Effects of a Cholecystokinin-Like Peptide on DNA and Polyamine Synthesis in the Rat Pancreas

Haarstad, H.; Winnberg, Asgeir; Petersen, H

doi:10.3109/00365528509089692

Cited by 33 publications

(23 citation statements)

References 12 publications

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“…In guinea pig pancreas, 4°70 of CCK receptors can be considered to be 'non-selective or gastrin receptors' [10]. These receptors are not linked to enzyme secretion but might be involved in Na+/H + exchange [11] (a phenomenon often linked to adenylate cyclase inhibition [12]) and in trophic effects [13].…”

Section: Discussionmentioning

confidence: 99%

CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin‐sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4‐2J

et al. 1988

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(Thr28,Nleat)CCK(23-33) (CCK-9) and gastrin(1-17)l (gastrin) inhibited adenylate cyclase activity in membranes from the tumoral rat pancreatic acinar cell line AR 4-2J through a Bordetella pertussis toxin-sensitive mechanism. This contrasted with the stimulatory effect exerted by CCK-9 on adenylate cyclase activity in membranes from normal rat pancreas. The relative potency of CCK-9, gastrin, and related peptides in inhibiting adenylate cyclase, when confronted with previous evidence, suggests that 'non-selective CCK-gastrin CCK-B receptors' predominating over 'selective CCK-A receptors' in the AR 4-2J cell line, favored the coupling of the first receptors to adenylate cyclase through G, while CCK-A receptors capable of stimulating the enzyme through Gs were detected only after Bordetella pertussis toxin pretreatment.

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Section: Discussionmentioning

confidence: 99%

CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin‐sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4‐2J

et al. 1988

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“…The DNA polymerase activity was calculated according to a modification of a method of Haarstad et al [25]. The amount [methyl- 3 H]thymidine triphosphate (1.78 TBq/nmol) incorporated in newly formed DNA was measured as picomoles per 30 min per milligram DNA.…”

Section: Methodsmentioning

confidence: 99%

“…It is well known that the polyamine metabolism is essentially involved in normal and adaptive pancreatic growth in rats [25, 26, 27, 28]. α-Difluoromethylornithine (DFMO) is a potent specific inhibitor of ornithine decarboxylase (ODC) which is the key enzyme of intracellular polyamine synthesis [5].…”

Section: Introductionmentioning

confidence: 99%

Effects of Insulin-Like Growth Factor I on Growth and Polyamine Metabolism in Various Organs in Rats

Höpfner¹,

Berger²,

Fölsch³

et al. 2002

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Background/Aim: Human insulin-like growth factor I (IGF-I) is known to be the mediator of growth hormone dependent proliferation and is responsible for growth-promoting effects in the gastrointestinal tract. Polyamines play an essential role in cell growth and differentiation. The aim of the present study was to investigate the growth-promoting potency of IGF-I in various organ systems simultaneously in rats and the potential role of the polyamine metabolism during IGF-I-induced gastrointestinal growth. Methods: Based on results of initial dose-response studies, male Wistar rats (150 g) were either treated by subcutaneous injections with (1) IGF-I (1 × 1,000 µg/kg/24 h); (2) IGF-I plus α-difluoromethylornithine (3 × 300 mg i.p./kg/24 h plus 2% in drinking water), a specific inhibitor of intracellular polyamine de novo synthesis, or (3) saline (controls). 9–10 animals per group were sacrificed after 5 days of treatment. Results: IGF-I caused a significant (p < 0.005) increase in the weight of small intestine and spleen due to hyperplasia in the small intestine and hypertrophy and hyperplasia in the spleen, while no trophic effects could be observed in stomach or pancreas. The amylase concentration in the pancreas was increased. Simultaneously administered α-difluoromethylornithine significantly (p < 0.005) abolished the IGF-I-induced trophic effects in small intestine and spleen. Conclusions: These data reveal different trophic effects of IGF-I in various organ systems: while significant growth stimulation was found in small intestine and spleen, no proliferation was seen in pancreas and stomach. Polyamines obviously play an important role in IGF-I-mediated gastrointestinal growth.

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“…The enzyme activity was determined by a modification of a method de scribed by Haarstad et al [9] by measuring the picomoles of ,4C02 liberated from the (l-l4C)-labeled sub strate ornithine. 500 pi of the above-mentioned cytosol/glycerol mixture were given to 1.5 ml of a stan dard reaction mixture containing 75 pmol Tris buffer (pH 7.5), 1.5 pmol EDTA, 3 pmol dithiothreitol, 0.3 pmol pyridoxal phosphate and 8.77 nmol (0.5 pCi) DL-( l-,4C)-omilhine (50 pCi/ml).…”

Section: Analytical Proceduresmentioning

confidence: 99%

“…5] and regeneration of the liver [6,7] is well-estab lished. However, though increased polyamine concentrations after hormonal stimulation of pancreatic growth were described [8][9][10]. their role in pancreatic adaptation has not been satisfactorily defined [4],…”

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confidence: 99%

Role of Ornithine Decarboxylase and Polyamines in Camostate (Foy-305)-Induced Pancreatic Growth in Rats

Löser¹,

Fölsch²,

Cleffmann³

et al. 1989

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This study was designed to investigate changes of ornithine decarboxylase and polyamines during pancreatic adaptation in response to feeding of the synthetic protease inhibitor camostate. α-Difluoromethylornithine, an irreversible and specific inhibitor of ornithine decarboxylase, was applied simultaneously to elucidate the essential role of polyamines in pancreatic growth. Cholecystokinin (CCK) plasma levels in camostate-fed rats increased from basal values of 3–4 pmol/l to a maximal level of 27.4 pmol/l after 2 h; they then decreased up to 12 h but remained elevated above controls throughout the 30-day experiments. In the camostate group pancreatic ornithine decarboxylase activity was elevated after 2 h, reaching a maximum after 6 h (1,858.5 pmol ¹⁴CO₂/h/mg DNA, about 200-fold above controls) followed by a significant increase in putrescine after 4 h and spermidine after 24 h while spermine remained unchanged. The trophic parameters increased in the following time sequence: thymidine kinase (12 h), DNA polymerase (12 h), protein (24 h), pancreatic weight (24 h) and DNA (5 days). α-Difluoromethylornithine significantly delayed and reduced the camostate-induced increase in ornithine decarboxylase activity and polyamine concentrations as well as the trophic parameters. Application of the CCK receptor antagonist L-364,718 resulted in complete inhibition of the increases in ornithine decarboxylase, polyamines and all trophic parameters. These data indicate an important role for ornithine decarboxylase and polyamines in camostate-induced pancreatic growth and hormonal mediated pancreatic adaptation in rats.

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Effects of a Cholecystokinin-Like Peptide on DNA and Polyamine Synthesis in the Rat Pancreas

Cited by 33 publications

References 12 publications

CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin‐sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4‐2J

CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin‐sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4‐2J

Effects of Insulin-Like Growth Factor I on Growth and Polyamine Metabolism in Various Organs in Rats

Role of Ornithine Decarboxylase and Polyamines in Camostate (Foy-305)-Induced Pancreatic Growth in Rats

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