glucose Cancer Research Results
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*antiOx↑, Blueberries contain polyphenolic compounds, most prominently anthocyanins, which have antioxidant and anti-inflammatory effects.
*Inflam↓,
*memory↑, anthocyanins have been associated with increased neuronal signaling in brain centers mediating memory function as well as improved glucose disposal, benefits that would be expected to mitigate neurodegeneration.
*neuroP↑, preliminary study suggest that moderate-term blueberry supplementation can confer neurocognitive benefit
*cognitive↑, At 12 weeks, we observed improved paired associate learning (p = 0.009) and word list recall (p = 0.04).
*Mood↑, In addition, there were trends suggesting reduced depressive symptoms (p = 0.08) and lower glucose levels (p = 0.10)
*glucose↓,
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ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
radioP↑, apigenin's radioprotective and radiosensitive properties
RadioS↑,
*COX2↓, When exposed to irradiation, apigenin reduces inflammation via cyclooxygenase-2 inhibition and modulates proapoptotic and antiapoptotic biomarkers.
*ROS↓, Apigenin's radical scavenging abilities and antioxidant enhancement mitigate oxidative DNA damage
VEGF↓, It inhibits radiation-induced mammalian target of rapamycin activation, vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP), and STAT3 expression,
MMP2↓,
STAT3↓,
AMPK↑, while promoting AMPK, autophagy, and apoptosis, suggesting potential in cancer prevention.
Apoptosis↑,
MMP9↓, radiosensitizer, apigenin inhibits tumor growth by inducing apoptosis, suppressing VEGF-C, tumor necrosis factor alpha, and STAT3, reducing MMP-2/9 activity, and inhibiting cancer cell glucose uptake.
glucose↓,
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CRC, |
HT29 |
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CRC, |
HCT116 |
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PKM2↓, berberine is directly bound to pyruvate kinase isozyme type M2 (PKM2) in colorectal cancer cells. Berberine inhibited PKM2 activity
Glycolysis↓, berberine was shown to inhibit the reprogramming of glucose metabolism and the phosphorylation of STAT3, down regulate the expression of Bcl-2 and Cyclin D1 genes
p‑STAT3↓,
Bcl-2↓,
cycD1/CCND1↓,
TumCG↓, n vivo experiments showed that tumor growth was inhibited in HT29 cell-bearing mice injected intraperitoneally with berberine (5 or 10 mg/kg body weight)
Ki-67↓, Berberine inhibited the proliferation index (Ki67 expression)
lactateProd↓, Berberine inhibited lactate production, glucose uptake, pyruvate production, and PKM2 activity in HWT tumor tissues, but no apparent effects were observed in both F244A mutant cells and I199S mutant tumor tissues
glucose↓,
*glucose↓, Boron supplementation in human subjects decreased serum glucose, creatinine, and calcitonin,
*creat↓,
*SOD↑, while it increased serum triglycerides, ceruloplasmin, and erythrocyte superoxide dismutase
*MMP↑, Boron administration had positive effects on mitochondrial membrane potential and function in multiple species, but entry into mitochondria was not confirmed
*ROS↓, The available evidence suggest that mitochondria may benefit from the availability of boron, which may promote metabolism and reduce redox stress.
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BC, |
T47D |
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MCF-7 |
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ROS↑, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
cJun↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
p38↑,
eff↓, The antioxidant N‐acetyl‐L‐cysteine (5 μM) abolished CA‐induced apoptosis.
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓,
Apoptosis↑, CA Induced Breast Cancer Apoptosis
BAX↑, Bax and PARP expression levels increased significantly while Bcl‐2 expression decreased with time
PARP↑,
Bcl-2↓,
TumCG↑, CA Suppressed Growth of Breast Cancer Xenografts in Nude Mice
Ki-67↓, down‐regulating Ki67 and Bcl‐2 in vivo.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,
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AntiTum↓, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
ROS↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
cJun↑, CA Activated JNK and p38 in Breast Cancer Cell Lines
p‑p38↑,
Apoptosis↑, CA induced apoptosis of hepatocellular carcinoma cells via the reactive oxygen species (ROS)‐mediated mitochondrial pathway
ROS↑,
eff↑, Furthermore, the combined application of CA and curcumin suppressed the proliferative activity and disrupted the mitochondrial function of metastatic prostate cancer cells compared with their individual uses
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓, Glucose consumption was accelerated by low concentrations of CA, but decreased with increasing time and CA concentration.
