2004
DOI: 10.1111/j.1365-2362.2004.01291.x
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Impaired neutrophil store‐mediated calcium entry in Type 2 diabetes

Abstract: In Type 2 diabetes there is a defect in neutrophil calcium signalling which results in a lesser increase in free cytosolic calcium owing to impaired influx across the plasma membrane. Abnormal calcium signalling is likely to be important in the pathogenesis of diabetic complications.

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Cited by 17 publications
(13 citation statements)
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“…The investigators had suggested that the abnormal calcium signalling was likely to be important in the pathogenesis of diabetic infectious complications. 14 Several clinical studies had showed the inhibitory effects of hyperglycemia on PMNL functions, thus contributing at least partly to altered host defence in diabetes mellitus. 5e17 These findings also supported the hypothesis that defective PMNL functions possibly were leading to infectious complications.…”
Section: Discussionmentioning
confidence: 99%
“…The investigators had suggested that the abnormal calcium signalling was likely to be important in the pathogenesis of diabetic infectious complications. 14 Several clinical studies had showed the inhibitory effects of hyperglycemia on PMNL functions, thus contributing at least partly to altered host defence in diabetes mellitus. 5e17 These findings also supported the hypothesis that defective PMNL functions possibly were leading to infectious complications.…”
Section: Discussionmentioning
confidence: 99%
“…Given that increased integrin exposure is associated with adverse cardiovascular outcomes, it can be hypothesized that correction of the cytoskeletal defect in Type 2 diabetes may have a positive effect on cardiovascular morbidity and mortality. Altered neutrophil cytoskeletal function is also associated with impaired calcium signalling in Type 2 diabetes, which regulates many neutrophil functions [45]. It can therefore be anticipated that correction of the downstream block to cytoskeletal function may improve other aspects of neutrophil function beyond that of integrin exposure.…”
Section: Discussionmentioning
confidence: 99%
“…However, literature to date is contradictory in regard to other host defense functions of neutrophil including oxidative burst activity [24][25][26] , migration 19,22,27 , phagocytosis [22][23][24]28 and apoptosis 27,29,30 . The changed neutrophil functions can be caused by upregulated expression of adhesion molecules 28 , downregulated receptors 31 , impaired calcium signaling 32 and anomalous activities of adenosine triphosphate synthases on neutrophils 33 . Although the neutrophil apoptosis rate was significantly correlated with glycated hemoglobin (HbA1c) levels in patients with type 2 diabetes 30 , research has shown that HbA1c level and history of infection did not seem to affect neutrophil functions in type 1 diabetes patients 28 .…”
Section: Neutrophil Counts and Functions In Type 1 Diabetesmentioning
confidence: 99%