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DL-Ethionine is the antagonist of methionine, which is one of the essential amino acids, and is known to cause pancreatic acinar cell necrosis in rats and other experimental animals by either intraperitoneal injection or oral administration. The mechanism of pancreatic damage is presumed to be abnormal metabolism in protein synthesis. There are also other chemical agents, such as 1-aminocyclopentane carboxylic acid (ACPC) and puromycin, which can cause pancreatic acinar cell necrosis and degeneration.

These chemical agents have therefore been used for experiments on pancreatic acinar cell regeneration. On the other hand, the chemical agents which produce pancreatic endocrine cell destruction, such as alloxan [4] and strepto-zotocin [5-7], have been used for various experiments on pancreatic endocrine regeneration, and it is also known that these chemical agents produce diabetic states in rats and guinea-pigs. Furthermore, studies on regeneration of pancreatic acinar cells and endocrine cells after partial or subtotal pancreatectomy of some experimental animals, have been reported [8]. My previous experiment on the characteristic histological patterns of regeneration in the chemically-injured animal pancreas suggested that pancreatic acinar cell regeneration followed by necrosis and destruction by DL-ethionine administration occurred as early as 3 days after the termination of DL-ethionine administration. Pancreatic endocrine cells also regenerated in an early phase, and these cells were found in ductal and/or ductular epithelia, as well as in isolated cases in the interstitium. Histochemically recognized 7-GTP activity in such pancreata was restored rapidly to the control value in parallel with the histopathological restoration. Electronmicroscopic observations supported this view, suggesting that functional restoration of pancreatic exocrine cells begins at an early stage and finishes within a shorter period. Recently, expression of some growth factors was proposed in close relation to pancreatic regeneration. Expression of platelet-derived growth factor-A (PDGF-A) and vascular endothelial growth factor (VEGF) in regeneration of rat pancreas was determined by immunohistochem-ical analysis [9], and epidermal growth factor and leukemia-inhibitor factor induced exocrine-endocrine transdifferentiation in vitro [10]. Furthermore, Renuka et al. [11] suggested that the increased muscarinic Ml and M3 receptor subtypes stimulated insulin secretion and islet cell proliferation during pancreas regeneration. Also, morphological examinations of experimental animals clarified the potential endocrine and exocrine progenitors as tubular complex [12] and acinoinsular and/or ductuloinsular transformation.


1 Fitzgerald PJ, Alvizouri M: Rapid restitution of the rat pancreas following acinar cell necrosis subsequent to ethione. Nature 1952;170:929-930.

2 Eguchi M, Suzuki F, Matsumoto M, et al: Regeneration of pancreatic acinar and endocrine cell after DL-ethionine administration in the rat; in Sato T, Yamauchi H (eds): Pancreatitis. Tokyo, University of Tokyo Press, 1985, pp 317-325.

3 Eguchi M, Matsumoto M, Shirai T, et al: Electronmicroscopic examination of localization of 7-GTP activity in regenerative rat pancreas. J Clin Electron Microsc 1991;24:740-741.

4 Jacob S: Regeneration of the islets of Langerhans in the guinea pig. Cell Tissue Res 1977;181: 277-286.

5 Buchanan KD, Mawhinney WAA: Glucagon release from isolated pancreas in streptozotocin-treated rats. Diabetes 1973;22:797-800.

6 Patel YO, Cameron DP, Brinkier A: Changes in somatostatin concentration in pancreas and other tissues of streptozotocin diabetic rats. Endocrinology 1978;103:917-923.

7 Cantenys D, Portha B, Dutrillaux MC, et al: Histogenesis of the endocrine pancreas in new born rats after destruction by streptozotocin. Virchows Arch B Cell Pathol Incl Mol Pathol 1981;35: 109-122.

8 Pearson KW, Scott D, Torrance B: Effect of partial surgical pancreatectomy in rats. Gastroenterology 1977;72:469-473.

9 Dembinski A, Warzecha Z, Ceranowicz P, et al: Effect of ischemic precondition on pancreatic regeneration and pancreatic expression of vascular endothelial growth factor and platelet-derived growth factor-A in ischemia/reperfusion-induced pancreatitis. J Physiol Pharmacol 2006;57: 39-58.

10 Lardon J, Bouwens L: Metaplasia in the pancreas. Differentiation 2005;73:278-286.

11 Renuka TR, Savitha B, Paulose CS: Muscarinic M1 and M3 receptor binding alterations in pancreas during pancreatic regeneration of young rats. Endocr Res 2005;31:259-270.

12 Wang GS, Rosenberg L, Scott FW: Tubular complexes as a source for islet neogenesis in the pancreas of diabetes-prone BB rats. Lab Invest 2005;85:675-688.

Masanobu Eguchi

Department of Clinical Pathology

Juntendo University, Nerima Hospital

Takanodai 3-10-10, Nerima, Tokyo 177-8521 (Japan)

Tel +81 3 5923 3111, E-Mail [email protected]

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  • Helen Michael
    How can i conclude on pancretitis?
    3 years ago

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