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Decreased numbers of platelet alpha-adrenergic binding sites in diabetes mellitus

Diabetes Care
|May 1, 1986
PubMed

Insights

Diabetic men have fewer platelet alpha-adrenergic binding sites compared to controls. These reduced sites correlate with higher glycosylated hemoglobin levels, indicating a link between diabetes control and platelet receptor density.

Area of Science:

  • Endocrinology
  • Cardiovascular Research
  • Platelet Physiology

Background:

  • Platelet alpha-adrenergic receptors play a role in hemostasis and cardiovascular regulation.
  • Alterations in platelet function are observed in diabetes mellitus.
  • Understanding these changes may offer insights into diabetic complications.

Purpose of the Study:

  • To investigate potential differences in platelet alpha-adrenergic binding sites between men with diabetes mellitus and healthy male controls.
  • To explore the relationship between the number of these binding sites and glycemic control indicators.

Main Methods:

  • Utilized [3H]dihydroergocryptine (DHE) as a radioligand antagonist to quantify platelet alpha-adrenergic binding sites.
  • Compared binding affinity and site density between 11 diabetic men and 45 male controls.
  • Assessed correlations with glycosylated hemoglobin, catecholamine levels, disease duration, body weight, and fasting blood sugar.

Main Results:

  • No significant difference in binding affinity was found between diabetic subjects and controls.
  • Diabetic men exhibited a significantly lower number of platelet alpha-adrenergic binding sites (430 +/- 30) compared to controls (574 +/- 29; P = .005).
  • The reduction in binding sites was inversely correlated with elevated glycosylated hemoglobin levels (P = .002), but not with other clinical parameters.

Conclusions:

  • Men with diabetes mellitus demonstrate a reduced density of platelet alpha-adrenergic binding sites.
  • This reduction is significantly associated with poorer glycemic control, as indicated by higher glycosylated hemoglobin levels.
  • Further research is warranted to elucidate the pathophysiological implications of these findings in diabetes.

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