Bonora Benedetta Maria, Cappellari Roberta, Grasso Marco, Mazzucato Marta, D'Anna Marianna, Avogaro Angelo, Fadini Gian Paolo
Department of Medicine, University of Padova, Via Giustiniani 2, 35128, Padua, Italy.
Venetian Institute of Molecular Medicine, 35128, Padua, Italy.
Diabetes Ther. 2022 Jul;13(7):1327-1337. doi: 10.1007/s13300-022-01273-5. Epub 2022 Jun 9.
Diabetes reduces the levels of circulating endothelial progenitor cells (EPCs), which contribute to vascular homeostasis. In turn, low EPCs levels predict progression of chronic complications. Several studies have shown that hyperglycaemia exerts detrimental effects on EPCs. Improvement in glucose control with glucose-lowering medications is associated with an increase of EPCs, but only after a long time of good glycaemic control. In the present study, we examined the effect of a rapid glycaemic amelioration on EPC levels in subjects hospitalized for decompensated diabetes.
We used flow cytometry to quantify EPCs (CD34/CD133KDR) in patients hospitalized for/with decompensated diabetes at admission, at discharge, and 2 months after the discharge. During hospitalization, all patients received intensive insulin therapy.
Thirty-nine patients with type 1 or type 2 diabetes were enrolled. Average (± SEM) fasting glucose decreased from 409.2 ± 25.9 mg/dl at admission to 190.4 ± 12.0 mg/dl at discharge and to 169.0 ± 10.3 at 2 months (both p < 0.001). EPCs (per million blood cells) significantly increased from hospital admission (13.1 ± 1.4) to discharge (16.4 ± 1.1; p = 0.022) and remained stable after 2 months (15.5 ± 1.7; p = 0.023 versus baseline). EPCs increased significantly more in participants with newly-diagnosed diabetes than in those with pre-existing diabetes. The increase in EPCs was significant in type 1 but not in type 2 diabetes and in those without chronic complications.
In individuals hospitalized for decompensated diabetes, insulin therapy rapidly increases EPC levels for up to 2 months. EPC defect, reflecting impaired vascular repair capacity, may be reversible in the early diabetes stages.
糖尿病会降低循环内皮祖细胞(EPCs)的水平,而内皮祖细胞有助于维持血管稳态。反之,低水平的内皮祖细胞预示着慢性并发症的进展。多项研究表明,高血糖对内皮祖细胞有有害影响。使用降糖药物改善血糖控制与内皮祖细胞数量增加有关,但这仅在长期良好的血糖控制之后。在本研究中,我们检测了血糖快速改善对因糖尿病失代偿而住院的患者内皮祖细胞水平的影响。
我们使用流式细胞术对因糖尿病失代偿而住院的患者入院时、出院时及出院后2个月的内皮祖细胞(CD34/CD133KDR)进行定量。住院期间,所有患者均接受强化胰岛素治疗。
共纳入39例1型或2型糖尿病患者。平均(±标准误)空腹血糖从入院时的409.2±25.9mg/dl降至出院时的190.4±12.0mg/dl,2个月时降至169.0±10.3mg/dl(均p<0.001)。内皮祖细胞(每百万血细胞)从入院时的(13.1±1.4)显著增加至出院时的(16.4±1.1;p=0.022),2个月后保持稳定(15.5±1.7;与基线相比p=0.023)。新诊断糖尿病患者的内皮祖细胞增加显著多于既往有糖尿病的患者。内皮祖细胞的增加在1型糖尿病患者中显著,而在2型糖尿病患者及无慢性并发症的患者中不显著。
对于因糖尿病失代偿而住院的患者,胰岛素治疗可使内皮祖细胞水平迅速升高,且这种升高可持续长达2个月。反映血管修复能力受损的内皮祖细胞缺陷在糖尿病早期可能是可逆的。