Suppression of ATP-dependent (S)-NAD(P)H-hydrate dehydratase expression inhibits adipocyte differentiation of 3T3-L1 preadipocytes by increasing excessive accumulation of NADHX.
Nakajima K., Takahashi K., Tanaka M., Kawashima M., Machida K., Nakao Y.
Animal Study, published in J Biochem (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Biochem (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40113573
- DOI
- 10.1093/jb/mvaf015
Abstract (original English)
ATP-dependent (S)-NAD(P)H-hydrate dehydratase (NAXD) is a crucial enzyme in the nicotinamide adenine dinucleotide repair system that regenerates NAD(P)H, an essential electron donor in metabolic redox reactions. NAD+-related metabolic pathways connect cellular metabolism and the expression of genes responsible for adipogenesis; however, the biological significance of the NAXD-mediated repair pathway remains unclear. Herein, we showed that NAXD is essential for normal adipocyte differentiation of 3T3-L1 murine preadipocytes. Silencing of the Naxd gene attenuated differentiation-induced lipid accumulation with excessive accumulation of hydrated NADH (NADHX) without altering NAD+ levels. FK866, a specific inhibitor of NAMPT, further reduced lipid accumulation even in Naxd-silenced cells with substantial decrease in NAD+. Supplementation with nicotinamide mononucleotide, a precursor of NAD+, restored NAD+ levels comparably in Naxd- and LacZ-silenced cells treated with FK866, but failed to recover adipocyte differentiation of Naxd-silenced cells to the level of LacZ-silenced cells. In contrast, exposure of wild-type 3T3-L1 cells to NADHX recapitulated the Naxd deficiency-elicited inhibitory effects on adipocyte differentiation with reduced expression of master transcriptional regulators of adipogenesis, peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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