In primary mouse hepatocytes, NMN blocked the SL010110-induced decrease in NAD+/NADH ratio.
In plain wordsIn cells from mouse liver, NMN blocked the decrease in NAD+/NADH ratio caused by SL010110.
- Outcome
- IncreaseNAD+/NADH ratio rescue
- Study
mousen: not reported in source
Primary mouse hepatocytes exposed to SL010110- Outcome group
- Receptor activity and mechanism · Liver
Source sentences
These effects were blocked by NMN, an NAD+ precursor, suggested that SL010110 inhibited gluconeogenesis by inhibiting SIRT2, activating p300, and subsequently promoting PEPCK1 acetylation.
2 context sentences(design, population, supporting numbers)
SL010110 decreased NAD+/NADH ratio, inhibited SIRT2 activity, and further promoted p300 acetyltransferase activation and PEPCK1 acetylation.
SL010110 activated p300 acetyltransferase activity in primary mouse hepatocytes.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).