Inactivation of cholecystokinin octapeptide by normal and cirrhotic liver in rats

Zoltán Berger, Ákos Pap, Imre Ungi, Vince Varro

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3 Citations (Scopus)


In anesthetized rats, a marked decrease in CCK-OP activity and, to a far lesser extent, in the pancreatic secretory effect of CCK-33 were found after portal administration, compared to the femoral route. Changes in the biological activity of CCK-OP were further investigated after 30 min incubation with different subcellular liver fractions (1000×g, 12 000 ×g, microsomal fraction with or without NADPH). All the subcellular liver fractions caused an approximately 70% decrease in the CCK-effect, as calculated from dose-response relationships. The inactivation of CCK-OP after incubation with microsomal fractions of thioacetamide (TAA)-induced cirrhotic liver did not differ from that of control rats. The CCK-OP doseresponse curves were similar in cirrhotic and control rats, but the pancreatic secretion was sustained to a greater extent and the inhibitory effect of supramaximal stimulation was delayed in cirrhotic rats. It was concluded that CCK-OP can be inactivated by liver proteins present in microsomal fractions, by a NADPH-independent mechanism. This inactivation did not diminish in liver cirrhosis. There were no changes in CCK-OP elimination in cirrhotic rats in vivo, thus pancreatic hypertrophy in experimental cirrhosis must be explained by other mechanisms.

Original languageEnglish
Pages (from-to)279-289
Number of pages11
JournalInternational Journal of Pancreatology
Issue number3-4
Publication statusPublished - Oct 1 1986



  • Cholecystokinin octapeptide
  • cirrhosis
  • rat liver

ASJC Scopus subject areas

  • Oncology
  • Endocrinology
  • Gastroenterology

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