Springer Online Journal Archives 1860-2000
Abstract Aim of the present study was to evaluate therole of cellular uptake of dietary [ H]putrescine forthe regulation of pancreatic, hepatic, and smallintestinal polyamine metabolism during normal andcamostate-induced pancreatic growth in rats in vivo. Initiallydose-response and time-course studies of[3H]putrescine uptake were performed. MaleWistar rats were either treated with the synthetictrypsin inhibitor camostate (200 mg/kg body wt orally twice daily),camostate plus the ornithine decarboxylase inhibitoralpha-difluoromethylornithine (DFMO) (2% in drinkingwater plus 3 × 300 mg/kg body wt intraperitoneallyduring daytime) or saline as controls. After 4, 8, 12,24, 36, 48, or 120 hr, five to seven animals per groupwere killed, respectively. Orally fed [ H]putrescine (10nmol/kg body wt. 2 hr prior to death) is rapidly taken up and further metabolized tospermidine in normal growing pancreas, liver, and smallintestine. Feeding of camostate significantly enhanceddietary [3H]putrescine uptake, whilesimultaneous inhibition of de novo synthesis ofintracellular polyamines by DFMO resulted in a highlysignificant further increase in cellular uptake oforally fed [3H]putrescine, which isimmediately metabolized to spermidine. The present in vivo data confirmthe important role of dietary putrescine uptake for themaintenance of intracellular polyamine pool in normaland stimulated pancreatic growth. Furthermore, dietary putrescine uptake is an importantregulatory mechanism to maintain the normal andgrowth-stimulated cellular polyamine pool in thepancreas after potent simultaneous inhibition ofintracellular de novo polyamine synthesis.
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