BAX↑, up‐regulating Bax and PARP and down‐regulating Bcl‐2.
PARP↑,
Bcl-2↓,
eff↓, We then abrogated the effect of CA‐induced ROS using the antioxidant NAC (5 mM).
Ki-67↓, These findings indicated that CA could accelerate tumor apoptosis by up‐regulating Bax expression and down‐regulating Ki67 and Bcl‐2 in vivo.
toxicity↝, Furthermore, CA did not injure vital organs.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,
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*Pain↓, capsaicin promotes pain relief when used in the right dosage and frequency.
*TRPV1↑, capsaicin-induced pain is also used to assess new molecules that target TRPV1 receptor. Capsaicin activates TRPV1
AMPK↑, The inhibitory effect of capsaicin on this process seems to involve the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK) in conjunction with intracellular ROS release
ROS↑,
TumCP↑, AMPK activation is also linked to inhibition of cell proliferation and apoptosis [153,154]
Apoptosis↑,
TumCCA↑, capsaicin targets preadipocyte proliferation by blocking the S-phase of the cell cycle [149].
Casp3↑, capsaicin induces apoptosis in preadipocytes via the activation of caspase-3, Bax, and Bak, cleavage of PARP, and down-regulation of Bcl-2
BAX↑,
Bak↑,
cl‑PARP↑,
Bcl-2↓,
RNS↑, capsaicin induces apoptosis in BMSC via increased production of ROS and reactive nitrogen species (RNS) [
*glucose↓, healthy male volunteers revealed that capsaicin lowers glucose and increases insulin levels shortly after oral administration
*Insulin↑,
*BP↓, Capsaicin stimulates the release of CGRP through the activation of TRPV1 and therefore decreases blood pressure
*AntiAg↑, Capsaicin has been shown to inhibit platelet aggregation [199,200], which may also provide protection against cardiovascular diseases
ER Stress↑, endoplasmic reticulum stress in human nasopharyngeal carcinoma and pancreatic cancer cells,
Hif1a↓, capsaicin increases the degradation of hypoxia inducible factor 1α in non-small cell lung cancer,
chemoPv↑, mounting evidence supporting a chemo-preventive role for capsaicin in cancer cell culture and animal models,
*glucose↓, OGTT showed that plasma glucose levels in volunteers who received capsicum were significantly lower than those in the placebo group at 30 and 45 minutes
*Insulin↑, Furthermore, plasma insulin levels were significantly higher at 60, 75, 105, and 120 minutes
*Dose↑, 5 grams of capsicum presented capsaicin levels that were associated with a decrease in plasma glucose levels and the maintenance of insulin levels.
*AntiDiabetic↑, The present result might have clinical implications in the management of type 2 diabetes
Apoptosis↑, Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress.
PPARγ↓,
mtDam↑,
ROS↑, Induced cell death via apoptosis and increased ROS levels.
EMT↓, It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity.
CD8+↑,
NK cell↑,
ChemoSen↑, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.
ATP↓, CBD decreases intracellular ATP and glucose levels
glucose↓,
Ca+2↑, CBD enhances calcium influx (mediated by TRPV2) and elevates p-ERK expression in CIK cells
TRPV2↑,
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*neuroP↑, including neuroprotection for neurodegenerative disorders and diabetic peripheral neuropathy, anti-inflammation, anti-oxidation, anti-pathogens, mitigation of cardiovascular disorders,
*Inflam↓,
*antiOx↑,
*cardioP↑, Cardiovascular Protective Effect
*NRF2↑, pivotal antioxidants by activating the Nrf2 pathway
*AMPK↑, It elevates AMPK pathways for the maintenance and restoration of metabolic homeostasis of glucose and lipids.
