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Molecular aspects of pancreatic islet cell defence mechanisms in type I diabetes

Molecular aspects of pancreatic islet cell defence mechanisms in type I diabetes
Molecular aspects of pancreatic islet cell defence mechanisms in type I diabetes

Insulin deficiency leading to developing of Type I diabetes may be associated not only with autoimmune beta cell destruction but also with the potential of the beta cell for adaptive repair and regeneration following cytotoxic injury. Activation or stimulation of islet cell defence mechanisms could provide a novel approach to the prevention and treatment of Type I diabetes.

Pancreatic reg gene expression was recently discovered to be closely associated with experimentally induced islet cell growth both in vivo and in vitro, and also responsive to beta-cytotoxic injury of islets maintained in culture. The present study investigated the role of the reg gene and its product in islet cell defence processes both in vivo and in vitro.

The best analogue to human Type I diabetes - the spontaneously diabetic BB rat was used in the in vivo study to investigate the correlation between the expression of the reg gene and the development of diabetes with respect to islet adaptive regeneration and repair. Using northern blot analysis of rat pancreatic RNA from serial pancreatic biopsies, it was found that the reg mRNA levels declined in control diabetes-resistant BB/S-C rats as age increased; whereas there was a significant increase in the reg mRNA levels in diabetes-prone BB/S rats at or around the mean age for onset of diabetes (90/100 days). This may indicate an activation of the reg gene expression in these animals following autoimmune attack of the islet cells.

The effects of rat reg protein on islet growth and protection from toxic injury were further studied in vitro. Isolated islets treated with exogenous rat recombinant reg protein did not show a Mitogenic effect on islet cell DNA synthesis; and such treatment failed to counteract the inhibitory effect of IL-1 B on islet cell growth and insulin release.

University of Southampton
Zhang, Shaoli
731ca399-f117-4aff-8d1d-36e59c919539
Zhang, Shaoli
731ca399-f117-4aff-8d1d-36e59c919539

Zhang, Shaoli (1993) Molecular aspects of pancreatic islet cell defence mechanisms in type I diabetes. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Insulin deficiency leading to developing of Type I diabetes may be associated not only with autoimmune beta cell destruction but also with the potential of the beta cell for adaptive repair and regeneration following cytotoxic injury. Activation or stimulation of islet cell defence mechanisms could provide a novel approach to the prevention and treatment of Type I diabetes.

Pancreatic reg gene expression was recently discovered to be closely associated with experimentally induced islet cell growth both in vivo and in vitro, and also responsive to beta-cytotoxic injury of islets maintained in culture. The present study investigated the role of the reg gene and its product in islet cell defence processes both in vivo and in vitro.

The best analogue to human Type I diabetes - the spontaneously diabetic BB rat was used in the in vivo study to investigate the correlation between the expression of the reg gene and the development of diabetes with respect to islet adaptive regeneration and repair. Using northern blot analysis of rat pancreatic RNA from serial pancreatic biopsies, it was found that the reg mRNA levels declined in control diabetes-resistant BB/S-C rats as age increased; whereas there was a significant increase in the reg mRNA levels in diabetes-prone BB/S rats at or around the mean age for onset of diabetes (90/100 days). This may indicate an activation of the reg gene expression in these animals following autoimmune attack of the islet cells.

The effects of rat reg protein on islet growth and protection from toxic injury were further studied in vitro. Isolated islets treated with exogenous rat recombinant reg protein did not show a Mitogenic effect on islet cell DNA synthesis; and such treatment failed to counteract the inhibitory effect of IL-1 B on islet cell growth and insulin release.

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Published date: 1993

Identifiers

Local EPrints ID: 462384
URI: http://eprints.soton.ac.uk/id/eprint/462384
PURE UUID: a715d038-0138-497d-8be4-4826cddde383

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Date deposited: 04 Jul 2022 19:06
Last modified: 23 Jul 2022 01:07

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Contributors

Author: Shaoli Zhang

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