Platelet Protein-Related Abnormalities in Response to Acute Hypoglycemia in Type 2 Diabetes
<h3>Introduction </h3><p dir="ltr">Patients with severe COVID-19 infections have coagulation abnormalities indicative of a hypercoagulable state, with thromboembolic complications and increased mortality. Platelets are recognized as mediators of inflammation, releasing pr...
محفوظ في:
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| مؤلفون آخرون: | , , , |
| منشور في: |
2021
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إضافة وسم
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| الملخص: | <h3>Introduction </h3><p dir="ltr">Patients with severe COVID-19 infections have coagulation abnormalities indicative of a hypercoagulable state, with thromboembolic complications and increased mortality. Platelets are recognized as mediators of inflammation, releasing proinflammatory and prothrombotic factors, and are hyperactivated in COVID-19 infected patients. Activated platelets have also been reported in type 2 diabetes (T2D) patients, putting these patients at higher risk for thromboembolic complications of COVID-19 infection. </p><h3>Methods </h3><p dir="ltr">A case-control study of T2D (n=33) and control subjects (n=30) who underwent a hyperinsulinemic clamp to induce normoglycemia in T2D subjects: T2D: baseline glucose 7.5 ± 0.3mmol/l (135.1 ± 5.4mg/dl), reduced to 4.5 ± 0.07mmol/l (81 ± 1.2mg/dl) with 1-hour clamp; Controls: maintained at 5.1 ± 0.1mmol/l (91.9 ± 1.8mg/dl). Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement was used to determine a panel of platelet proteins. </p><h3>Results </h3><p dir="ltr">Prothrombotic platelet proteins were elevated in T2D versus controls: platelet factor 4 (PF4, p<0.05); platelet glycoprotein VI (PGVI p<0.05); P-selectin (p<0.01) and plasminogen activator inhibitor I (PAI-1, p<0.01). In addition, the antithrombotic platelet-related proteins, plasmin (p<0.05) and heparin cofactor II (HCFII, p<0.05), were increased in T2D. Normalization of glucose in the T2D cohort had no effect on platelet protein levels. </p><h3>Conclusion </h3><p dir="ltr">T2D patients have platelet hyperactivation, placing them at higher risk for thromboembolic events. When infected with COVID-19, this risk may be compounded, and their propensity for a more severe COVID-19 disease course increased.</p><h2>Other Information</h2><p dir="ltr">Published in: Frontiers in Endocrinology<br>License: <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank">https://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.3389/fendo.2021.651009" target="_blank">https://dx.doi.org/10.3389/fendo.2021.651009</a></p><p dir="ltr">Clinical Trial Registration: <a href="https://clinicaltrials.gov/ct2/show/NCT03102801" target="_blank">https://clinicaltrials.gov/ct2/show/NCT03102801</a>, identifier NCT03102801</p> |
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