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Role of miR-146a of the peripheral blood mononuclear cell in the pathogenesis of type 2 diabetic peripheral neuropathy / 中华内分泌代谢杂志
Chinese Journal of Endocrinology and Metabolism ; (12): 552-555, 2016.
Artículo en Chino | WPRIM | ID: wpr-496197
ABSTRACT
Objective To explore the possible role of miR-146a in the pathogenesis of diabetic peripheral neuropathy( DPN) by investigating the correlation of miR-146a level in the peripheral blood mononuclear cells (PBMCs)with tumor necrosis factor α(TNF-α), interleukin-6(IL-6), and C reactive protein(CRP). Methods The expression levels of miR-146a in the PBMCs were measured using realtime PCR in 81 patients and 34 healthy individuals. The correlation of miR-146a expression with clinical parameters was analyzed. Results Compared to those in the healthy individuals and patients without DPN, miR-146a level was significantly decreased in diabetic patients with DPN while TNF-α, CRP, IL-6, HbA1C, systolic blood pressure, and homeostasis model assessment of insulin resistance index(HOMA-IR) were significantly increased(all P<0.05). Duration of diabetes, blood uric acid, serum creatinine, and urinary albumin to creatinine ratio in diabetics with DPN were higher compared with diabetics without DPN(all P<0. 05). The expression level of miR-146a was negatively correlated with diabetes duration, HOMA-IR, HbA1C, TNF-α, and IL-6. Multiple linear regression showed that HOMA-IR, HbA1C, TNF-α, and IL-6 were independent factors of miR-146a. Conclusion miR-146a may be involved in the development of DPN through inflammation, glucose metabolism, and insulin resistance.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Tipo de estudio: Estudio de etiología / Estudio pronóstico Idioma: Chino Revista: Chinese Journal of Endocrinology and Metabolism Año: 2016 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Tipo de estudio: Estudio de etiología / Estudio pronóstico Idioma: Chino Revista: Chinese Journal of Endocrinology and Metabolism Año: 2016 Tipo del documento: Artículo