MicroRNA-24/MODY Gene Regulatory Pathway Mediates Pancreatic β-Cell Dysfunction

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FIG. 7.
FIG. 7.

Knockdown of miR-24 expression rescued the GSIS defect in islets from HFD-fed mice. C56BL/6 mice aged 8 weeks were fed an HFD or standard diet (SD) for 10 weeks. Mice were fasted for 8 h before measuring body weight (A) and blood glucose (B). Islets from HFD-fed mice (n = 9) and SD-fed mice (n = 16) were isolated and cultured for 3 h before GSIS (C) was performed. HFD mice exhibited high body weight, hyperglycemia, and defective GSIS compared with SD mice. Secreted insulin was normalized to relative insulin content (**P < 0.01 vs. SD group). D: Islets from HFD mice were transfected with 100 nmol/L Cy3-labled Anti-Neg. After 48 h post-transfection, photographs of Cy3-labeled islets were acquired by fluorescent microscopy and used to quantify the transfection efficiency of miRNAs in primary isolated islets. After 3-h recovery in culturing medium, islets isolated from HFD mice were transfected with 100 nmol/L Anti-Neg or Anti-miR miRNA-24 inhibitor (Anti-miR-24) for 48 h, at which time qRT-PCR (E) and GSIS (F) were carried out. U6 was used as an internal control for miRNA analysis. Insulin secretion was normalized to relative insulin content (**P < 0.01 vs. Anti-Neg + SD; #P < 0.05 or ##P < 0.01 vs. Anti-Neg + HFD).

This Article

  1. Diabetes vol. 62 no. 9 3194-3206