C-peptide reduces pro-inflammatory cytokine secretion in LPS-stimulated U937 monocytes in condition of hyperglycemia

Haidet, Jaime; Cifarelli, Vincenza; Trucco, Massimo; Luppi, Patrizia

doi:10.1007/s00011-011-0384-8

Cited by 44 publications

(40 citation statements)

References 44 publications

(62 reference statements)

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“…It was also observed that the shorter the interval between preceding infection and T1D diagnosis, the lower the release of C-peptide. It has recently been shown that monocytes represent an additional cellular target for C-peptide anti-inflammatory activity (24). Monocytes are pivotal cells in inflammatory responses as they serve as the principal reservoir of proinflammatory cytokines, e.g., TNF-α.…”

Section: Discussionmentioning

confidence: 99%

General immune dampening is associated with disturbed metabolism at diagnosis of type 1 diabetes

et al. 2013

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Section: Discussionmentioning

confidence: 99%

General immune dampening is associated with disturbed metabolism at diagnosis of type 1 diabetes

et al. 2013

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“…Inhibited cytokines include IL-6, IL-8, macrophage inflammatory protein- (MIP-) 1 α , MIP-1 β [17], TNF- α , and reactive oxygen species [18]. …”

Section: Hyperglycemia and Innate Immune Cellsmentioning

confidence: 99%

Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells

Xiu

Stanojcic

et al. 2014

International Journal of Endocrinology

113

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Hyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Recent studies have proposed a fundamental role of the immune system towards the development of insulin resistance in traumatic patients. A comprehensive review of published literatures on the effects of hyperglycemia and insulin on innate immunity in critical illness was conducted. This review explored the interaction between the innate immune system and trauma-induced hypermetabolism, while providing greater insight into unraveling the relationship between innate immune cells and hyperglycemia. Critical illness substantially disturbs glucose metabolism resulting in a state of hyperglycemia. Alterations in glucose and insulin regulation affect the immune function of cellular components comprising the innate immunity system. Innate immune system dysfunction via hyperglycemia is associated with a higher morbidity and mortality in critical illness. Along with others, we hypothesize that reduction in morbidity and mortality observed in patients receiving insulin treatment is partially due to its effect on the attenuation of the immune response. However, there still remains substantial controversy regarding moderate versus intensive insulin treatment. Future studies need to determine the integrated effects of HG and insulin on the regulation of innate immunity in order to provide more effective insulin treatment regimen for these patients.

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“…An investigation into insulin's and C-peptide's roles in modulation of human saphenous vein neointima formation revealed that C-peptide increased endothelial cell number by about 40%, thus indicating that C-peptide may promote re-endothelialization and thus limiting neointimal development (70). C-peptide has also been shown to reduce systemic inflammatory responses that are deleterious to the endothelium by lowering circulating levels of the proinflammatory cytokines IL-1, IL-6, macrophage inflammatory protein (MIP)-1␣, and TNF-␣, effects that most likely occur through inhibition of activated monocytes (11,34,108). Vascular smooth muscle cells are yet another cell type that plays a critical role in vascular disease and atherosclerotic plaque formation.…”

Section: E959 Physiology Of C-peptidementioning

confidence: 99%

Physiological effects and therapeutic potential of proinsulin C-peptide

Yosten

Maric‐Bilkan

Luppi

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Connecting Peptide, or C-peptide, is a product of the insulin prohormone, and is released with and in amounts equimolar to those of insulin. While it was once thought that C-peptide was biologically inert and had little biological significance beyond its role in the proper folding of insulin, it is now known that C-peptide binds specifically to the cell membranes of a variety of tissues and initiates specific intracellular signaling cascades that are pertussis toxin sensitive. Although it is now clear that C-peptide is a biologically active molecule, controversy still remains as to the physiological significance of the peptide. Interestingly, C-peptide appears to reverse the deleterious effects of high glucose in some tissues, including the kidney, the peripheral nerves, and the vasculature. C-peptide is thus a potential therapeutic agent for the treatment of diabetes-associated long-term complications. This review addresses the possible physiologically relevant roles of C-peptide in both normal and disease states and discusses the effects of the peptide on sensory nerve, renal, and vascular function. Furthermore, we highlight the intracellular effects of the peptide and present novel strategies for the determination of the C-peptide receptor(s). Finally, a hypothesis is offered concerning the relationship between C-peptide and the development of microvascular complications of diabetes.

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C-peptide reduces pro-inflammatory cytokine secretion in LPS-stimulated U937 monocytes in condition of hyperglycemia

Abstract: We conclude that, in conditions of hyperglycemia, C-peptide reduces monocytes activation via inhibition of the NF-κB pathway.

Cited by 44 publications

References 44 publications

General immune dampening is associated with disturbed metabolism at diagnosis of type 1 diabetes

General immune dampening is associated with disturbed metabolism at diagnosis of type 1 diabetes

Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells

Physiological effects and therapeutic potential of proinsulin C-peptide

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