Abstract
Diabetes is a chronic, endocrine disorder that effects millions of people worldwide. Cardiovascular complications are the major cause of diabetes-related morbidity and mortality. Cardiac β1- and β2-adrenoceptor (AR) stimulation mediates positive inotropy and chronotropy, whereas β3-AR mediates negative inotropic effect. Changes in β-AR responsiveness are thought to be an important factor that contributes to the diabetic cardiac dysfunction. Diabetes related changes in β-AR expression, signaling, and β-AR mediated cardiac function have been studied by several investigators for many years. In the present review, we have screened PubMed database to obtain relevant articles on this topic. Our search has ended up with wide range of different findings about the effect of diabetes on β-AR mediated changes both in molecular and functional level. Considering these inconsistent findings, the effect of diabetes on cardiac β-AR still remains to be clarified.
Highlights
Diabetes is an endocrine disorder due to partial or complete insulin deficiency or to insulin resistance in the target tissues
Ventricular myocytes have been isolated from Wistar rats and the isoprenaline-induced contractile response was not affected after 24 h of hyperglycemic exposure [129]
It is important to understand underlying mechanisms that contributes to diabetes-induced cardiac dysfunction to allow researchers and physicians to prevent or treat it
Summary
Diabetes is an endocrine disorder due to partial or complete insulin deficiency or to insulin resistance in the target tissues. In line with the change in protein expression level, mRNA expression of β3 -AR was shown to increased in 14-week STZ diabetic rat heart [42]. The same investigator group have determined the change of β-AR subtypes at 10 and 16 weeks of diabetes in ZDF rats They have reported that protein expression of β1 - AR was preserved at 10th week, it was decreased at 16th week. Stimulation of heterotrimeric G protein has been shown to result in similar AC activity [50,62,117,118] or decreased AC activity [81,82,105,119] or increased AC activity [85] in diabetic animals compared to control group. ENOS expression did not change in T1DM rats after 8 weeks of diabetes [36,40] Contrary to these findings, Kleindienst et al found increased eNOS and p-eNOS, both at Ser1177 and Thr495 site, expression in T2DM mice compared to the control group [98]. Β-AR functional changes in cardiac tissue is described, firstly, the contraction and/or relaxation responses obtained in in vitro studies and Ca++ -mediated responses, if any, and the responses obtained from in vivo studies in T1DM and T2DM separately
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