citation statements)
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“…It has been shown also that intra-duodenal infusion of 100 mg/kg body weight FOY-305, the same dose as that used in the present study, caused release of CCK into the portal vein of an isolated perfused duodenum, and that the CCK release was not blocked by tetrodotoxin but by vascular perfusion of a calcium-deficient solution (KANNO et al, 1979b(KANNO et al, , 1980. Furthermore, chronic treatment of CCK or caerulein is known to cause hypertrophy and hyperpyknia (MAINZ et al, 1973;YANATORI and FUJITA, 1976;FOLSCH et al, 1978;PETERSEN et al, 1978;SOLOMON et al, 1978SOLOMON et al, , 1979. The present results together with the above reported data support the view that FOY-305-induced effects on rat pancreas may be mediated mainly by endogenous CCK, though the possible participation of other humoral or neuronal factors cannot be excluded.…”
Section: Discussionmentioning
confidence: 99%
“…It has been shown also that intra-duodenal infusion of 100 mg/kg body weight FOY-305, the same dose as that used in the present study, caused release of CCK into the portal vein of an isolated perfused duodenum, and that the CCK release was not blocked by tetrodotoxin but by vascular perfusion of a calcium-deficient solution (KANNO et al, 1979b(KANNO et al, , 1980. Furthermore, chronic treatment of CCK or caerulein is known to cause hypertrophy and hyperpyknia (MAINZ et al, 1973;YANATORI and FUJITA, 1976;FOLSCH et al, 1978;PETERSEN et al, 1978;SOLOMON et al, 1978SOLOMON et al, , 1979. The present results together with the above reported data support the view that FOY-305-induced effects on rat pancreas may be mediated mainly by endogenous CCK, though the possible participation of other humoral or neuronal factors cannot be excluded.…”
Section: Discussionmentioning
confidence: 99%
“…Gastrin is implicated in a marked proliferative action on the proximal small intestine which diminishes distally, but evidence for a trophic effect on the colon is very limited Thomas et al 2003). CCK stimulates growth of the pancreas in experimental studies (Brants & Morisset, 1976;Folsch et al 1978). However, evidence for CCK playing a major role in the growth of the GI mucosa (stomach, small bowel and colon) is limited .…”
Section: Local Effects Of Cholecystokinin and Gastrin In The Gutmentioning
confidence: 99%
“…CCK is released mainly from the I cells of the small intestine and induces gallbladder contraction and pancreatic enzyme secretion in mammals (Folsch et al 1978, Sonobe et al 1995. Furthermore, CCK is expressed in the central and peripheral nervous system and is implicated in neural functions such as food intake, sleep and memory (Crawley & Corwin 1994, Moran & Schwartz 1994.…”
Section: Introductionmentioning
confidence: 99%