*SOD↑, figure1
*Catalase↑,
*GSH↑,
*GPx↑,
*ROS↓,
*TNF-α↓,
*IL6↓,
*NF-kB↓,
*COX2↓,
*glucose↓, CGA can attenuate glucose absorption
*TRPC1↓, CGA suppresses the levels of transient receptor potential canonical channel 1 (TRPC1) and decreases ROS and Ca2+, thus mitigating lysophosphatidylcholine (LPC)-induced endothelial injuries
*Ca+2↓,
*HO-1↑, enhancing superoxide dismutase (SOD), and producing NO and heme oxygenase (HO)-1
*NF-kB↓, CGAs can regulate NF-κB and PPARα pathways, lower HIF-1α expression, and suppress cardiac apoptotic signaling, thus executing beneficial effects against cardiac hypertrophy
*PPARα↝,
*Hif1a↓,
*JNK↓, CGA can inhibit NF-κB and JNK pathways, exhibiting cardioprotection
*BP↓, GCE (93 or 185 mg for 4 weeks) could lead to a reduction of 4.7 and 5.6 mmHg in levels of systolic blood pressure (SBP) and a decrease of 3.3 and 3.9 mmHg in levels of diastolic blood pressure (DBP)
*AntiDiabetic↑, CGA has shown its functions in protecting β cells from apoptosis, improving β cell function, facilitating glycemic control, and mitigating DM complications.
*hepatoP↑, CGA can mediate hepatoprotective roles in various pathological conditions of the liver via antioxidant and anti-inflammatory features
*TLR4↓, (1) It can inhibit TLR4-mediated activation of NF-κB, thus suppressing pro-inflammatory responses;
*NRF2↑, (3) it can increase the activity of the Nrf2 pathway
*Casp↓, (4) it can inhibit caspases’ activation to suppress hepatic apoptosis induced by chemicals or toxins.
*neuroP↑, CGA has shown diverse neuroprotective effects on various neuropathological conditions which may be exerted through inhibition of neuroinflammation, reduction in ROS production, prevention of oxidation, and suppression of neuronal apoptosis
*Aβ↓, CGA or extracts containing CGA can inhibit Aβ aggregation-caused cellular injury in SH-SY5Y cells, a neuroblastoma cell line
*LDH↓, CGA increases survival and decreases apoptosis via decreasing activities of lactate dehydrogenase (LDH) and the levels of MDA and raising the levels of SOD and GSH-Px
*MDA↓,
*memory↑, CGA prevents Aβ deposition and neuronal loss and ameliorates learning and memory deterioration in APP/PS2 mice
*AChE↓, CGA inhibits acetylcholinesterase (AChE) activity in rat brains, suggesting its beneficial effect against cognitive impairment
*eff↑, CGA protects against injury caused by cerebral ischemia/reperfusion
EMT↝, It also modulates the epithelial–mesenchymal transition (EMT) process of breast cancer cells by downregulation of N-cadherin and upregulation of E-cadherin
N-cadherin↓,
E-cadherin↑,
TumCCA↑, CGA can stall the cells in the S phase and cause DNA injury in human colon cancer cell lines such as HCT116 and HT29 by increasing ROS production, upregulation of phosphorylated p53, HO-1, and Nrf2
ROS↑,
p‑P53↑,
HO-1↑,
NRF2↑,
ChemoSen↑, CGA in combination with doxorubicin suppresses cellular metabolic activity, colony formation, and cell growth of U2OS and MG-63 cells by upregulating caspase-3 and PARP and suppressing the p44/42 MAPK pathway, thus inducing apoptosis
mtDam↑, mechanism involves CGA-mediated excessive ROS production, causing mitochondrial dysfunction, leading to increases in cleaved levels of caspase-3, caspase-9, PARP, and Bax/Bcl-2 ratio
Casp3↑,
Casp9↑,
PARP↑,
Bax:Bcl2↑,
TumCG↓, in vivo experiments showing that CGA can reduce tumor growth and volume in pancreatic cancer cell-bearing nude mice by modifying cancer cell metabolism through decreasing levels of cyclin D1, c-Myc, and cyclin-dependent kinase-2 (CDK-2),
cycD1/CCND1↓,
cMyc↓,
CDK2↓,
mitResp↓, interrupting mitochondrial respiration, and suppressing aerobic glycolysis
Glycolysis↓,
Hif1a↓, CGA arrests cells at the phase of G1 and inhibits cell viability of prostate cancer cell DU145 by suppressing the levels of HIF-1α and SPHK-1, PCNA, cyclin-D, CDK-4, p-Akt, p-GSK-3β, and VEGF
PCNA↓,
p‑GSK‐3β↓,
VEGF↓,
PI3K↓, inhibition of the PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,
OS↑, Extending Lifespan in Worms
lipid-P↓,
chemoPv↑, Amongst various chemo-preventive agents, phytochemicals especially curcumin and resveratrol in combination have shown great potential in combating cancer
GSH↑, However, supplementation with curcumin and resveratrol resulted in significant increase in the reduced glutathione levels in DMAB treated rats.
