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Protective effect of vitamin D on high glucose-induced podocyte insulin resistance / 临床儿科杂志
Journal of Clinical Pediatrics ; (12): 471-475, 2014.
Artículo en Chino | WPRIM | ID: wpr-447430
ABSTRACT
Objectives To study the protective effects of vitamin D (VitD) on podocyte insulin resistance and its mecha-nisms. Methods Immortalized mouse podocytes in vitro were randomly divided into 4 groupspodocytes+5 mmol/L glucose group (group A);podocytes+5 mmol/L glucose+1 nmol/L propylene glycol group (group B);podocytes+30 mmol/L glucose+1 nmol/L propylene glycol group (group C); podocytes+30 mmol/L glucose+1 nmol/L propylene glycol+1 nmol/L VitD group (group D). The percentage of podocyte apoptosis was determined after 48 h of incubation. Podocyte viability was assessed by MTT assay. The mRNA expressions of vitamin D receptor (VDR) and insulin receptor substrate protein 1 (IRS1) in podocyte were detected by RT-PCR. Western blot analysis was performed to measure the protein levels of p-IRS1/IRS, p-Akt/Akt and p-ERK1/2/ERK1/2. Results There were significant differences in apoptosis percentage, viability and the expression of VDR, IRS1, p-ERK1/2 of podoctyes(P0.05). Compared with group A, B , and D, the percentage of podocyte apoptosis in group C was significantly increased, the cell viabi-lity was decreased, the expressions of VDR and IRS1 mRNA and p-IRS1 and p-Akt proteins were down-regulated, whereas p-ERK1/2 was up-regulated in group C. The levels of p-IRS1/IRS1, p-Akt/Akt, p-ERK1/2/ERK1/2 had no statistical differences in group A, B, and D (P>0.05). Conclusions VitD-VDR system alleviates podocyte apoptosis induced by high glucose, and acti-vates insulin signaling pathway and counteracts insulin resistance signal to improve podocyte insulin resistance.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Journal of Clinical Pediatrics Año: 2014 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Journal of Clinical Pediatrics Año: 2014 Tipo del documento: Artículo