N-Methylpyridinium

N-Methylpyridinium at a Glance

N-methylpyridinium, or NMP (1-methylpyridinium), is a small pyridinium alkaloid that does not occur in the living coffee plant at all. It is created by roasting: the heat of the roaster decarboxylates and decomposes trigonelline, the abundant pyridine alkaloid of green coffee, into NMP ^{1,2Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}. In practice it is a roast-marker of coffee — the darker the roast, the more of it there is — and it is specific enough to roasted coffee that it has been proposed as a dietary biomarker of coffee intake ^{10,11Reference 10Lang R et al. · 2011Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumptionView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}.

Its research interest is cytoprotective and metabolic. In cell and animal models NMP is a potent inducer of the Nrf2/ARE pathway and the phase-II detoxifying enzymes it controls ^{3,4Reference 3Boettler U et al. · 2011In vitroCoffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivoView study →Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →}, and it down-regulates the machinery of gastric acid secretion in human stomach-cell lines — a candidate explanation for why darker-roast coffee is gentler on the stomach ^{5,6Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}. Alongside these it stimulates cellular energy metabolism ^{7Reference 7Riedel A et al. · 2014N-methylpyridinium, a degradation product of trigonelline upon coffee roasting, stimulates respiratory activity and promotes glucose utilization in HepG2 cellsView study →} and eases inflammatory insulin resistance in cultured fat cells ^{8Reference 8Quarta S et al. · 2021Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytesView study →}.

The honest posture is thin. Almost everything below is in-vitro or animal work on the isolate, plus one small human roast-comparison trial that tested whole coffee, not purified NMP. There is no controlled human trial of isolated N-methylpyridinium, and its dietary contribution sits inside the whole-coffee matrix alongside caffeine, chlorogenic acids and dozens of other roast products.

A Roast Product of Trigonelline

The single most compound-defining fact about NMP is that it is a cooking artefact of its own source. Green coffee beans contain essentially no N-methylpyridinium; they are rich in trigonelline (~1–2% dry weight), the N-methyl betaine of nicotinic acid. When coffee is roasted, trigonelline is heat-labile and breaks down along two routes — demethylation to niacin (vitamin B3), and decarboxylation to N-methylpyridinium ^{1,2Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}.

Model-system pyrolysis pinned the chemistry down: heating trigonelline salts under roasting-like conditions yields 1-methylpyridinium as a major product, with formation rising with temperature between about 220 and 245 °C ^{1Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →}. In real beans the consequence is a clean inverse relationship with roast degree — as trigonelline (and the caffeoylquinic acids) fall with darker roasting, NMP climbs, reaching up to roughly 0.25% of bean dry weight in dark roasts while remaining absent from green beans ^{2Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}.

This is the mirror image of the trigonelline story: the same roast that destroys trigonelline generates NMP. No single roast maximises both — a light roast is the higher-trigonelline exposure; a dark roast trades that for more N-methylpyridinium (and more niacin). During brewing NMP is efficiently extracted into the cup, so a mug of dark-roast coffee delivers the most ^{2,9Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →}.

Coffee, Nrf2 & Cytoprotection

NMP’s headline research thread is antioxidant defence by induction, not scavenging. Rather than mopping up radicals directly, it switches on the cell’s own protective program — the Nrf2/ARE (antioxidant-response element) pathway that governs phase-II detoxifying and antioxidant enzymes such as glutathione-S-transferases, NAD(P)H:quinone oxidoreductase and heme oxygenase-1.

Boettler, Somoza and colleagues showed that pyridinium derivatives, and NMP in particular, are potent activators of Nrf2 nuclear translocation and ARE-dependent gene expression, with the substitution pattern on the pyridinium ring determining potency ^{4Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →}. In a companion study they built two model coffees by varying the roast — a light roast rich in chlorogenic acid and a heavy roast rich in NMP — and found both induced chemopreventive phase-II enzymes via Nrf2/ARE in vitro and in vivo (in mice), establishing NMP as one of the roast-formed constituents behind coffee’s cytoprotective signal ^{3Reference 3Boettler U et al. · 2011In vitroCoffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivoView study →}.

This reframes a share of coffee’s antioxidant reputation as a dark-roast phenomenon carried by a roast product, complementing the light-roast chlorogenic-acid fraction. It remains cell-and-mouse evidence, and in the whole brew NMP acts alongside — and is partly opposed by residual trigonelline, which interfered with NMP-driven Nrf2 activation in one assay ^{4Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →}.