SOD↑, Similar trends were noticed in the enzyme activities of super-oxide disumutase and glutathione-s- transferase in DMAB treated rats, when supplemented with combination of phytochemicals.
GSTs↑,
glucose↓, combined treatment of curcumin and resveratrol resulted in appreciable moderation in the uptakes and turnover of glucose in the prostates of DMAB treated rats
*adiP↑, metabolic responses include reduced adiposity, reduced circulating and tissue lipid levels, increased plasma adiponectin and fibroblast growth factor 21 (FGF-21), and reduced fasting insulin and blood glucose
*FGF↑,
*Insulin↓,
*glucose↓,
*Akt↑, activation of Akt was significantly higher in methionine-restricted HepG2 cells
*GSH↓, MR produces a significant decrease in hepatic GSH
*PTEN↓, MR in HepG2 cells limits the capacity of the cells to reactivate oxidized PTEN, resulting in amplification of insulin activation of Akt by increasing PIP3.
*FGF21↑, MR produced a threefold increase in FGF-21 mRNA that was mirrored by a fourfold increase in serum FGF-21.
*PIP3↑,
Weight↓, Mice on the MR diet had reduced body weight and decreased adiposity
TumVol↓, They also had smaller tumors when compared to the mice bearing tumors on the CF diet
P21↑, Elevated expression of P21 occurred in both MCF10AT1-derived tumor tissue and endogenously in mammary gland tissue of MR mice.
p27↑, Breast cancer cell lines MCF10A and MDA-MB-231 grown in methionine-restricted cysteine-depleted media for 24 h also up-regulated P21 and P27 gene expression
*adiP↑, In rodents, a diet low in methionine (20-35 % of regular chow) reduced adiposity in the fat depots and reduced blood levels of lipids, glucose, IGF-1, and leptin, while elevating levels of FGF21 and adiponectin
*glucose↓,
*IGF-1↓,
*FGF21↑,
*OS↑, MR in rodents promotes longevity and delays onset of age-related impairments and chronic diseases
Ki-67↓, number of Ki67-positive stained cells was reduced in the tissue from mice on the MR diet
Casp3↑, MR mice had significantly elevated levels of activated caspase-3
cycD1/CCND1↓, Methionine restriction increases cell cycle inhibitors P21 and P27, while decreasing cyclin D1
GH↓, These effects of fasting/FMD on normal and cancer cells are mediated at least in part by the reduction in GH and IGF-I signaling.
IGF-1↓,
glucose↓, In mice, cycles of a 4-day FMD have been shown to lower blood glucose levels by 40 % and IGF-I by 45 % while increasing ketone bodies 9-fold and IGFBP-1, which inhibits IGF-I, by the end of the FMD
IGFBP1↑,
OS↑, FMD cycles adopted twice a month starting in middle age extend health span and longevity, reduce visceral fat and skin lesions, promote hippocampal neurogenesis, rejuvenate the immune system, and delay bone mineral density loss in mice
Imm↑,
neuroP↑,
BMD↑,
Dose↝, FMD is a plant-based caloric-restricted dietary regimen (typically between 300 and 1100 kcal per day) characterized by low proteins, sugars, and relatively high unsaturated fats.
Risk↓, Remarkably, these bi-monthly FMD cycles started in middle age reduce tumor incidence and delay cancer onset.
other↑, The robust epidemiological evidence that high animal protein consumption increases serum IGF-I levels in humans
TumCP↓, For these reasons, the GH/IGF-I axis emerged as a promising target for cancer treatments and prevention aimed at inhibiting cell proliferation by down-regulating IGF-I
IGF-1↓, Long-term CR is reported to reduce IGF-1 serum levels in rodents by ~30–40%, protecting them against several types of cancers
OS↑, effects of CR in retarding aging, by increasing lifespan by ~35%, reducing the incidence of kidney disorders, chronic pneumonia and tumors [
AntiAge↑,
glucose↓, underline mechanisms could be mediated by the decrease in blood glucose, IGF-1 and insulin levels
Insulin↓,
*glucose↓, Following short-term fasting, blood glucose levels in the sMF and sSF groups were significantly lower than those in the ND group
ROS↑, reactive oxygen species (ROS) levels were significantly higher in the sSF group compared to the sMF and ND groups
LC3B↑, sSF groups exhibited a significant upregulation of LC3B protein levels
p62↓, Conversely, p62 levels (1.00 ± 0.08, 0.58 ± 0.09 & 0.28 ± 0.05, P < 0.01) and the phosphorylation ratio of mTOR (p-mTOR/mTOR) (1.00 ± 0.04, 0.70 ± 0.10 & 0.35 ± 0.03, P < 0.01) were significantly reduced.
