adiP Cancer Research Results

adiP, adiponectin: Click to Expand ⟱
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Adiponectin is an adipokine with anti-inflammatory and insulin-sensitizing properties, and its effects on tumor biology are thought to be mediated through influences on cell proliferation, apoptosis, and metabolic regulation.

Adiponectin is a key metabolic hormone whose levels have been associated with cancer risk and prognosis across multiple tumor types. Generally, lower adiponectin levels tend to correlate with more aggressive tumor phenotypes and poorer outcomes, while higher levels may offer a degree of protection.
Scientific Papers found: Click to Expand⟱
4282- ALA,    Effect of add-on alpha lipoic acid on psychopathology in patients with treatment-resistant schizophrenia: a pilot randomized double-blind placebo-controlled trial
- Trial, NA, NA
*antiOx↑, Alpha lipoic acid (ALA) is a naturally occurring antioxidant that plays an important role in the functioning of enzymes involved in mitochondrial oxidative metabolism
*Inflam↓, act as antioxidant and anti-inflammatory agents
*lipid-P↓, ALA supplementation has been shown to decrease lipid peroxidation in healthy controls but not in patients with schizophrenia
*adiP↑, ALA has also been shown to improve adiponectin levels, prevent weight gain or weight loss
*cognitive∅, no significant difference between placebo and the ALA groups in scores of cognitive functions
*BDNF↑, median BDNF levels increased from 5.06 to 5.50 ng/mL

3549- ALA,    Important roles of linoleic acid and α-linolenic acid in regulating cognitive impairment and neuropsychiatric issues in metabolic-related dementia
- Review, AD, NA
*Inflam↓, LA and ALA attenuate neuroinflammation by modulating inflammatory signaling.
*other↝, ratio of LA to ALA in typical Western diets is reportedly 8–10:1 or higher, which is rather higher than the ideal ratio of LA to ALA (1–2:1) required to reach the maximal conversion of ALA to its longer chain PUFAs
*other↝, LA and ALA are essential PUFAs that must be obtained from dietary intake because they cannot be synthesized de novo
*neuroP↑, several studies have also suggested that lower dietary intake of LA influences AA metabolism in brain and subsequently causes progressive neurodegenerative disorders
*BioAv↝, LA cannot be synthesized in the human body
*adiP↑, study suggested that LA-rich oil consumption leads to the high levels of adiponectin in the blood [114], which could stimulate mitochondrial function in the liver and skeletal muscles for energy thermogenesis
*BBB↑, Although LA can penetrate the BBB, most of the LA that enters the brain cannot be changed into AA [48,49], and 59 % of the LA that enters the brain is broken down by fatty acid β-oxidation
*Casp6↓, In neurons, LA and ALA attenuate the activation of cleaved caspase-3/-9, p-NF-Kb and the production of TNF-a, IL-6, IL-1b, and ROS by binding GPR40 and GPR120.
*Casp9↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*ROS↓,
*NO↓, LA reduces NO production and inducible nitric oxide synthases (iNOS) protein expression in BV-2 microglia
*iNOS↓,
*COX2↓, ALA increases antioxidant enzyme activities in the brain [182] and inhibits the activation of COX-2 in AD models
*JNK↓, ALA has also been shown to suppress the activation of c-Jun N-terminal kinases (JNKs) and p-NF-kB p65 (Ser536), which is involved in inflammatory signaling
*p‑NF-kB↓,
*Aβ↓, and to inhibit Aβ aggregation and neuronal cell necrosis
*BP↓, LA also improves blood pressure, blood triglyceride and cholesterol levels, and vascular inflammation
*memory↑, One study suggested that long-term intake of ALA enhances memory function by increasing hippocampal neuronal function through activation of cAMP response element-binding protein (CREB) [192], extracellular signal-regulated kinase (ERK), and Akt signa
*cAMP↑,
*ERK↑,
*Akt↑,
cognitive?, Furthermore, ALA administration inhibits Aβ induced neuroinflammation in the cortex and hippocampus and enhances cognitive function

