diet FMD Fasting Mimicking Diet / PFK1 Cancer Research Results

dietFMD, diet FMD Fasting Mimicking Diet: Click to Expand ⟱
Features:
5-day diet to mimic fasting without fasting.
FMDs are caloric-restricted plant–based diets containing low proteins, low sugar and high fats which represent a more feasible and safer option to water-only fasting.
Fasting modality                         Approx CRIS
--------------------------------------   ----------
Time-restricted eating (12–16 h)          –3 to –4
Early time-restricted eating (eTRE)        –4
Intermittent fasting (24 h 1–2x/week)     –4
Periodic fasting / FMD                    –4 to –5*
Calorie restriction (chronic)             –3 (risk tradeoffs)

Compare STF(short term Fasting) to FMD
IGF-1 / insulin suppression (core driver)
| Aspect            | STF                 | FMD      |
| ----------------- | ------------------- | -------- |
| Depth             | **Very deep**       | Moderate |
| Speed             | **Rapid (24–48 h)** | Gradual  |
| Tumor stress      | **High**            | Medium   |
| Normal protection | High                | High     |
Fasting-Mimicking Diet (FMD; ~5-day low-protein, low-calorie cycle) Cancer vs Normal Cell Effects
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Insulin / IGF-1 signaling ↓ IGF-1 signaling (chronic stress) ↓ IGF-1 with regenerative priming Driver Sustained growth factor suppression Repeated IGF-1 lowering impairs tumor growth programs
2 AMPK → mTOR nutrient sensing ↓ mTOR; ↑ AMPK (growth inhibition) ↓ mTOR; ↑ AMPK (maintenance mode) Driver Prolonged anabolic suppression More sustained but less acute than STF
3 Autophagy / mitophagy ↑ autophagy → loss of tumor robustness ↑ autophagy → rejuvenation Driver Cellular renewal vs destabilization Repeated cycles promote organelle quality control
4 Mitochondrial metabolism ↓ metabolic resilience ↑ mitochondrial fitness Secondary Energy efficiency divergence Normal cells adapt better across cycles
5 Inflammatory signaling (NF-κB / cytokines) ↓ pro-tumor inflammation ↓ systemic inflammation Secondary Anti-inflammatory milieu Inflammation reduction contributes to chemopreventive effects
6 Reactive oxygen species (ROS) ↑ ROS (secondary, context-dependent) ↓ ROS Secondary Metabolism-linked redox shift ROS effects are indirect and less pronounced than STF
7 NRF2 antioxidant response ↔ modest activation ↑ NRF2 (protective) Adaptive Stress adaptation NRF2 supports normal-cell recovery between cycles
8 Cell cycle / regeneration ↓ proliferation ↑ regeneration post-cycle Phenotypic Degrowth vs regeneration FMD uniquely promotes regeneration upon refeeding


PFK1, Phosphofructokinase-1: Click to Expand ⟱
Source:
Type:
Phosphofructokinase-1 (PFK1) is a key regulatory enzyme in glycolysis that catalyzes the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate.
– As a rate-limiting enzyme in glycolysis, PFK1 is subject to complex regulation through allosteric effectors including ATP, AMP, and fructose-2,6-bisphosphate.
• Metabolic Control:
–PFK1 activity is central to controlling the pace of glycolysis, thereby influencing energy production and intermediary metabolite supply.
– In highly proliferative cells or cells under growth conditions, increased glycolytic flux (and, by extension, PFK1 activity) supports the biosynthetic demands of cell division.

– Many tumors (including breast, colorectal, and lung cancers) have been reported to have increased PFK1 expression/activity relative to normal tissues.
– High glycolytic flux, driven partly by enhanced PFK1, supports rapid cell proliferation and survival in the nutrient/stress-challenged tumor microenvironment.

Inhibitors:(typically glycolysis is targeted more broadly)
-Citrate
-Hydrogen ions (pH) – Acidic conditions can have inhibitory effects.
-3PO: inhibits PFKFB3, thereby indirectly reducing PFK1 activity.
-Resveratrol can downregulate glycolytic flux in cancer cells, which may indirectly affect PFK1 activity.
- FMDs offer an indirect strategy to modulate cancer metabolism by broadly reducing glycolysis. Their impact on PFK1 is likely part of a complex network of metabolic adaptations rather than a direct inhibitory effect.
Scientific Papers found: Click to Expand⟱
1861- dietFMD,  Chemo,    Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models
- in-vitro, Colon, CT26 - in-vivo, NA, NA
selectivity↑, ChemoSen↑, BG↓, AminoA↓, Warburg↓, OCR↑, ATP↓, ROS↑, Apoptosis↑, GlucoseCon↓, PI3K↓, PTEN↑, GLUT1↓, GLUT2↓, HK2↓, PFK1↓, PKA↓, ATP:AMP↓, Glycolysis↓, lactateProd↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

AminoA↓, 1,   ATP:AMP↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PFK1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

PKA↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PFK1, Phosphofructokinase-1
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#:79  Target#:988  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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