Slc12a8 is a nicotinamide mononucleotide transporter.
Level 5 - mechanism / opinion, no new human data
Bench and animal mechanistic research with no human data.
PubMed 31131364 · doi:10.1038/s42255-018-0009-4
What was done
Investigated the molecular mechanism of cellular nicotinamide mononucleotide (NMN) uptake using in vitro assays and murine models. The authors evaluated the expression and NAD+-mediated regulation of Slc12a8 in the murine small intestine, tested the effects of Slc12a8 knockdown on NMN uptake in vitro and in vivo, assessed substrate specificity against nicotinamide riboside and dependence on sodium ions, quantified NAD+ levels and uptake using doubly labeled isotopic NMN in Slc12a8-deficient mice, and measured Slc12a8 expression in aged murine ileum.
What was found
The abstract reports directional findings without providing numerical values or effect sizes. Slc12a8 was identified as a specific, sodium-dependent NMN transporter that does not transport nicotinamide riboside. Slc12a8 knockdown or deficiency abrogated NMN uptake in vitro and in vivo and significantly decreased NAD+ levels in the jejunum and ileum. In aged mice, Slc12a8 expression was upregulated in the ileum, maintaining local NAD+ levels.
Why it matters
Identifies Slc12a8 as a dedicated direct transporter for NMN, outlining a specific mechanism for intestinal NMN absorption and tissue NAD+ regulation.
Limits
Conducted entirely in cell culture and mouse models with no human subjects. The abstract provides no sample sizes, numerical values, transport kinetics, or statistical measures of uncertainty.
Cited by
- contradicts NMN cannot enter cells directly because it has a phosphate group; orally ingested NMN must be converted back to NR before cellular entry.