Effects of insulin on N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe)-stimulated production of reactive oxygen metabolites from normal human neutrophils

Oldenborg, Per‐Arne

doi:10.1007/s000110050479

Cited by 8 publications

(2 citation statements)

References 44 publications

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“…Insulin seemed to also possess a down-regulating action on enzymes involved in ROS elimination, as shown in this study for MPO. It was also found that MPO activity was reduced by in vitro insulin treatment in the cell-free supernatant of healthy PMN [37] and was altered in noncontrolled diabetic patients [38]. In addition, intravenous insulin infusion to induce hypoglycemia in healthy humans provoked an increase in the PMN count with associated elevation in plasma PMN elastase concentration [39].…”

Section: Discussionmentioning

confidence: 98%

In vivo evidences that insulin regulates human polymorphonuclear neutrophil functions

Walrand

Guillet

Boirie‌

et al. 2004

Journal of Leukocyte Biology

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Polymorphonuclear neutrophils (PMN) are able to destroy invasive mircoorganisms by a wide variety of functions. Whereas insulin does not stimulate hexose transport in PMN, previous reports have clearly shown that this hormone regulates glucose metabolism inside this cell, raising the question of insulin action on PMN functions in humans. It is interesting that in vitro studies established a strong relationship between specific binding of insulin to its PMN membrane receptor and the activation of the main PMN functions. Therefore, investigation in healthy subjects under strict euglycemia and physiological insulinemia was performed to understand the in vivo-specific action of insulin on PMN functions without hyperglycemia interferences. We determined numerous PMN functions before and after hyperinsulinemia (0.5 mU/kg/min) and euglycemia (0.9 g/l) clamp for 4 h in eight adult healthy volunteers (24+/-6 years). The total number of PMN and the number of PMN expressing CD11b, CD15, CD62L, and CD89 were significantly increased over baseline (P<0.001), whereas the density of these receptors was down-regulated (P<0.01) by insulin. PMN chemotaxis (+117%, P<0.05), phagocytosis (+29%, P<0.001), and bactericidal (+17-25%, P<0.001) capacities were increased during the insulin clamp (P<0.05). Therefore, insulin treatment may modulate PMN functions not only by attainment of a better metabolic control, as suggested by in vivo studies in diabetic patients, but also through a direct effect of insulin.

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Section: Discussionmentioning

confidence: 98%

In vivo evidences that insulin regulates human polymorphonuclear neutrophil functions

Walrand

Guillet

Boirie‌

et al. 2004

Journal of Leukocyte Biology

View full text Add to dashboard Cite

show abstract

“…Much work has been conducted to study the effects of hyperglycemia on the function of neutrophils [4] but knowledge on the effects of hyperinsulinemia on neutrophil function is scanty. In normal human neutrophils, physiological or moderately elevated levels of insulin was shown to stimulate chemokinesis [5,6] but to inhibit respiratory burst activation by the bacterial factor fMet-Leu-Phe [7]. The stimulating effect of insulin on neutrophil motility was found to be mediated through a tyrosine kinase and PI3-kinase-dependent signaling pathway [6].…”

Section: Introductionmentioning

confidence: 96%