Insulin-induced hypoglycemia induces a rise in C-reactive protein.

Galloway, Peter; Thomson, George; Fisher, B. M.; Semple, C. G.

doi:10.2337/diacare.23.6.861

Cited by 49 publications

(30 citation statements)

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“…Several studies have reported that hypoglycaemia increases the levels of a variety of inflammatory cytokines [9,10]. These in turn cause endothelial dysfunction, resulting in increased risk of cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

“…Strict glycaemia control using intensive insulin therapy increases the risk of hypoglycaemia. While it is well known that hypoglycaemia affects cognition, mood and consciousness, it also has profound effects on blood constituents [7,8], inflammatory cytokine level [9,10], and coagulation and fibrinolysis factors [11,12], mainly through the sympathoadrenal response to hypoglycaemia. These data suggest that hypoglycaemia induced by insulin injection may be implicated in the progression of atherosclerosis; however, there are no convincing in vivo data in support of this hypothesis.…”

Section: Introductionmentioning

confidence: 99%

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Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

et al. 2011

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Aims/hypothesis Severe hypoglycaemia associated with diabetes management is a potential risk for cardiovascular diseases. However, the effect and mechanism of hypoglycaemia on the progression of atherosclerosis remains largely unknown. As a first step towards elucidating the above, we investigated the effect of hypoglycaemia on monocyte-endothelial interaction. Methods Insulin was injected intraperitoneally once every 3 days for 5 weeks in Goto-Kakizaki rats, a non-obese rat model of type 2 diabetes. We counted the number of monocytes adherent to the endothelium of thoracic aorta as an index of early atherosclerogenesis. Cultured HUVEC were used to investigate the mechanism of action. Results Insulin treatment increased the number of monocytes adherent to the vascular endothelium. This increase was abrogated by injection of glucose with insulin. Amosulalol, an α-1 and β-adrenoreceptor antagonist, suppressed monocyte adhesion to endothelium and levels of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in the endothelial surface, which had been enhanced by insulin-induced hypoglycaemia. In HUVEC, adrenaline (epinephrine) significantly increased nuclear translocation of nuclear factor-κB (NF-κB) p65 and levels of adhesion molecules, effects that were abrogated following addition of SQ22536, a specific adenyl cyclase inhibitor. Conclusions/interpretation Our data indicate that repetitive hypoglycaemia induced by insulin enhanced monocyte adhesion to endothelial cells in Goto-Kakizaki rat aorta through enhanced adrenaline activity and that the latter stimulated intracellular cAMP, leading to nuclear translocation of NF-κB with subsequent production of adhesion molecules in endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

et al. 2011

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“…Galloway et al [101] have reported a significant increase in CRP at 24 h after acute insulin-induced hypoglycaemia, both in subjects with type 1 diabetes (0.77-2.31 mg/L) and in healthy volunteers (0.32-0.96 mg/L). While it is unclear as to the role of CRP in the causation of atherogenesis, increasing evidence has implicated its involvement in acute vascular events, with data in vitro and in vivo demonstrating its possible pathogenetic qualities, and additionally CRP levels are predictive of outcome following cardiovascular events [102,103].…”

Section: Inflammation and Endothelial Dysfunctionmentioning

confidence: 99%

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

Wright

Frier

2008

Diabetes Metabolism Res

301

242

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Acute hypoglycaemia provokes profound physiological changes affecting the cardiovascular system and several haematological parameters, principally as a consequence of sympatho-adrenal activation and counter-regulatory hormonal secretion. Many of these responses have an important role in protecting the brain from neuroglycopenia, through altering regional blood flow and promoting metabolic changes that will restore blood glucose to normal. In healthy young adults the cardiovascular effects are transient and have no obvious detrimental consequences. However, some of the effected changes are potentially pathophysiological and in people with diabetes who have developed endothelial dysfunction, they may have an adverse impact on a vasculature that is already damaged. The acute haemodynamic and haematological changes may increase the risk of localized tissue ischaemia, and major vascular events can certainly be precipitated by acute hypoglycaemia. These include myocardial and cerebral ischaemia and occasionally infarction. Established diabetic retinopathy often deteriorates after strict glycaemic control is instituted, the latter being associated with a threefold increase in frequency of severe hypoglycaemia, and enhanced exposure to mild hypoglycaemia. The possible mechanisms underlying these hypoglycaemia-induced effects include haemorrheological changes, white cell activation, vasoconstriction, and the release of inflammatory mediators and cytokines. The concept that acute hypoglycaemia could aggravate vascular complications associated with diabetes is discussed in relation to evolving comprehension of the pathogenesis of atherosclerosis and blood vessel disease.

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“…Hypoglycaemia induces sympatho-adrenal stimulation with potentially adverse cardiovascular consequences, 22 including QT interval prolongation, 23 and release of inflammatory cytokines that have an adverse impact on endothelial function. 24 These effects may trigger arrhythmias and exacerbate ischaemia, and this has been proposed as an explanation for the increased mortality seen with tightly controlled diabetes in the ACCORD study. 25 However, hypoglycaemia was reported in only 4.1% of patients in TITAN-ACS, and for the majority it was a single episode, this rate is lower than that in the other published randomised controlled trials (Table 4).…”

Section: Discussionmentioning

confidence: 99%

An evaluation of the safety and efficacy of a variable rate intravenous insulin infusion in the management of hyperglycaemia in acute coronary syndrome: experience of the TITAN-ACS

et al. 2015

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Aim: To assess the safety and efficacy of a variable rate intravenous insulin infusion to lower blood glucose (BG) in patients presenting with acute coronary syndrome and hyperglycaemia. Methods: We evaluated the response over 24 hours of a variable rate insulin infusion with 5% dextrose and potassium chloride (40 mEq/L), to control hyperglycaemia in 776 patients with an admission BG ≥10 mmol/L in 36 UK hospitals. Patients had either ST segment elevation or non-ST segment elevation myocardial infarction and the study included both patients with or without a diagnosis of diabetes. We measured blood glucose, initially hourly, and serum potassium at admission, at 24 hours and at the time of major arrhythmias. We measured survival to 30 days.

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Insulin-induced hypoglycemia induces a rise in C-reactive protein.

Abstract: Sane , Saito H: Endogenous glucose production and glucose effectiveness in type 2 diabetic subjects derived from stablelabeled minimal model approach.

Cited by 49 publications

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Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

An evaluation of the safety and efficacy of a variable rate intravenous insulin infusion in the management of hyperglycaemia in acute coronary syndrome: experience of the TITAN-ACS

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