Impact of glycemic variability on the levels of endothelial progenitor cells in patients with type 1 diabetes

Abstract

Objective A reduction in endothelial progenitor cell (EPC) count is considered to correlate with cumulative cardiovascular risk factors including hyperglycemia. This study was conducted to elucidate the influence of glycemic variability on EPC count in patients with diabetes. Methods In study 1, we examined the number of EPCs in 57 patients with type 1 diabetes and 43 patients with type 2 diabetes. The number of EPCs (CD34 ? , CD34 ? CD133 ? , CD34 ? CD309 ? , and CD34 ? CD133 ? CD309 ?) was counted as the number of cells per 10 6 events. In study 2, we examined 37 outpatients with type 1 diabetes without macrovascular complications. We assessed associations between EPC count and seven parameters of glycemic variability (blood glucose standard deviation, mean amplitude of glycemic excursion, J index, M value, mean of daily differences, low blood glucose index, and high blood glucose index), as measured by continuous glucose monitoring. We further analyzed the correlation between EPC count and the carotid intima-media thickness (IMT) in 24 patients. Results In study 1, the number of circulating CD34 ? and CD34 ? CD133 ? cells was significantly decreased in patients with type 1 diabetes relative to that in patients with type 2 diabetes (p = 0.020 and 0.036, respectively). In study 2, a univariate analysis showed that the J index was negatively correlated with logCD34 ? (r =-0.342, p = 0.039). LogCD34 ? was significantly negatively associated with the max IMT (r =-0.486, p = 0.012) and the mean IMT (r =-0.503, p = 0.016). Conclusions An increase in the J index, which reflects both hyperglycemia and glycemic variability, is associated with a reduction in the EPC count, which might result in the progression of diabetic vascular complications. Keywords Endothelial progenitor cells Á Type 1 diabetes Á J index Á Glycemic variability Á Intima-media thickness Á Glycated albumin Á Continuous glucose monitoring

NGF receptors and PI3K/AKT pathway involved in glucose fluctuation-induced damage to neurons and α-lipoic acid treatment

“…Poor diet control, improper treatment with insulin and hypoglycemic drugs, and inadequate compliance are associated with blood glucose fluctuation during the course of T2DM [ 33 ]; thus, glucose fluctuations are difficult to avoid in patients with diabetes. Several studies have demonstrated that IHG-induced damage is more serious than CHG in vascular endothelial cells, olfactory neuroepithelial cells, retinal epithelial cells, and Schwann cells [ 15 , 21 , 38 , 44 ]. However, the effects of IHG on neuronal cells and their potential mechanisms are unknown.…”

Glucose Variability: How Does It Work?

“…The direct influence of IHG on EPCs has not been tested. Nonetheless, in patients with the T1D, the J-index, a GV parameter, correlated negatively with CD34 + EPC count [77]. In turn, reducing GV with continuous subcutaneous insulin infusion increased the EPC levels in subjects with T1D [78].…”

Glucose Fluctuation and Severe Internal Carotid Artery Siphon Stenosis in Type 2 Diabetes Patients

“…Compared with chronic sustained hyperglycemia, glucose fluctuations induce a more specific effect on oxidative stress [ 8 ]. Severe blood glucose fluctuation is known to lower the number of vascular endothelial progenitor cells [ 28 ]. Blood glucose fluctuation is also correlated with carotid intima media thickness (IMT) [ 29 ], which is an indicator of subclinical atherosclerosis.…”