Buty Cancer Research Results

Buty, Butyrate: Click to Expand ⟱
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Butyrate (butyric acid) is a four-carbon short-chain fatty acid produced primarily by intestinal microbial fermentation of dietary fibre and resistant starch. It is a major energy source for normal colonocytes and also functions as a signalling metabolite through inhibition of histone deacetylases (HDACs) and activation of receptors including GPR109A/HCAR2 and FFAR2/GPR43. In colorectal cancer cells, butyrate ↑ commonly causes intracellular accumulation, HDAC inhibition, cell-cycle arrest, differentiation, and apoptosis while reducing proliferation and inflammatory signalling. This contrasting effect in normal versus malignant colonocytes is sometimes called the butyrate paradox: normal colonocytes efficiently oxidize butyrate as fuel, whereas glycolytic cancer cells may metabolize less butyrate, permitting greater nuclear accumulation and HDAC inhibition. Butyrate is an individual metabolite and microbial postbiotic, separate from the broader short-chain fatty acid group and from acetate and propionate. Effects outside the colon are dose-, tissue-, microbiome-, and metabolism-dependent, and most direct anticancer evidence remains preclinical. Colorectal cancer reference; Intestinal biology review; HDAC inhibition reference.



Scientific Papers found: Click to Expand⟱
7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7669- IP,    Colorectal cancer and inulin supplementation: the good, the bad, and the unhelpful
- Review, CRC, NA
GutMicro↑, The primary prebiotic function of inulin is linked to stimulating the growth of beneficial bacteria, mostly strains from Bifidobacterium and Lactobacillus genera, and reducing the expansion of harmful bacteria
Buty↑, Inulin supplementation specifically was shown to promote the growth of Clostridium cluster XIVa butyrate producers
eff↓, Despite the promising results shown with inulin supplementation and a general consensus surrounding the benefits of inulin for gut health, more recent studies in mice show that inulin may produce harmful effects.
Inflam↑, When bacteria capable of fermenting inulin are absent, inulin remains unfermented in the gut and can trigger inflammation.
eff∅, In most clinical studies, inulin supplementation (ranging from 10 to 15 g/day during 1–6 months) failed to convincingly demonstrate a preventive effect on CRC development
SCFAs↑, Even if inulin supplementation modulates the gut microbiota and increases concentrations of SCFAs, these changes may be insufficient to provide a better disease outcome.

7659- IP,    Inulin-type fructans and reduction in colon cancer risk: review of experimental and human data
- in-vivo, Colon, NA
GutMicro↑, Inulin-type fructans (beta(2,1)fructans) extracted from chicory roots (Cichorium intybus) are prebiotic food ingredients, which in the gut lumen are fermented to lactic acid and SCFA
SCFAs↑,
eff↑, Higher beneficial effects were achieved by synbiotics (mixtures of probiotics and prebiotics), long-chain inulin-type fructans compared to short-chain derivatives, and feeding high-fat Western style diets
Buty↑, The effects have been reported to be associated with gut flora-mediated fermentation and production of butyrate.
Risk↓, evidence has been accumulated that shows that inulin-type fructans and corresponding fermentation products reduced the risks for colon cancer.

7660- IP,    Overview of experimental data on reduction of colorectal cancer risk by inulin-type fructans
- Review, CRC, NA
SCFAs↑, Important products formed by fermentation of inulin-type fructans with human gut flora are short-chain fatty acids.
Buty↑, Of these, butyrate and propionate inhibit growth of colon tumor cells and histone deacetylases.
PA↑,
TumCG↓,
HDAC↓,
Apoptosis↑, Butyrate also causes apoptosis, reduces metastasis in colon cell lines, and protects from genotoxic carcinogens by enhancing expression of enzymes involved in detoxification.
TumMeta↓,

7661- IP,    Enhancement of carbohydrate metabolism by probiotic and prebiotic intake promotes short-chain fatty acid production in the gut microbiome: a randomized, double-blind, placebo-controlled crossover trial
- Trial, Nor, NA
*PA↑, Two weeks of BL + IN intake significantly increased acetate, propionate, and butyrate concentrations and Bifidobacterium abundance compared to placebo.
*Buty↑,
*GutMicro↑,
*SCFAs↑, suggesting an enhanced capacity for SCFA production.

7664- IP,  GCL2505,    Administration of bifidobacteria and dietary fiber improves cognitive function by increasing short-chain fatty acid-producing bacteria and reducing inflammation
- Trial, AD, NA
*cognitive↑, A randomized, double-blind, placebo-controlled, parallel-group clinical trial of this probiotic strain in combination with inulin (a prebiotic) reported an improvement of cognitive function in the elderly.
*SCFAs↑, After probiotic and prebiotic administration, short-chain fatty acid producers such as Faecalibacterium and Bifidobacterium were increased in the gut.
*GutMicro↑, GCL2505 and inulin can improve cognitive function by alleviating inflammation via an increase of short-chain fatty acid-producing bacteria, which appears to elevate levels of short-chain fatty acids, particularly acetate and butyrate, in the gut.
*Buty↑,
*AcOH↑,
*neuroP↑, 12 weeks of administration of GCL2505 and inulin significantly improved scores in the Neurocognitive Index domain, an assessment of overall cognitive function,

7666- IP,    Short-chain fatty acid kinetics and concentrations are higher after inulin supplementation in young and older adults: a randomized trial
- Trial, Nor, NA
*Dose↝, placebo-controlled, double-blind crossover study, 21 YAs (20-29 y) and 40 OAs (59-87 y) adults were supplemented with inulin or placebo (maltodextrin) for 7 d (final intake: 30 g/d)
*Buty↑, Inulin evoked a 44% increase in butyrate production (μmol/min) in the inaccessible pool
*PA↑, In addition, a 34% increase in propionate production in YA only
*AcOH↑, We found a 50%-60% increase in fecal acetate, propionate, and butyrate and a 34% increase in plasma butyrate in OA, whereas in YA only 34% increase in fecal acetate.
*SCFAs↑, Inulin intake increases SCFA production.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 3,   PA↑, 1,   SCFAs↑, 3,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

HDAC↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumMeta↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,   eff↑, 1,   eff∅, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 2,  

Functional Outcomes(tgid=23) ⓘ

Risk↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AcOH↑, 2,   Buty↑, 4,   diuretic↑, 1,   GLP-1R↑, 1,   PA↑, 2,   SCFAs↑, 4,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   uricA↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   MAPK↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↑, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

COL1↓, 1,   Fibrosis↓, 1,   RAGE↓, 1,   TGF-β1↓, 1,   TJ↑, 1,   α-SMA↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   GutMicro↑, 3,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 44

Scientific Paper Hit Count for: Buty, Butyrate
6 Inulin Prebiotic
1 Fucoidan
1 Bifidobacterium animalis subsp. lactis GCL2505
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1564  State#:%  Dir#:2
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