What is behind Fatty Liver (NAFLD)
The cell's master energy sensor — when fuel runs low it ignites fat-burning, glucose uptake and mitochondrial renewal while standing down growth. Evidence A — Human trial evidence.
Fatty-acid synthesis — the de-novo line that converts surplus carbohydrate into stored fat and liver triglyceride. Evidence A — Human trial evidence.
The mitochondrial pathway that dismantles fatty acids into cellular energy — the engine that empties stored and circulating fat. Evidence A — Human trial evidence.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
Glutathione — the body's main built-in antioxidant, made inside cells throughout the body (liver, eyes, lungs, immune cells and more) to neutralize harmful oxidants and help clear toxins. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
The intestinal barrier — the selective wall that admits nutrients, excludes toxins and anchors the gut–brain and immune dialogue.
Hepatic steatosis — the accumulation of fat in the liver, the first step of metabolic liver disease. Evidence A — Human trial evidence.
Bile acids acting through the FXR and TGR5 receptors — not merely emulsifiers but hormones. Evidence A — Human trial evidence.
The cell's quality-control system for newly made proteins — and what happens when the backlog becomes permanent. Evidence B — Preclinical.
An adipose-derived hormone that sharpens insulin sensitivity and steers fat toward burning rather than storage. Evidence A — Human trial evidence.
TGF-β / Smad signaling — the builder that lays down collagen and directs repair, and the same hand that, overused, drives fibrosis. Evidence B — Preclinical.
Evidence on these pathways
AMPK → Insulin Sensitivity. “In model systems, sustained decreases in AMPK activity accompany IR, whereas AMPK activation increases insulin sensitivity.” — AMPK, insulin resistance, and the metabolic syndrome. The Journal of Clinical Investigation, 2013, volume 123, issue 7, pages 2764-2772. doi:10.1172/JCI67227
Intestinal Barrier → Ammonia. “This weakens the paracellular seal of the intestinal epithelium, enabling microbial products such as endotoxins, ammonia, and even whole microorganisms to translocate into the portal circulation.” — How the gut-liver axis shapes hepatic encephalopathy: mechanistic and therapeutic perspectives. Exploration of Digestive Diseases 2025;4:100597. doi:10.37349/edd.2025.100597 (no PMID exists — the journal is not MEDLINE-indexed; absence confirmed on file, not derived)
Intestinal Barrier → Oxygen-Carrying Capacity. “The two main causes are the villous atrophy of the mucosa at the site of iron absorption (the duodenum) and the resulting inflammation, which triggers the mechanism that leads to the anemia of chronic disease.” — Persistent Iron Deficiency Anemia in Patients with Celiac Disease Despite a Gluten-Free Diet. Nutrients, 2020, 12(8), 2176. doi:10.3390/nu12082176
Intestinal Barrier → Micronutrient Status. “Micronutrient deficits, such as those in zinc and iron, can be caused by intestinal permeability and gut inflammation brought on by environmental enteric dysfunction.” — Environmental Enteropathy and Anaemia Status Among Under-Five Children, in Slum Areas of Jimma Town, Ethiopia. Pediatric Health, Medicine and Therapeutics, 2023, vol 14, 33-43. doi:10.2147/PHMT.S387747
Formulas that act on these pathways
Acts on 9 of these pathways: AMPK, Fatty-Acid Synthesis, Nrf2, Glutathione, NF-κB, Intestinal Barrier, Hepatic Steatosis, Bile Acid Signaling, ER Stress / Unfolded Protein Response.
Acts on 9 of these pathways: AMPK, Fatty-Acid Synthesis, Nrf2, Glutathione, NF-κB, Intestinal Barrier, Hepatic Steatosis, ER Stress / Unfolded Protein Response, Adiponectin.
Acts on 8 of these pathways: AMPK, Fatty-Acid β-Oxidation, Nrf2, Glutathione, NF-κB, Hepatic Steatosis, Bile Acid Signaling, ER Stress / Unfolded Protein Response.
Acts on 7 of these pathways: AMPK, Nrf2, Glutathione, NF-κB, Intestinal Barrier, Hepatic Steatosis, TGF-β / Smad.
Acts on 7 of these pathways: AMPK, Nrf2, Glutathione, NF-κB, Intestinal Barrier, ER Stress / Unfolded Protein Response, Adiponectin.
Acts on 6 of these pathways: AMPK, Nrf2, Glutathione, NF-κB, Intestinal Barrier, Adiponectin.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Fatty Liver (NAFLD). A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.