The effect of diabetes on expression of beta(1)-, beta(2)-, and beta(3)-adrenoreceptor in rat hearts

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DIABETES, vol.50, no.2, pp.455-461, 2001 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 50 Issue: 2
  • Publication Date: 2001
  • Doi Number: 10.2337/diabetes.50.2.455
  • Title of Journal : DIABETES
  • Page Numbers: pp.455-461


Diabetic hearts exhibit decreased responsiveness to stimulation by beta -adrenoreceptor (beta -AR) agonists. This decrease in activity may be due to changes in expression and/or signaling of beta -AR. Recently we showed that right atrial strips from 14-week streptozotocin (STZ)induced diabetic rat hearts exhibit decreased responsiveness to beta (1)-AR agonist stimulation, but not to beta (2)-AR agonist. In the present study, we investigated the effects of long-term diabetes on the expression of cardiac beta (1)-, beta (2)-, and beta (3)-ARs and looked at whether these changes could be restored with insulin treatment. Using reverse transcription-polymerase chain reaction (RT-PCR), PAGE, and Western blot analysis, we found that beta (1)-AR mRNA and protein levels decreased by 34.9 +/- 5.8 and 44.4 +/- 5.8%, respectively, in 14 week-STZ-treated diabetic rat hearts when compared with age-matched controls. On the other hand, mRNA levels encoding beta (2)- and beta (3)-ARs increased by 72.5 +/- 16.6 and 97.3 +/- 26.1%, respectively. Although the latter translated into a proportional increase in beta (3)-AR protein levels (100.0 +/- 17.0%), beta (2)-AR protein levels decreased to 82.6 +/- 1.1% of control. Insulin treatment for 2 weeks, after 12 weeks of untreated diabetes, partially restored beta (1)-AR mRNA and protein levels to 60.1 +/- 8.4 and 83.2 +/- 5.0%, respectively, of control. Although insulin treatment minimally attenuated the rise in mRNA levels encoding beta (2)- and beta (3)-ARs, the steady-state levels of these proteins returned to near control values. These data suggest that the decreased responsiveness of diabetic hearts to stimulation of beta -AR agonists may be due to a decrease in beta (1)-AR and an increase beta (3)-AR expression.