What It's Used For

The evidence is broad in mechanism but shallow in tier: several coherent cell/animal signals, one small human trial of whole coffee (not the isolate), and no controlled trial of purified NMP.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Scores stay low: no application rests on a controlled human trial of isolated NMP, so read the per-row basis.

01Nrf2 / Phase-II CytoprotectionShaky38%Isolate + model-coffee, in vitro and in mice ^{3,4Reference 3Boettler U et al. · 2011In vitroCoffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivoView study →Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →}

02Gastric Acid ModulationShaky36%HGT-1 stomach cells + one small human roast-comparison trial (whole coffee) ^{5,6Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}

03Cellular Energy & Glucose MetabolismShaky28%HepG2 liver-cell isolate ^{7Reference 7Riedel A et al. · 2014N-methylpyridinium, a degradation product of trigonelline upon coffee roasting, stimulates respiratory activity and promotes glucose utilization in HepG2 cellsView study →}

04Anti-Inflammatory / Insulin SensitisingShaky24%Human adipocyte isolate, in vitro ^{8Reference 8Quarta S et al. · 2021Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytesView study →}

Mechanisms

The load-bearing mechanism is Nrf2/phase-II induction ^{3,4Reference 3Boettler U et al. · 2011In vitroCoffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivoView study →Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →} — NMP acts by switching on the cell’s own antioxidant program rather than by direct radical scavenging, which is why it registers as bioactive at sub-micromolar concentrations.

Pharmacokinetics

NMP is a small, permanently charged, water-soluble quaternary pyridinium cation, yet it is readily and concentration-dependently absorbed after coffee consumption ^{9,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. It is essentially absent from plasma until coffee is drunk, then rises to a peak within about 1–2 h — reported maxima around 0.8 µmol/L (roughly 777 nmol/L in women, 804 nmol/L in men) after a coffee dose — before being excreted unchanged in the urine over the following hours ^{9,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. It is chemically very stable and is not appreciably metabolised, which (together with its coffee-only origin) is exactly why it works as a dietary biomarker of recent roasted-coffee intake ^{10,11Reference 10Lang R et al. · 2011Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumptionView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. Robust isolate parameters — absolute oral bioavailability, definitive half-life, tissue distribution — have not been formally established in humans; the data are dietary appearance-and-excretion curves, not a purified-compound PK study ^{9Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →}.

Clinical Trials

There are no controlled efficacy trials of isolated N-methylpyridinium. The only human intervention data are (a) a small whole-coffee crossover comparing a dark, NMP-rich roast against a medium roast for gastric acid secretion ^{6Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}, and (b) human PK/biomarker studies measuring NMP appearance in plasma and urine after drinking coffee ^{9,10,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 10Lang R et al. · 2011Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumptionView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. Everything mechanistic is cell or mouse.

Last checked: July 2026.

Isolate vs. Plant Studies

This molecule has an unusual profile because it is a roast artefact, not a plant constituent — so the usual “isolate vs. whole plant” axis becomes “isolate vs. whole roasted coffee.” The mechanistic work is overwhelmingly the isolate: purified NMP drives the Nrf2/ARE induction ^{4Reference 4Boettler U et al. · 2011Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expressionView study →}, the HGT-1 gastric down-regulation ^{5Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →}, the HepG2 energy/glucose effects ^{7Reference 7Riedel A et al. · 2014N-methylpyridinium, a degradation product of trigonelline upon coffee roasting, stimulates respiratory activity and promotes glucose utilization in HepG2 cellsView study →} and the adipocyte anti-inflammatory response ^{8Reference 8Quarta S et al. · 2021Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytesView study →}. As a preclinical isolate base that is a genuine strength — these are NMP-specific findings, not whole-extract assays.

The human evidence, however, is never the isolate. The one intervention trial dosed whole dark- vs. medium-roast coffee ^{6Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}, and the biomarker/PK studies measure NMP that appears after drinking coffee ^{9,10,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 10Lang R et al. · 2011Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumptionView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. Because NMP is generated by the same roasting that reshapes chlorogenic acids, trigonelline, melanoidins and caffeine, its dietary effect is inseparable from the roast matrix it rides in. The correct framing: strong isolate mechanism + a coffee-specific human PK/biomarker record + zero controlled human trials of purified NMP — so the cell data and the coffee data must not be equated.

