AI Article Synopsis

  • The study examined how nicotinamide mononucleotide (NMN) affects insulin secretion and the expression of important transcription factors PDX-1 and FoxO1.
  • Results showed that combining NMN with repaglinide significantly increased insulin secretion in RIN-m5f cells compared to control groups.
  • NMN also boosted the mRNA levels of PDX-1, indicating its potential to enhance insulin production, while no significant changes were observed in FoxO1 or PDX-1 protein levels with NMN treatment.

Article Abstract

Objective: To investigate the effect of nicotinamide mononucleotide (NMN) on insulin secretion and gene expressions of pancreatic and duodenal homeobox 1(PDX-1) and forkhead box-containing protein O-1 (FoxO1), which were important transcription factors for insulin secretion.

Methods: Insulin secretion level in RIN-m5f cells was detected by rat insulin ELISA detection kit. The mRNA expression levels of PDX-1 and FoxO1 in RIN-m5f cells were analyzed by real-time PCR. The protein expression of PDX-1 was measured by Western blot.

Results: Insulin secretion levels in RIN-m5f cells treated with repaglinide (10 nmol/L) plus NMN (100 μmol/L) was significantly higher than those in the blank control, the DMSO control group, and the NMN (50 μmol/L) treated group (P<0.05). The mRNA expression levels of PDX-1 in RIN-m5f cells treated with NMN (10, 50 and 100 μmol/L) for 36 h were significantly higher than those in the control group (P<0.05, P<0.01, and P<0.001, respectively). There was marked differences in the mRNA expression levels of PDX-1 among different concentrations of NMN (P<0.001), but no significant differences in the mRNA expression level of FoxO1 (P>0.05). No significant difference was found in the protein expression levels of PDX-1 in RIN-m5f cells treated by NMN (50, 100, and 200 μmol/L) for 36 or 48 h compared with the control group (P>0.05).

Conclusion: NMN can stimulate insulin secretion and upregulate the mRNA expression of PDX-1 in RIN-m5f cells.

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Source
http://dx.doi.org/10.3969/j.issn.1672-7347.2011.10.005DOI Listing

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