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Research ArticleOriginal Article
Open Access

Insulin enhances amylase and lipase activity in the pancreas of streptozotocin-diabetic rats. An in vivo study

Adib A. Aughsteen and Faisal I. Mohammed
Saudi Medical Journal July 2002, 23 (7) 838-844;
Adib A. Aughsteen
Faculty of Pharmacy and Medical Laboratories, Al-Zaytoonah University, PO Box 130, Amman 11733, Jordan. Tel. +962 (6) 4291511 Ext. 314. Fax. +962 (6) 4291432. E-mail: [email protected]
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Faisal I. Mohammed
Department of Physiology and Biochemistry, Faculty of Medicine, University of Jordan, Amman, Jordan.
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Abstract

OBJECTIVE: To analyze the biochemical effect of in vivo insulin therapy on the amylase and lipase activities in the pancreatic acinar cells of streptozotocin-diabetic rats, and to detect any possible regeneration in the beta cells of the islets of Langerhans using transmission electron microscopy.

METHODS: Adult male albino Fischer-344 rats were divided into 3 groups, the first group received drug vehicle and served as controls, the 2nd group was made diabetic with a single intravenous dose of streptozotocin (75 mg/kg body weight), while the 3rd group was made diabetic as in its 2nd group but the rats were treated with Lente human insulin. Their body weight, blood glucose and glucosuria were regularly recorded, and blood samples for serum immunoreactive insulin assay were taken from each rat at sacrifice. The largest part of each excised pancreas was homogenized for biochemical assay of amylase, lipase and insulin, while only a small part of the gland was used for morphological survey. The study was conducted in the Faculty of Medicine, University of Jordan, Amman, Jordan.

RESULTS: The serum immunoreactive and pancreatic-homogenate insulin levels of the untreated diabetic rats were reduced by 85% and 37% compared with those of the controls. Their pancreatic amylase and lipase levels were also reduced by 66% and 43%. Insulin treatment of diabetic rats resulted in a 65-fold increase in serum immunoreactive insulin, and approximately 61%, 47%, and 25% increase in the pancreatic-homogenate levels of amylase, lipase, and insulin. Electron microscopic examination of the pancreas of untreated and insulin-treated diabetic rats showed no evidence of beta cell regeneration.

CONCLUSION: Inspite of the controversies in an extensively studied field of in vivo and in vitro influence of insulin on pancreatic enzymes, our present biochemical data clearly indicates that in vivo insulin administration has a stimulant effect on both amylase and lipase activity in the pancreatic acinar cells of streptozotocin-diabetic rats. It also proposes that insulin might play an important role in beta cell regeneration although no morphological evidence of beta cell mitosis was demonstrable. We finally suggest that the biochemical assay of pancreatic enzymes might be of value in determining the severity and chronicity of human insulin-dependent diabetes, and can be used as a parameter in evaluating the response to treatment.

  • Copyright: © Saudi Medical Journal

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Saudi Medical Journal: 23 (7)
Saudi Medical Journal
Vol. 23, Issue 7
1 Jul 2002
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Insulin enhances amylase and lipase activity in the pancreas of streptozotocin-diabetic rats. An in vivo study
Adib A. Aughsteen, Faisal I. Mohammed
Saudi Medical Journal Jul 2002, 23 (7) 838-844;

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Insulin enhances amylase and lipase activity in the pancreas of streptozotocin-diabetic rats. An in vivo study
Adib A. Aughsteen, Faisal I. Mohammed
Saudi Medical Journal Jul 2002, 23 (7) 838-844;
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© 2025 Saudi Medical Journal Saudi Medical Journal is copyright under the Berne Convention and the International Copyright Convention.  Saudi Medical Journal is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work. Electronic ISSN 1658-3175. Print ISSN 0379-5284.

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