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Relationship between fluctuations in glucose levels measured by continuous glucose monitoring and vascular endothelial dysfunction in type 2 diabetes mellitus

DOI: 10.1186/1475-2840-12-1

Keywords: Atherosclerosis, Type 2 diabetes mellitus, Endothelium, Glucose, Continuous glucose monitoring (CGM)

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Fluctuations in blood glucose levels were measured over 24?hours by continuous glucose monitoring (CGM) on admission day 2 in 57 patients with type 2 diabetes mellitus. The reactive hyperemia index (RHI), an index of vascular endothelial function, was measured using peripheral arterial tonometry (EndoPAT) on admission day 3.The natural logarithmic-scaled RHI (L_RHI) correlated with SD (r=?0.504; P<0.001), the mean amplitude of glycemic excursions (MAGE) (r=?0.571; P<0.001), mean postprandial glucose excursion (MPPGE) (r=?0.411; P=0.001) and percentage of time ≥200?mg/dl (r=?0.292; P=0.028). In 12 patients with hypoglycemia, L_RHI also correlated with the percentage of time at hypoglycemia (r=?0.589; P=0.044). L_RHI did not correlate with HbA1c or fasting plasma glucose levels. Furthermore, L_RHI did not correlate with LDL cholesterol, HDL cholesterol, and triglyceride levels or with systolic and diastolic blood pressures. Finally, multivariate analysis identified MAGE as the only significant determinant of L_RHI.Fluctuations in blood glucose levels play a significant role in vascular endothelial dysfunction in type 2 diabetes.UMIN000007581Death due to ischemic heart disease and onset of myocardial infarction are approximately 2 to 6 times greater and the risk of stroke is approximately 2 to 3 times greater in patients with type 2 diabetes than normal population [1-5]. Microvascular complications may be ameliorated and/or inhibited by the control of blood glucose levels through maintenance of hemoglobin A1c (HbA1c) below a critical level. However, the outcome of recent large-scale clinical studies suggested that strict glycemic control using HbA1c alone is not sufficient to reduce the risk of macrovascular complications [6,7]; rather, the total number of deaths remained significantly high after intensive therapy [7]. In this regard, severe hypoglycemia has been reported to be an important cause of increased incidence of sudden cardiovascular death [8].In addition to


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