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Glucagon Inhibition of Cerulein‐Induced Hypertrophy of the Exocrine Pancreas

 

作者: Fred Kash,   John Wood,   Travis Solomon,  

 

期刊: Pancreas  (OVID Available online 1988)
卷期: Volume 3, issue 1  

页码: 11-17

 

ISSN:0885-3177

 

年代: 1988

 

出版商: OVID

 

关键词: Glucagon;Cholecystokinin;Pancreas;Small intestine;Hypertrophy;Brush-border enzymes

 

数据来源: OVID

 

摘要:

Glucagon is structurally related to secretin but inhibits the effects of secretin and cholecystokinin (CCK) on pancreatic secretion in vivo. Because secretin is a weak stimulant of pancreatic growth and potentiates the trophic effects of CCK, we hypothesized that glucagon might inhibit CCK-induced pancreatic growth. Four groups of 10 rats were injected with saline, glucagon (30 μg, equimolar to a known trophic dose of secretin), cerulein (0.67 μg/kg), or glucagon plus cerulein every 8 h for 5 days. The pancreas was excised, weighed, and assayed for total content of DNA, protein, amylase, chymotrypsinogen, and lipase. In control and glucagon-alone groups, the small intestine was also removed, weighed, and assayed for DNA, protein, and disaccharidase content. Glucagon alone decreased pancreatic DNA and increased lipase content. Compared with cerulein-treated animals, animals treated with glucagon and cerulein showed significant decreases in pancreatic weight and content of protein, amylase, and chymotrypsinogen. Although glucagon had significant effects on intestinal protein, maltase, and sucrase contents in certain segments, there was no clear pattern of response. The data suggest that glucagon may be an inhibitory regulator of pancreatic growth, acting to block the effects of CCK on pancreatic hypertrophy.

 

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