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Related Experiment Videos

Bromocriptine/SKF38393 ameliorates islet dysfunction in the diabetic (db/db) mouse

Y Liang1, T L Jetton, M Lubkin

  • 1Ergoscience, Charlestown, Massachusetts 02129, USA. yliang@ergo.com

Cellular and Molecular Life Sciences : CMLS
|August 26, 1998
PubMed
Summary

Dopamine agonists (bromocriptine/SKF38393) improved pancreatic islet function in diabetic mice by reducing hyperglycemia and hyperlipidemia. This treatment enhanced insulin release and content, suggesting an indirect mechanism via the neuroendocrine system.

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Neuroendocrinology

Background:

  • Pancreatic islet dysfunction is central to type II diabetes.
  • Chronic high blood sugar (hyperglycemia) and high blood lipids (hyperlipidemia) can impair islet function.
  • Previous research indicated dopaminergic agonists could improve hyperglycemia and hyperlipidemia in diabetic rodents.

Purpose of the Study:

  • To investigate the therapeutic effect of dopamine D2/D1 receptor agonists (bromocriptine/SKF38393, BC/SKF) on pancreatic islet dysfunction in a mouse model of type II diabetes (db/db mice).

Main Methods:

  • db/db mice were treated with BC/SKF for two weeks.
  • Evaluated effects on hyperglycemia, hyperlipidemia, and islet function (insulin release, insulin content).
  • Assessed the impact on daily corticosterone, blood glucose, and plasma lipid levels.

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Main Results:

  • BC/SKF treatment significantly reduced hyperglycemia and hyperlipidemia.
  • Islet function improved, evidenced by increased secretagogue-stimulated insulin release and a fourfold rise in pancreatic insulin content.
  • The beneficial effects were not observed in pair-fed animals and BC/SKF did not directly stimulate insulin secretion, indicating an indirect mechanism.
  • Treatment normalized elevated corticosterone, blood glucose, and plasma lipid levels.

Conclusions:

  • Dopamine D2/D1 receptor agonist treatment (BC/SKF) ameliorates pancreatic islet dysfunction in a mouse model of type II diabetes.
  • The mechanism appears indirect, potentially involving the neuroendocrine system's regulation of peripheral metabolism.
  • BC/SKF demonstrates potential as a therapeutic strategy for type II diabetes by improving metabolic parameters and islet function.