1854- dietFMD,    How Far Are We from Prescribing Fasting as Anticancer Medicine?
- Review, Var, NA
ChemoSideEff↓, ample nonclinical evidence indicating that fasting can mitigate the toxicity of chemotherapy and/or increase the efficacy of chemotherapy.
ChemoSen↑, Fasting-Induced Increase of the Efficacy of Chemotherapy
IGF-1↓,
IGFBP1↑, biological activity of IGF-1 is further compromised due to increased levels of insulin-like growth factor binding protein 1 (IGFBP1)
adiP↑, increased levels of adiponectin stimulate the fatty acid breakdown.
glyC↓, After depletion of stored glycogen, which occurs usually 24 h after initiation of fasting, the fatty acids serve as the main fuels for most tissues
E-cadherin↑, upregulation of E-cadherin expression via activation of c-Src kinase
MMPs↓, decrease of cytokines, chemokines, metalloproteinases, growth factors
Casp3↑, increase of level of activated caspase-3
ROS↑, it is postulated that the beneficial effects of fasting are ascribed to rapid metabolic and immunological response, triggered by a temporary increase in oxidative free radical production
ATP↓, Glucose deprivation leads to ATP depletion, resulting in ROS accumulation
AMPK↑, Additionally, ROS activate AMPK
mTOR↓, Under conditions of glucose deprivation, AMPK inhibits mTORC1
ROS↑, Beyond glucose deprivation, another mechanism increasing ROS levels is the AA (amino acids) starvation
Glycolysis↓, Indeed, in cancer cells, limited glucose sources impair glycolysis, decrease glycolysis-based NADPH production due to reduced utilization of the pentose phosphate pathway [88,89,90,91],
NADPH↓,
OXPHOS↝, and shift the metabolism from glycolysis to oxidative phosphorylation (OXPHOS) (“anti-Warburg effect”), leading to ROS overload [92,93,94,95].
eff↑, Fasting compared to long-term CR causes a more profound decrease in insulin (90% versus 40%, respectively) and blood glucose (50% versus 25%, respectively).
eff↑, FMD have been demonstrated to result in alterations of the serum levels of IGF-I, IGFBP1, glucose, and ketone bodies reminiscent of those observed in fasting
*RAS↓, A plausible explanation of the differential protective effect of fasting against chemotherapy is the attenuation of the Ras/MAPK and PI3K/Akt pathways downstream of decreased IGF-1 in normal cells
*MAPK↓,
*PI3K↓,
*Akt↓,
eff↑, Starvation combined with cisplatin has been shown in vitro to protect normal cells, promoting complete arrest of cellular proliferation mediated by p53/p21 activation in AMPK-dependent and ATM-independent manner
ROS↑, generation of ROS due to paradoxical activation of the AKT/S6K, partially via the AMPK-mTORC1 energy-sensing pathways malignant cells
Akt↑, cancer cells
Casp3↑, combination of fasting and chemotherapy was in part ascribed to enhanced apoptosis due to activation of caspase 3

2269- dietMet,    Mechanisms of Increased In Vivo Insulin Sensitivity by Dietary Methionine Restriction in Mice
- in-vivo, Nor, NA
*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↑,

2265- dietMet,    Cysteine supplementation reverses methionine restriction effects on rat adiposity: significance of stearoyl-coenzyme A desaturase
- in-vivo, Nor, NA
*SCD1↓, Dietary methionine restriction in rats decreases hepatic Scd1 mRNA and protein,
*Weight↓, MR markedly lowered weight gain, as previously reported (21, 22, 28), despite food intake/g body weight being consistently higher than CF group throughout the study
*Insulin↓, MR significantly decreased serum concentrations of insulin, leptin, IGF-1, and raised adiponectin compared with CF.
*IGF-1↓,
*adiP↑,
*eff↓, these effects were reversed by cysteine