p‑mTOR↓,
p‑AMPK↑, IMF group exhibited a significant increase in the LC3B-II/I ratio and the phosphorylation ratio of AMPK (p-AMPK/AMPK)
Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types
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Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods
*PGC-1α↑, figure 1
*AMPK↑,
*adiP↑,
*glucose↓,
*Insulin↓,
*mTOR↓,
*IL6↓,
*TNF-α↓,
*cognitive↑, or even enhanced—cognitive performance
*Inflam↓, fasting suppresses inflammation, reducing the expression of pro-inflammatory cytokines such as interleukin 6 (IL6) and tumor necrosis factor α (TNFα)
*eff↑, mice fasted on alternate days can eat twice as much on the feeding day, such that their net weekly calorie intake remains similar to mice fed ad libitum; despite the lack of overall calorie restriction, the former still display beneficial metabolic e
*neuroP↑, Fasting can also prevent and treat many neurological disorders in animals;
ChemoSen↑, fasting has been shown to improve the therapeutic responses of a variety of rodent cancer models, including gliomas, to chemotherapy
eff↓, shorter nightly fasts were associated with an increased recurrence of cancer
chemoP↑, fasting before or after chemotherapy decreased chemotherapy-related adverse effects, such as weakness, fatigue, and gastrointestinal upset
*eff↑, implementation of a fasting regimen after a traumatic brain injury confers neuroprotection and improves functional recovery
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Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,
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Stroke, |
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*Risk↓, Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases
*Dose↝, Adequate intake: 51+ years Male:3,400 mg Female:2,600 mg
*Risk↓, those who consumed an average of more than 4,099 mg of potassium per day had a 35% lower risk of kidney stones. The potassium citrate salts significantly reduced the risk of new stones and reduced stone size.
*BMD↑, Observational studies suggest that increased consumption of potassium from fruits and vegetables is associated with increased bone mineral density
*glucose↓, Numerous observational studies of adults have found associations between lower potassium intakes or lower serum or urinary potassium levels and increased rates of fasting glucose, insulin resistance, and type 2 diabetes
*AntiDiabetic↑,
*glucose↓, magnolol administered to rats with type 2 diabetes reduced fasting blood glucose and plasma insulin levels, without affecting their body weight
*SOD↑, increase in SOD and CAT activity
*Catalase↑,
*ROS↓, Magnolol acts as a free radical scavenger which was proven in numerous in vitro and in vivo studies
*MDA↓, decrease in MDA level
*GPx↑, increase in SOD, CAT and GPx activities, decrease in MDA level and CYP2E1 activity in the liver
*CYP2E1↓,
*AGEs↓, decrease in AGEs level in kidney glomeruli
*IL10↑, increase in IL-10 level in the plasma
*neuroP↑, numerous reports on the protective effect of magnolol on the nervous system, it can be assumed that this lignan may also have neuroprotective effects in the course of diabetes
*GutMicro↑, In the case of the intestinal microflora, honokiol had a beneficial effect on obtaining microbiota homeostasis increasing the amount of Akkermansia bacteria and reducing the amount of Oscillospira bacteria
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AD, |
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Park, |
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Diabetic, |
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*AntiDiabetic↑, Metformin has been designated as one of the most crucial first-line therapeutic agents in the management of type 2 diabetes mellitus.
*AMPK↑, acts majorly by activating AMPK (Adenosine Monophosphate-Activated Protein Kinase) in the cells and reducing glucose output from the liver.
*glyC↓, It also decreases advanced glycation end products and reactive oxygen species production in the endothelium apart from regulating the glucose and lipid metabolism
*ROS↓,
*cardioP↑, hence minimizing the cardiovascular risks.
