Peripheral blood cell changes in response to acute hypoglycaemia in man

Frier, Brian M.; Corrall, R. J. M.; Davidson, Neil; Webber, Rachel; Dewar, A E; French, E. B.

doi:10.1111/j.1365-2362.1983.tb00061.x

Cited by 47 publications

(50 citation statements)

References 18 publications

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“…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%

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: 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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“…8 -10 These observations have supported the suggestion that the tachycardia and the rise in blood pressure observed during a hypoglycemic episode might destabilize an atherosclerotic plaque. 11 These hemodynamic changes, the increased myocardial work, and hypoglycemia-induced increases in platelet aggregation, platelet activity, [12][13][14] and hematocrit 15,16 may precipitate cardiac and cerebral ischemic events in patients at high risk of cardiovascular disease. 17 Support for this possibility comes from a number of small studies and case reports.…”

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confidence: 99%

Serious Cardiovascular Outcomes in Diabetes

Yakubovich

Gerstein

2011

Circulation

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H ypoglycemia is a well-recognized side effect of glucoselowering therapies in patients with diabetes mellitus. The incidence of mild self-reported hypoglycemic episodes in patients with type 1 diabetes mellitus is approximately 30 episodes per patient per year, whereas the incidence of severe hypoglycemic episodes (ie, those that require third-party assistance) may be as high as 3.2 episodes per patient per year. 1-3 Hypoglycemic episodes occur much less frequently in patients with type 2 diabetes mellitus, in whom the incidence of mild and severe hypoglycemic episodes is 2 to 10 per patient per year and 0.1 to 0.7 per patient per year, respectively. 2 When patients are alerted to the occurrence of a hypoglycemic episode by symptoms such as tremor, diaphoresis, tachycardia, malaise, hunger, and anxiety, they can abort these episodes by consuming carbohydrates. However, if hypoglycemic episodes occur rapidly or are unrecognized and untreated, the resulting neuroglycopenia may cause confusion, seizures, accidents, angina, and, rarely, death or permanent cognitive impairment. 3,4 Patients who experience frequent episodes of hypoglycemia are especially at risk of having unrecognized hypoglycemic episodes (and their sequelae), because their counterregulatory response to hypoglycemia becomes blunted. Indeed, the rare occurrence of sudden death during sleep in young patients with type 1 diabetes mellitus (the so-called dead-in-bed syndrome) has been attributed to hypoglycemia, although this cause is seldom proven. [5][6][7] It is well known that hypoglycemic episodes are associated with a surge of sympathetic activity and a release of catecholamines. 8 -10 These observations have supported the suggestion that the tachycardia and the rise in blood pressure observed during a hypoglycemic episode might destabilize an atherosclerotic plaque. 11 These hemodynamic changes, the increased myocardial work, and hypoglycemia-induced increases in platelet aggregation, platelet activity, 12-14 and hematocrit 15,16 may precipitate cardiac and cerebral ischemic events in patients at high risk of cardiovascular disease. 17 Support for this possibility comes from a number of small studies and case reports. For example, continuous glucose and ECG monitoring in 19 patients with coronary artery disease and type 2 diabetes mellitus 18 revealed a higher frequency of ischemic ECG changes when glucose levels fell below 3.9 mmol/L (70 mg/dL). A similar study in 24 patients with type 1 diabetes mellitus 19 revealed a nocturnal increase in the corrected QT interval and some minor rhythm disturbances when nocturnal glucose levels fell below 3.5 mmol/L (63 mg/dL) that were not observed when nocturnal glucose levels were Ͼ5 mmol/L (90 mg/dL). Experimentally induced hypoglycemia prolonged the corrected QT interval and reduced potassium levels in healthy adults 10 and in people with type 1 and type 2 diabetes mellitus. 20,21 Finally, case reports have shown a relationship between ischemic cerebral changes and concurrent severe hypoglycemia in patie...

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“…Insulin does not need to cause hypoglycaemia to cause the increase in haematocrit but the increment is larger if it does. It can be seen from Table 2 that the increase in haematocrit did not occur in sympathectomized patients [26,27]. This suggests that the fall in plasma volume which may occur after insulin is mediated by catecholamines.…”

Section: Changes In Plasma Volume and Haematocritmentioning

confidence: 67%

“…The increase in haematocrit after insulin administration is, however, unlikely to be explained by an increase in blood flow. Frier et al [27] observed that beta-adrenoceptor blockade with propranolol did not influence the rise in haematocrit after insulin. During insulin-induced hypoglycaemia plus propranolol, or during infusion of adrenaline plus propranolol, forearm blood flow and calf blood flow do not increase [31,32,33].…”

Section: Changes In Plasma Volume and Haematocritmentioning

confidence: 99%

Acute effects of insulin on cardiovascular function and noradrenaline uptake and release

Christensen

1983

Diabetologia

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Peripheral blood cell changes in response to acute hypoglycaemia in man

Cited by 47 publications

References 18 publications

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

Serious Cardiovascular Outcomes in Diabetes

Acute effects of insulin on cardiovascular function and noradrenaline uptake and release

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