Deranged platelet calcium homeostasis in poorly controlled IDDM patients
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Published on: April 6, 2017
F Pellegatta1, F Folli, P Ronchi
1Department of Medicine, IRCCS H. San Raffaele, Milano, Italy.
Insights
Platelet hyperfunction in type 1 diabetes is linked to poor metabolic control, affecting calcium levels. Acute blood sugar changes do not influence this platelet activation.
Area of Science:
- Endocrinology
- Hematology
- Cell Biology
Background:
- Platelet hyperfunction is common in insulin-dependent diabetes mellitus (IDDM).
- Cytosolic free calcium ([Ca2+]i) is crucial for platelet activation.
Purpose of the Study:
- To investigate the role of cytosolic free calcium ([Ca2+]i) in platelet activation in IDDM patients.
- To correlate [Ca2+]i levels with metabolic control and diabetic complications.
Main Methods:
- Measured [Ca2+]i in platelets of 60 IDDM patients and 31 controls using the fura-2 fluorescent probe.
- Studied platelets under resting conditions and after thrombin stimulation.
- Analyzed correlation between [Ca2+]i, HbA1c, and blood cholesterol.
Main Results:
- No overall difference in [Ca2+]i between IDDM patients and controls.
- Higher resting [Ca2+]i in IDDM patients with poor metabolic control (HbA1c > 8%).
- Increased thrombin-induced rise in [Ca2+]i observed in uncomplicated IDDM patients with good metabolic control.
- Significant correlation between resting [Ca2+]i, HbA1c, and cholesterol levels in diabetic patients.
Conclusions:
- Platelet hyperfunction in IDDM is associated with unsatisfactory metabolic control and involves calcium homeostasis.
- Acute fluctuations in blood glucose levels do not appear to influence platelet [Ca2+]i or activation in this context.
Objective:
Platelet hyperfunction frequently occurs in IDDM. As in many other cellular systems, cytosolic free Ca plays a key role in platelet activation.
Research Design And Methods:
We measured cytosolic free Ca concentration ([Ca2+]i) by means of the fluorescent probe fura-2 in 60 IDDM patients (mean age 30.8 yr, range 18-50 yr) and in 31 age-matched healthy control subjects. Platelets were studied in both resting conditions and after stimulation with thrombin at 0.05, 0.1, and 0.5 U/ml.
Results:
No differences were noted between control subjects and diabetic patients, as a whole. Patients with a poor metabolic control (HbA1c > 8%) had significantly (P < 0.01 and P < 0.03) higher [Ca2+]i in resting platelets. The presence or absence of retinopathy did not modify resting platelet [Ca2+]i. After stimulation with thrombin, a significantly (P < 0.009) higher rise of platelet [Ca2+]i was observed only in those patients who were both free from complications and had good metabolic control. A highly significant (P < 0.001) correlation was found between resting [Ca2+]i and both blood cholesterol and HbA1c in the diabetic patients. Platelets from 10 young healthy subjects also were studied after in vitro incubation with various glucose concentrations (from 1.68 to 56 mM): resting and thrombin-stimulated platelet [Ca2+]i and thrombin-induced aggregation were not modified.
Conclusions:
These data confirm that platelet hyperfunction is present in IDDM patients who have unsatisfactory metabolic control, and give evidence that such an activation involves Ca homeostasis. Acute variations of blood glucose concentration are probably not influent, in this respect.
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