*neuroP↑, Preclinical studies have also shown some evidence of metformin’s neuroprotective role in Parkinson’s disease, Alzheimer’s disease, multiple sclerosis and Huntington’s disease.
*Half-Life↝, The plasma half-life of metformin is 2–3 hours, and the active duration is about 6–10hrs.
*toxicity↝, Metformin use for an extended period is linked to a deficiency of vitamin B12.
*BioAv↑, Absolute bioavailability 50–60% in healthy individuals
*glucose↓, Conventionally, it is quite established that metformin lowers blood glucose primarily by its action on the liver
*AGEs↓, Metformin decreases the synthesis of AGE (“Advanced Glycation End”) product formation and hyperglycaemic-induced ROS (“Reactive Oxygen Species”) production
AntiCan↑, There is growing evidence that metformin has anti-cancer effects based on clinical and preclinical studies.
Risk↓, reported that metformin use might decrease the risk of lung cancer within T2D patients as compared to other conventional agents.
TumCP↓, Several studies on cancer cell lines have observed that metformin treatment leads to inhibition of development and proliferation and induces apoptosis of the cancer cells
Apoptosis↑,
TumCCA↑, Metformin was found to block the cell cycle in the “G(0)/G(1)” phase
cycD1/CCND1↓, and this was observed with a sharp drop in the cyclin D1 levels, pRb phosphorylation, and elevated p27(kip) expression.
pRB↓,
p27↓,
mTOR↓, as well as inhibits the mTOR pathway that is activated by insulin.
Casp↑, Metformin is also responsible for inducing caspase-dependent apoptosis along with c- JNK (“Jun N-Terminal Kinase”) activation, oxidative stress and mitochondrial depolarization.
ROS↑,
MMP↓,
ChemoSen↑, patients who received metformin along with the chemotherapy had better pathologic responses as compared to the group without metformin
*hepatoP↑, effects including cardioprotective, hepatoprotective, anti-malignant, and geroprotective effects
*CRM↑, mechanism behind the process of calorie restriction is a reduction in insulin
*Insulin↓,
glucoNG↓, Metformin, the universal first-line treatment for type 2 diabetes, exerts its therapeutic glucose-lowering effects by inhibiting hepatic gluconeogenesis
glucose↓, metformin suppressed hepatic glucose production from gluconeogenic substrates that depend on cytosolic NADH (lactate and glycerol), but not from gluconeogenic substrates independent of cytosolic NADH
*glucose↓, Metformin therapy lowers blood glucose in type 2 diabetes by targeting various pathways including hepatic gluconeogenesis.
*glucoNG↓, inhibits gluconeogenesis
*AMPK↑, The activation of AMPK by metformin
*glucoNG↓, Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase
*glucose↓, Acute and chronic low-dose metformin treatment effectively reduced endogenous glucose production (EGP)
*mitResp↓, These findings are supported by our data showing that metformin significantly inhibited mitochondrial respiration from G-3-P
*glucose↓, RES played a protective role on the IR in PCOS rats, which significantly decreased the levels of blood glucose and serum insulin, up regulated the expression of IGF1R, and down regulated the expression of IGF1.
*Insulin↓,
*IGFR↓,
*IGF-1↓,
*LDHA↑, RES overtly repaired the glycolysis process by reversing the levels of lactic acid and pyruvate, together with up regulating the expression level of LDHA, HK2, and PKM2, after AGK2 treatment.
*HK2↑,
*PKM2↑,
*Glycolysis↝, RES could eectively improve insulin resistance and restore the glycolysis pathway by regulating SIRT2, which may contribute to attenuating the ovarian damage of PCOS rat
*SIRT2↑, activating SIRT2 in PCOS granulosa cells
*glucose↓, MO-SeNPs treatment significantly reduced blood glucose levels (p < 0.05) and restored insulin resistance, with lower dose demonstrating better glycaemic control than larger dose.
*antiOx↑, MO-SeNPs also increased hepatic antioxidant enzyme activity, including GSH-Px, CAT, and T-SOD, which neutralise oxidative stress
*GPx↑,
*Catalase↑,
*SOD↑,
*ROS↓,
*cardioP↑, MO-SeNPs also improves cardiovascular health by raising HDL and lowering LDL.