Prevalence in Nature

N-methylpyridinium is not a natural plant product in the usual sense: it is essentially confined to roasted coffee, formed on the roaster from trigonelline and absent from the green bean ^{1,2Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}. Because it is a thermal decarboxylation product, its abundance is governed almost entirely by roast degree rather than by species, soil or variety:

• Roasted coffee (Coffea spp.) — the dominant and effectively sole dietary source. NMP correlates inversely with roast colour: dark roasts reach up to ~0.25% of bean dry weight, light roasts carry little, and green beans carry none ^{2Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}. Brewed coffee delivers roughly 20–40 mg/L, extracted efficiently into the cup ^{9,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}.
• Other roasted/pyrolysed foods carry it only where trigonelline is heated — traces can arise in other thermally processed plant materials, but roasted coffee is the overwhelming exposure ^{1Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →}.

This coffee-specificity is the basis for NMP’s proposed role as a biomarker of roasted-coffee consumption: it is present in plasma and urine essentially only after coffee is drunk, is chemically stable, and its abundance tracks intake ^{10,11Reference 10Lang R et al. · 2011Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumptionView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}.

Discovery & Synthesis

N-methylpyridinium as a chemical entity — 1-methylpyridinium — is a simple, long-known quaternary pyridinium salt of classical heterocyclic chemistry. Its identity as a coffee/trigonelline roasting product was established by Richard Stadler and colleagues at Nestlé Research in 2002, who subjected trigonelline to roasting-like pyrolysis and identified 1-methylpyridinium as a major decarboxylation product, with formation increasing with temperature from 220–245 °C ^{1Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →}. Subsequent quantitative work by Lang, Hofmann and Somoza mapped its formation across real coffee roasts and its appearance in human plasma and urine ^{2,9Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →}.

Chemically, NMP is trivially prepared by N-methylation of pyridine (e.g. with methyl iodide, giving 1-methylpyridinium iodide) — a textbook quaternisation — so the pure salt is a defined laboratory reagent rather than a substance extracted from plants. In the diet, however, its only meaningful origin is in-situ generation during coffee roasting from trigonelline; it is not manufactured as a supplement.

Patents: not yet researched.

Toxicity & Safety

N-methylpyridinium carries a low toxicity flag. It is a normal constituent of roasted coffee, one of the most widely consumed beverages in the world, and humans have therefore ingested it routinely for centuries with no signal of acute toxicity at dietary levels ^{6,11Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. It is water-soluble, chemically stable, readily absorbed and excreted unchanged in urine within hours — it is not bioaccumulated or extensively metabolised ^{9,11Reference 9Bresciani L et al. · 2020Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention studyView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}. Its documented bioactivities occur at nanomolar-to-low-micromolar concentrations that are consistent with ordinary coffee exposure, and its best-characterised gastric effect is a protective down-regulation of acid secretion rather than an irritant one ^{5,6Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}.

The caveats are the honest ones of a thin dataset. Concentrated or supplemental NMP has not been characterised for repeat-dose, genotoxicity or drug-interaction endpoints; there are no isolate human safety studies and no enzyme- or transporter-level interaction data. As a permanently charged quaternary cation it is structurally reminiscent of other N-methylpyridinium species used as tool toxins in the laboratory, but there is no evidence that the dietary coffee ion behaves that way at food-relevant exposure — the point is only that its isolated, high-dose toxicology is simply uncharacterised, not that it is implicated. Pregnancy and lactation are decided on the coffee page, where intake is decided, not on this molecule page.

Safety at a Glance

✅ Low / no toxicity

• A dietary roast constituent with low toxicity. A normal component of roasted coffee, consumed routinely with no acute-toxicity signal at food levels ^{6,11Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →Reference 11Lang R et al. · 2008Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysisView study →}.
• Gastric-protective in the relevant models. Down-regulates rather than stimulates gastric acid secretion in human stomach cells and a small human roast-comparison trial ^{5,6Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →Reference 6Rubach M et al. · 2014A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blendView study →}.
• Isolated/supplemental exposure is uncharacterised. No repeat-dose, genotoxicity or drug-interaction data exist for concentrated NMP ^{5,8Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →Reference 8Quarta S et al. · 2021Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytesView study →}.
• Exposure depends entirely on roast. Dark-roast coffee carries far more NMP than light roast; green coffee carries none ^{1,2Reference 1Stadler RH et al. · 2002AlkylpyridiniumsView study →Reference 2Lang R et al. · 2013Quantitative studies on roast kinetics for bioactives in coffeeView study →}.

