Platelet insulin receptor

Hajek, Anthony S.; Joist, J. Heinrich

doi:10.1016/0076-6879(92)15079-r

Cited by 13 publications

(8 citation statements)

References 10 publications

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“…Platelets express insulin and IGF-1 receptors, which may be activated by insulin (13–15), but the literature on insulin effects on platelet activation is inconsistent. We have found mild platelet-activating effects of insulin at physiologic concentrations (10–100 µU/mL [60–600 pmol/L]) in vitro (9,16).…”

Section: Discussionmentioning

confidence: 99%

Postprandial Platelet Activation Is Related to Postprandial Plasma Insulin Rather Than Glucose in Patients With Type 2 Diabetes

Spectre

Östenson

et al. 2012

Diabetes

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Postprandial hyperglycemia is associated with platelet activation. We thus investigated if meal-induced platelet activation could be attenuated by meal insulin. A randomized, double-blind, cross-over study was performed to compare postprandial platelet activation after premeal injections of placebo or insulin aspart (0.1 and 0.2 units/kg) in 18 patients with type 2 diabetes mellitus (T2DM). Platelet activation was assessed by flow cytometry, without and with stimulation by the thromboxane analog U46619 or ADP. Measurements were before and after premeal blood glucose standardization (to 6–7 mmol/L by insulin infusion, if needed) and at 90 min after the meal. Premeal insulin reduced postprandial hyperglycemia by 2–3 mmol/L compared with placebo. Postmeal insulin levels were doubled with placebo and further elevated with insulin injections. The standardized meal enhanced U46619-induced platelet P-selectin expression by 23% after placebo; this response was more than doubled after premeal insulin. U46619-induced fibrinogen binding was unchanged after meal intake with placebo but was markedly enhanced (by ∼50–60%) after premeal insulin. Postprandial platelet activation correlated positively to postprandial insulin levels and inversely to glucose levels. Premeal insulin infusion was also associated with platelet activation. Our results suggest that postprandial insulin rather than glucose accounts for postprandial platelet activation in T2DM patients.

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Section: Discussionmentioning

confidence: 99%

Postprandial Platelet Activation Is Related to Postprandial Plasma Insulin Rather Than Glucose in Patients With Type 2 Diabetes

Spectre

Östenson

et al. 2012

Diabetes

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“…It is also suggested that the relevance of these effects can be restricted by dimerization of subunits of IR and insulin-like growth factor 1 (IGF-1) receptor [171]. Alike IR, IGF-1 receptors are also expressed in platelets [172]. However, binding of IGF-1 to the IGF-1 receptor leads to activation of downstream IR mediators (IRS-1 and IRS-2), resulting in increased platelet reactivity [173].…”

Section: Platelets Hyperactivity In T2dmmentioning

confidence: 99%

Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies

Kaur

Singh

2018

Cardiovasc Diabetol

493

363

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The incidence and prevalence of diabetes mellitus is rapidly increasing worldwide at an alarming rate. Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes, accounting for approximately 90–95% of the total diabetes cases worldwide. Besides affecting the ability of body to use glucose, it is associated with micro-vascular and macro-vascular complications. Augmented atherosclerosis is documented to be the key factor leading to vascular complications in T2DM patients. The metabolic milieu of T2DM, including insulin resistance, hyperglycemia and release of excess free fatty acids, along with other metabolic abnormalities affects vascular wall by a series of events including endothelial dysfunction, platelet hyperactivity, oxidative stress and low-grade inflammation. Activation of these events further enhances vasoconstriction and promotes thrombus formation, ultimately resulting in the development of atherosclerosis. All these evidences are supported by the clinical trials reporting the importance of endothelial dysfunction and platelet hyperactivity in the pathogenesis of atherosclerotic vascular complications. In this review, an attempt has been made to comprehensively compile updated information available in context of endothelial and platelet dysfunction in T2DM.

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“…34 Platelets express both insulin receptors and insulin-like growth factor-1 (IGF-1) receptors. 35,36 Among other effects, the binding of insulin to platelets increases surface expression of adenylate cyclase-linked prostacyclin receptor. 37 However, insulin receptor expression is relatively low because the majority of its subunits heterodimerize with those of the IGF-1 receptor to form an insulin/IGF-1 hybrid receptor, which avidly binds IGF-1 but not insulin.…”

Section: Insulin Deficiency and Resistancementioning

confidence: 99%

“…34 A vérlemezkéken mind az inzulin, mind az inzulinszerű nö-vekedési faktor-1 (IGF-1) receptorai megtalálhatók. 35,36 Az inzulin, egyéb hatásai mellett, a vérlemezkékhez kapcsolódva megnöveli az adenil-cikláz-kapcsolt prosztaciklinreceptor felszíni expresszióját. 37 Az inzulinreceptor-expresszió azonban viszonylag alacsony, mivel alegységeinek nagy része az 50 Circulation -Magyar Kiadás 2011. március 1. ábra A cukorbetegekben észlelt vérlemezke-mûködési zavar kialakításában szerepet játszó mechanizmusok.…”

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