*HDL↑,
*LDL↓,
*hepatoP↑, MO-SeNPs showed hepatoprotective benefits by lowering inflammatory markers such TNF-α, IL-6, IL-1β, iNOS, and AGEs, and reduced lipid peroxidation.
*TNF-α↓,
*IL6↓,
*IL1β↓,
*lipid-P↓,
*Inflam↓, The reduction in these indicators shows MO-SeNPs reduce liver inflammation and protect the liver.
*ALAT↓, The normalisation of liver enzyme levels (ALT, AST, ALP) showed improved liver function.
*AST↓,
*ALP↓,
*Dose↝, For the aqueous extract, 20 g of powdered leaves were homogenized in 800 mL of boiling distilled water, shaken at 150 rpm for 4 hours, centrifuged at 4000 rpm for 20 minutes, and filtered using Whatman filter paper No. 1 (Cat No. 1001 125) from GE H
*Dose↝, Selenium nanoparticles (MO-SeNPs) were synthesized by adding 5 mL of a 50 mM sodium selenite solution dropwise to 20 mL of Moringa oleifera extract under magnetic stirring, followed by incubation at 37 °C for 48 hours at pH 8 to facilitate the green
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*hepatoP↑, It improves hepatic function, lessens hepatotoxicity caused by high acetaminophen intake, and can lessen oxidative stress in experimental mice, according to a study on animals
*Inflam↓,
*chemoP↑, moreover reducing the side effect of chemotherapeutic agents.
*glucose↓, Silymarin is effective anti-diabetic as it lowers serum glucose levels thus preventing the development of diabetic nephropathy
*antiOx↑, Various studies revealed that Silymarin could exert antioxidant properties in several mechanisms, which includes direct hindrance in free radical production,
*ROS↓,
*ACC↓, down-regulation of acetyl-CoA carboxylase, fatty acid synthase, and peroxisome proliferator-activated receptor
*FASN↓,
*radioP↑, More studies have revealed radioprotective properties of Silymarin in the testis tissues of mice and rats
*NF-kB↓, Silymarin inhibits NF-kB, down-regulates TGF-ß1 mRNA
*TGF-β↓,
*AST↓, Silymarin significantly decreased the elevation of aspartate aminotransferase (AST), alanine aminotransferase, and alkaline phosphatase in serum, and also reversed the altered expressions of α-smooth muscle actin in fibrotic tissue
*α-SMA↝,
*eff↑, Okda et al.[Citation76] currently reported that silymarin with ginger has significantly decreased the severity and incidence of liver fibrosis.
*neuroP↑, Researchers demonstrated that silymarin inhibits microglia activation, and protects dopaminergic neurons from lipopolysaccharide (LPS)-induced neurotoxicity
eff↑, The Silymarin with a selenium dose of 570 mg/d, for 6 months caused no side effects and was effective in reducing prostate cancer growth
ROS↓, Silymarin shows anti-cancerous properties considered to be linked to oxidative stress inhibition, apoptosis induction, growth cycle arrest, and mitochondrial pathway inhibition
*glucose↓, Vitamin C supplementation resulted in significant decreases in blood glucose 16, BP 17, TG and LDL-C 1
*BG↓,
*antiOx↑, vitamin C is a powerful antioxidant because it acts as a reducing agent preventing other compounds from being oxidised.