Dosage

There is no established or recommended human dose for isolated N-methylpyridinium. The cited effect concentrations are cell-culture exposures — nanomolar in the HepG2 energy studies ^{7Reference 7Riedel A et al. · 2014N-methylpyridinium, a degradation product of trigonelline upon coffee roasting, stimulates respiratory activity and promotes glucose utilization in HepG2 cellsView study →}, ~1 µmol/L in the adipocyte study ^{8Reference 8Quarta S et al. · 2021Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytesView study →}, and low-micromolar in the gastric-cell work ^{5Reference 5Rubach M et al. · 2012Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretionView study →} — and are not convertible to human self-dosing.

Real human exposure is dietary and roast-dependent:

Because NMP is generated by roasting alongside dozens of other changes to the coffee matrix, coffee’s human health associations cannot be re-created by dosing purified NMP. These are dietary exposures and research-model concentrations, not a personal recommendation.

References

1. Stadler RH, Varga N, Hau J, Arce Vera F, Welti DH (2002). Alkylpyridiniums. 1. Formation in model systems via thermal degradation of trigonelline. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/11853503/
2. Lang R, Yagar EF, Wahl A, Beusch A, Dunkel A, Dieminger N, Eggers R, Bytof G, Stiebitz H, Lantz I, Hofmann T (2013). Quantitative studies on roast kinetics for bioactives in coffee. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/24274681/
3. Boettler U, Volz N, Pahlke G, Teller N, Kotyczka C, Somoza V, Stiebitz H, Bytof G, Lantz I, Lang R, Hofmann T, Marko D (2011). Coffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivo. Molecular Nutrition & Food Research. https://pubmed.ncbi.nlm.nih.gov/21448860/
4. Boettler U, Sommerfeld K, Volz N, Pahlke G, Teller N, Somoza V, Lang R, Hofmann T, Marko D (2011). Coffee constituents as modulators of Nrf2 nuclear translocation and ARE (EpRE)-dependent gene expression. The Journal of Nutritional Biochemistry. https://pubmed.ncbi.nlm.nih.gov/20655719/
5. Rubach M, Lang R, Seebach E, Somoza MM, Hofmann T, Somoza V (2012). Multi-parametric approach to identify coffee components that regulate mechanisms of gastric acid secretion. Molecular Nutrition & Food Research. https://pubmed.ncbi.nlm.nih.gov/22147653/
6. Rubach M, Lang R, Bytof G, Stiebitz H, Lantz I, Hofmann T, Somoza V (2014). A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blend. Molecular Nutrition & Food Research. https://pubmed.ncbi.nlm.nih.gov/24510512/
7. Riedel A, Hochkogler CM, Lang R, Bytof G, Lantz I, Hofmann T, Somoza V (2014). N-methylpyridinium, a degradation product of trigonelline upon coffee roasting, stimulates respiratory activity and promotes glucose utilization in HepG2 cells. Food & Function. https://pubmed.ncbi.nlm.nih.gov/24448391/
8. Quarta S, Scoditti E, Carluccio MA, Calabriso N, Santarpino G, Damiano F, Siculella L, Wabitsch M, Verri T, Favari C, Del Rio D, Mena P, De Caterina R, Massaro M (2021). Coffee bioactive N-methylpyridinium attenuates tumor necrosis factor (TNF)-α-mediated insulin resistance and inflammation in human adipocytes. Biomolecules. https://pubmed.ncbi.nlm.nih.gov/34680177/
9. Bresciani L, Tassotti M, Rosi A, Martini D, Antonini M, Dei Cas A, Bonadonna R, Brighenti F, Del Rio D, Mena P (2020). Absorption, pharmacokinetics, and urinary excretion of pyridines after consumption of coffee and cocoa-based products containing coffee in a repeated dose, crossover human intervention study. Molecular Nutrition & Food Research. https://pubmed.ncbi.nlm.nih.gov/32776430/
10. Lang R, Wahl A, Stark T, Hofmann T (2011). Urinary N-methylpyridinium and trigonelline as candidate dietary biomarkers of coffee consumption. Molecular Nutrition & Food Research. https://pubmed.ncbi.nlm.nih.gov/21618426/
11. Lang R, Yagar EF, Eggers R, Hofmann T (2008). Quantitative investigation of trigonelline, nicotinic acid, and nicotinamide in foods, urine, and plasma by means of LC-MS/MS and stable isotope dilution analysis. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/19007232/

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