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Cellular and structural study

Slc12a8 is a nicotinamide mononucleotide transporter

Alessia Grozio, Kathryn F Mills, Jun Yoshino, Santina Bruzzone, Giovanna Sociali, Kyohei Tokizane, Hanyue Cecilia Lei, Richard Cunningham, Yo Sasaki, Marie E Migaud, Shin-Ichiro Imai

Nature Metabolism · 2019 · 1(1):47–57

Original publication PubMed Full text on PMC

Study at a glance

Design
Cellular, genetic and mouse tracer study of candidate NMN transport
Population or model
Murine intestinal models and cultured cells
Sample size
Multiple cellular and animal experiments; see publication
Intervention
NMN exposure with Slc12a8 knockdown and isotopic tracing
Publication type
Preclinical mechanistic study
Evidence class
preclinical-mechanistic
Research area
NMN transport mechanisms
Trial registration
Not applicable.

Study endpoints

  • NMN uptake
  • Slc12a8 expression
  • Sodium dependence
  • Intestinal NAD+
  • Isotopic NMN transport

Plain-language summary

This study proposed that the Slc12a8 gene encodes a specific NMN transporter, based on cell experiments, mouse intestinal biology, gene knockdown and isotopic tracing.

The authors reported that reducing Slc12a8 impaired NMN uptake and that transport showed sodium dependence, supporting direct NMN transport in their experimental systems.

The interpretation became scientifically contested. A subsequent Nature Metabolism Matters Arising by Schmidt and Brenner argued that the evidence did not establish SLC12A8 as an NMN transporter. Both papers should therefore be read together.

Key findings

  • The study proposed SLC12A8 as a specific NMN transporter.
  • Slc12a8 knockdown reduced NMN uptake in the reported experiments.
  • Transport was reported as sodium dependent and selective relative to NR.
  • A later published critique disputed whether the evidence establishes SLC12A8 as an NMN transporter.

Limitations

  • Cell and mouse evidence, not direct human transport measurements.
  • Transporter assignment depends on interpretation of genetic, kinetic and tracer data.
  • A published Matters Arising directly challenged the transporter conclusion.
  • The question should be presented as scientifically contested rather than settled.

Funding and transparency

Funding

A.G. was supported as the Tanaka Scholar by Tsunemaru Tanaka and Megumi Tanaka. M.E.M. was supported by U.K. Research Councils and Biotechnology and Biological Sciences Research Council grant BB/N001842/1. The work was mainly supported by National Institute on Aging grants AG024150, AG037457, and AG047902 to S.I., with core-facility support from Diabetes Research Center P30 DK020579, Nutrition Obesity Research Center P30 DK56341, the Hope Center for Neurological Disorders, and NCRR grant C06 RR015502.

Competing interests

A.G. and S.I. are inventors of a patent (PCT/US18/46233) about the Slc12a8 NMN transporter, whose applicant is Washington University and which has been licensed by Teijin Limited (Japan). Other authors declare no competing financial interests.

HealthspanX observation

This transporter claim is contested in the literature and should never be presented without the Schmidt and Brenner response.

Interpretive weight

Mechanistic context

Influential mouse/cell study proposing SLC12A8 as an NMN transporter; the interpretation was challenged in a published Matters Arising and should not be treated as settled.

This record summarizes a publication; it is not medical advice or a claim that a HealthspanX product reproduces the study's results. Report a correction.

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