*ROS↓,
Showing Research Papers: 1 to 31 of 31
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 31
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↑, 1, GSTs↑, 1, HO-1↑, 1, lipid-P↓, 1, lipid-P↑, 1, NRF2↑, 1, OXPHOS↑, 1, RNS↑, 1, ROS↓, 1, ROS↑, 11, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 2, Insulin↓, 2, mitResp↓, 1, MMP↓, 1, MMP↑, 1, mtDam↑, 2,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 3, p‑AMPK↑, 1, cMyc↓, 1, glucoNG↓, 1, glucose↓, 10, GLUT2↓, 1, Glycolysis↓, 2, lactateProd↓, 2, PKM2↓, 1, PPARγ↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 4, p‑Akt↓, 1, Apoptosis↑, 8, BAD↑, 1, Bak↑, 2, BAX↑, 3, Bax:Bcl2↑, 1, Bcl-2↓, 4, Casp↑, 1, Casp3↑, 4, Casp8↓, 1, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1, Fas↑, 1, Myc↓, 1, p27↓, 1, p27↑, 1, p38↑, 1, p‑p38↑, 1,
Kinase & Signal Transduction ⓘ
TRPV2↑, 1,
Transcription & Epigenetics ⓘ
cJun↑, 2, other↑, 1, other↝, 1, pRB↓, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 2, GRP78/BiP↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3B↑, 2, LC3II↑, 1, p62↓, 1, TumAuto↓, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, P53↝, 1, p‑P53↑, 1, PARP↑, 4, cl‑PARP↑, 1, PCNA↓, 1, TP53↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, cycD1/CCND1↓, 4, P21↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, EMT↝, 1, GH↓, 1, p‑GSK‐3β↓, 1, IGF-1↓, 4, IGF-1R↑, 1, IGFBP1↑, 1, mTOR↓, 5, p‑mTOR↓, 1, mTORC1↓, 1, NOTCH3↓, 1, PI3K↓, 4, STAT↓, 1, STAT3↓, 3, p‑STAT3↓, 1, TumCG↓, 3, TumCG↑, 1, Wnt↑, 1,
Migration ⓘ
Ca+2↑, 1, E-cadherin↑, 1, Ki-67↓, 4, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, N-cadherin↓, 1, TumCMig↓, 1, TumCP↓, 6, TumCP↑, 1, TumMeta↓, 1, Zeb1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, ATF4↑, 1, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 2, VEGF↓, 3,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
Imm↑, 2, Inflam↓, 1, JAK1↓, 1, NK cell↑, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 6, Dose↝, 1, eff↓, 3, eff↑, 8, RadioS↑, 2,
Clinical Biomarkers ⓘ
BMD↑, 1, Ki-67↓, 4, Myc↓, 1, TP53↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiTum↓, 1, chemoP↑, 2, chemoPv↑, 2, ChemoSideEff↓, 1, neuroP↑, 1, OS↑, 3, QoL↑, 2, radioP↑, 1, Risk↓, 4, toxicity↝, 1, TumVol↓, 1, Weight↓, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 141
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 6, Catalase↑, 3, CYP2E1↓, 1, GPx↑, 3, GSH↓, 1, GSH↑, 1, HDL↑, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 2, MPO↓, 1, NRF2↑, 2, ROS↓, 9, SOD↑, 4,
Mitochondria & Bioenergetics ⓘ
Insulin↓, 4, Insulin↑, 2, mitResp↓, 1, MMP↑, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis ⓘ
ACC↓, 1, adiP↑, 3, ALAT↓, 1, AMPK↑, 4, CRM↑, 1, FASN↓, 1, FGF21↑, 2, glucoNG↓, 2, glucose↓, 21, glyC↓, 1, Glycolysis↝, 1, HK2↑, 1, LDH↓, 1, LDHA↑, 1, LDL↓, 4, PIP3↑, 1, PKM2↑, 1, PPARα↝, 1, SIRT2↑, 1,
Cell Death ⓘ
Akt↑, 1, BAX↓, 1, Casp↓, 1, Cyt‑c↓, 1, JNK↓, 1, TRPV1↑, 1,
Proliferation, Differentiation & Cell State ⓘ
FGF↑, 1, IGF-1↓, 2, IGFR↓, 1, mTOR↓, 1, PTEN↓, 1,
Migration ⓘ
AntiAg↑, 1, Ca+2?, 1, Ca+2↓, 1, TGF-β↓, 1, TRPC1↓, 1, α-SMA↝, 1,
Angiogenesis & Vasculature ⓘ
Hif1a↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CRP↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 3, Inflam↓, 7, NF-kB↓, 4, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission ⓘ
AChE↓, 1,
Protein Aggregation ⓘ
AGEs↓, 2, Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, Dose↑, 1, Dose↝, 6, eff↑, 5, Half-Life↝, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 2, BG↓, 1, BMD↑, 1, BP↓, 3, creat↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 3, LDH↓, 1,
Functional Outcomes ⓘ
AntiDiabetic↑, 6, Bone Healing↑, 1, cardioP↑, 5, chemoP↑, 1, cognitive↑, 3, hepatoP↑, 4, memory↑, 4, Mood↑, 1, neuroP↑, 9, OS↑, 2, Pain↓, 1, QoL↑, 1, radioP↑, 1, Risk↓, 2, toxicity↝, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 104
Scientific Paper Hit Count for: glucose, glucose
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
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