Mechanisms for pancreatic hypertrophy induced by long-term administration of bethanechol

Kato, Masato; Ohkuma, Seitaro; Kataoka, Keisuke; Kashima, Kei; Mukainaka, Teruo; Kuriyama, Kinya

doi:10.1016/0926-6917(94)90025-6

Cited by 3 publications

(1 citation statement)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, there is much evidence to suggest that CCK stimulates secretion of pancreatic juice and growth of the pancreas via CCK-A receptors on the acinar cells. Recently, however, Li & Owyang (1994), reported that CCK stimulates pancreatic enzyme secretion via vagal afferent pathways, and Kato et al (1994) have suggested that direct stimulation of muscarinic receptors induces pancreatic hypertrophy. Thus, the mode of action of CCK is far from clear, and the popular view that CCK acts directly on the acinar cells may have to be reconsidered (LaMont 1994).…”

Section: Discussionmentioning

confidence: 99%

The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

Nylander¹,

Chen²,

Ding³

et al. 1997

Pharmacology & Toxicology

View full text Add to dashboard Cite

Cholecystokinin (CCK) stimulates pancreatic enzyme secretion and growth. This study establishes the dose/ plasma concentration -and time -response relationships for the trophic effect of CCK on the rat pancreas and evaluates the importance of vagal innervation and muscarinic receptors for the trophic effect. Rats received sulfated CCK-8 (CCK8s) by continuous subcutaneous infusion. Different doses and different times of treatment were tested. The trophic effect was determined as wet weight and DNA content of the pancreas. The pancreatic weight and DNA content were found to depend not only on the plasma concentration of CCK-8s but also on the duration of treatment. The ECSo value was 40 pmoles CCK-8s per liter. This value should be compared with plasma CCK-8s concentrations of 2 4 pmol/l in intact fed rats. Maximum trophic effect was observed after 7-14 days of infusion. We conclude that although physiologically relevant concentrations of CCK-8s may be important for the maintenance of the pancreas they do not induce growth. In another experiment atropinized, vagally denervated and intact rats were treated with a maximally effective dose of CCK for four days. The trophic effect of CCK-8s was unaffected by vagotomy or atropinization.

show abstract

Section: Discussionmentioning

confidence: 99%

The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

Nylander¹,

Chen²,

Ding³

et al. 1997

Pharmacology & Toxicology

View full text Add to dashboard Cite

show abstract

Toxicology of the Exocrine Pancreas

Foster¹

2009

General, Applied and Systems Toxicology

View full text Add to dashboard Cite

The exocrine pancreas is not a common target organ for toxic drugs and chemicals. It is however the fifth most common human cancer in the western world, and acute and chronic pancreatitis, through various identifiable and unidentified causes, is a common disease in both the developed and developing countries of the world. Both inflammatory disease and cancer of the pancreas is correlated to lifestyle with poor diet and habits, such as moderate to high alcohol intake and smoking, having positive correlations to developing the disease. The chapter describes the functional anatomy of the organ together with its biochemistry that determines toxicity, in particular the role of oxidant damage in the development of cell and tissue damage is thought to be important. The consequences of toxic damage to the acinar cells are severe and primarily result from the auto‐activation and hence autodigestion of the tissue by the digestive enzymes normally contained within the exocrine cells, a cascade of apoptosis/necrosis and fibrosis with the ultimate collapse of the organ, subsequent shock, multi‐organ collapse and death. The organ has complex molecular mechanisms to prevent premature activation of the digestive enzymes and also has defence mechanisms present to neutralise any premature enzyme activation but these can be rendered ineffectual by factors such as alcohol abuse and a poor diet. Chemical exposure, through both occupational and consumer product usage, has been associated with the development of both pancreatic neoplastic and non‐neoplastic disease but the relationship between exposure and disease has never developed further than a simple association and it is likely that the development of pancreatic disease is a multi‐faceted combination of inter‐related events, none of which in isolation can induce disease. The pancreas has its own array of phase 1 and 2 metabolic enzyme systems and the role of pancreatic drug and chemical activation and detoxification in inducing toxicity is discussed together with the possible secondary effects of hepatic drug/chemical activation and detoxification. Finally the role of animal models of pancreatic disease is discussed in terms of their contribution to understanding the aetiology of the human conditions and the possible use of therapeutic intervention in treating the disease.

show abstract

Pancreatic enlargement in a patient receiving therapy with vasodilators for pulmonary arterial hypertension: a case report

et al. 2022

View full text Add to dashboard Cite

Mechanisms for pancreatic hypertrophy induced by long-term administration of bethanechol

Cited by 3 publications

References 21 publications

The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

Toxicology of the Exocrine Pancreas

Pancreatic enlargement in a patient receiving therapy with vasodilators for pulmonary arterial hypertension: a case report

Contact Info

Product

Resources

About