2270- dietMet,    Methionine-restricted diet inhibits growth of MCF10AT1-derived mammary tumors by increasing cell cycle inhibitors in athymic nude mice
- in-vivo, Var, NA
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

5192- dietMet,    Intermittent methionine restriction reduces IGF‐1 levels and produces similar healthspan benefits to continuous methionine restriction
OS↑, A sustained state of methionine restriction (MR) dramatically extends the healthspan of several model organisms.
eff↝, we show for the first time that IMR produces similar beneficial metabolic effects to continuous MR,
IGF-1↓, like continuous MR, IMR confers beneficial changes in the plasma levels of the hormones IGF‐1, FGF‐21, leptin, and adiponectin.
adiP↑, Plasma levels of the energy‐regulating hormones adiponectin and leptin are increased and decreased, respectively, by continuous MR
Leptin↓,
Weight↓, both continuous MR and the IMR2 regimen resulted in animals remaining lean over the course of the experiment

3708- dietSTF,    Fasting as a Therapy in Neurological Disease
*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

4328- VitB5,    Pantethine
- Review, AD, NA
*BBB↝, BBB: not penetrant, but cysteamine (metabolite) is penetrant
*LDL↓, Pantethine has reduced total and LDL cholesterol though effects have been modest.
*lipid-P↓, Therapeutic Lifestyle Change (TLC) diet alone did not significantly affect lipid profiles but when combined with pantethine supplementation, significantly decreased lipid levels.
*AST↓, significantly reduced levels of liver enzymes (AST reduced from 66 to 33 IU/L, and ALT reduced from 113 to 51 IU/L, or by 58%)
*ALAT↓,
*TGF-β↓, mean serum TGF-β level was significantly decreased
*adiP↑, while the mean serum level of high molecular adiponectin was increased.
*Inflam↓, inflammation was improved,
TumCG↓, mouse model of ovarian tumor, pantethine treatment (750 mg/kg/day, i.p.) for 4 weeks resulted in slower tumor progression,
FASN↓, Pantethine inhibits fatty acid synthase (FAS). Inhibition of FAS activity has been shown to be cytotoxic to human cancer cells in vitro and in vivo [17].


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↝, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 2,   AMPK↑, 1,   FASN↓, 1,   glyC↓, 1,   Glycolysis↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Casp3↑, 3,   p27↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 2,   IGFBP1↑, 1,   mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   MMPs↓, 1,  

Hormonal & Nuclear Receptors ⓘ

Leptin↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↓, 1,   eff↑, 3,   eff↝, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   ChemoSideEff↓, 1,   cognitive?, 1,   OS↑, 1,   TumVol↓, 1,   Weight↓, 2,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↓, 1,   lipid-P↓, 2,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

Insulin↓, 3,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 7,   ALAT↓, 1,   AMPK↑, 1,   cAMP↑, 1,   FGF21↑, 2,   glucose↓, 3,   LDL↓, 1,   PIP3↑, 1,   SCD1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 2,   Casp6↓, 1,   Casp9↓, 1,   iNOS↓, 1,   JNK↓, 1,   MAPK↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   FGF↑, 1,   IGF-1↓, 2,   mTOR↓, 1,   PI3K↓, 1,   PTEN↓, 1,   RAS↓, 1,  

Migration ⓘ

TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   BBB↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 4,   p‑NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   eff↓, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

cognitive↑, 1,   cognitive∅, 1,   memory↑, 1,   neuroP↑, 2,   OS↑, 1,   Weight↓, 1,  
Total Targets: 55

Scientific Paper Hit Count for: adiP, adiponectin
4 diet Methionine-Restricted Diet
2 Alpha-Lipoic-Acid
1 diet FMD Fasting Mimicking Diet
1 diet Short Term Fasting
1 Vitamin B5,Pantothenic Acid
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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