Open AccessEndothelial impairment and bone marrow‐derived CD 34 + /133 + cells in diabetic patients with erectile dysfunction
Author(s) -
Murata Miho,
Tamemoto Hiroyuki,
Otani Taeko,
Jinbo Sachimi,
Ikeda Nahoko,
Kawakami Masanobu,
Ishikawa Sane
Publication year - 2012
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/j.2040-1124.2012.00230.x
Subject(s) - medicine , erectile dysfunction , diabetes mellitus , endothelial dysfunction , cd34 , progenitor cell , bone marrow , endothelial progenitor cell , gastroenterology , urology , endocrinology , stem cell , biology , genetics
Aims/Introduction The present study was undertaken to determine vascular endothelial impairment and endothelial progenitor cells ( EPC s) in patients with type 2 diabetes mellitus and erectile dysfunction ( ED ). Materials and Methods A total of 100 type 2 diabetic men were enrolled. Flow‐mediated dilatation ( FMD ) and anaerobic threshold ( AT ) were measured. Also, EPC s in the peripheral blood were determined by flow cytometry. Results In the 42 ED diabetic patients, FMD and AT were significantly less than those in the 58 patients with normal erectile function ( FMD 2.84 vs 3.82%, P = 0.038, and AT 11.2 vs 12.7 mL/kg/min, P = 0.022). Exercise tolerance significantly increased the number of EPC s in the patients with and without ED (49–60 cells/100 μL, P = 0.015, and 72–99 cells/100 μL, P = 0.003). In the diabetic patients without autonomic neuropathy, FMD was significantly reduced in the patients with ED than those without ED ( P = 0.015). In response to exercise tolerance, the number of EPC s increased in both the diabetic patients with ED ( P = 0.003) and without ED ( P = 0.007). In contrast, in the diabetic patients with autonomic neuropathy, there was no difference in FMD between the patients with and without ED . The exercise tolerance increased the number of EPC s in the patients without ED ( P = 0.023), but it disappeared in those with ED . Conclusions ED diabetic patients have endothelial impairment during the early period of diabetic complications, whose deranged endothelial function is concomitantly repaired by promoting bone marrow‐derived EPC s.