Clears liver fat
Steatosis↓
Also searched as Steatosis.
You want it cleared: reversing liver fat restores metabolic and hepatic health.
In depth
Hepatic steatosis — the accumulation of fat in the liver, the first step of metabolic liver disease.
What drives it
Fat burning reduces it.
Hashimoto 2000, J Biol Chem 275:28918 — a defect in PPARα-inducible fatty-acid oxidation determines the severity of hepatic steatosis; robust β-oxidation clears hepatic fat.
Exports liver fat reduces it.
Hepatic VLDL-secretion study 2010 — impaired VLDL secretion (loss of microsomal triglyceride transfer protein) drives hepatic triglyceride accumulation and steatohepatitis; VLDL export protects the liver from steatosis. PMID 20392512. Human genetics settles the direction: people carrying rare variants in APOB or MTTP have VLDL secretion virtually eliminated, with a resulting increase in hepatic steatosis — and familial abetalipoproteinemia shows near-complete absence of apoB-containing lipoproteins. Export is the drain; block the drain and the liver fills. MTP is described as absolutely required for VLDL assembly. And fat blocks its own exit — A self-amplifying loop: free-fatty-acid accumulation in the liver causes chronic endoplasmic reticulum stress, ER stress increases apoB100 degradation, and losing apoB100 reduces the liver's ability to export triglyceride, worsening the steatosis that started it. Insulin does the same thing deliberately: insulin directly targets apoB100 for degradation, so hyperinsulinemia suppresses the export route. PMID 20392512
Limits fat uptake increases it.
10.2337/db07-0907 — Koonen 2007, Diabetes 56:2863 — increased hepatic CD36 raises fatty-acid uptake and triglyceride accumulation, contributing to diet-induced hepatic steatosis. The quantitative fact that reframes liver fat, and it argues against the popular story: in the liver, fatty acids derived from uptake of plasma free fatty acids released from adipose tissue account for approximately 70 to 80 percent of hepatic triglyceride synthesis. De-novo lipogenesis and the breakdown of remnant particles make up the remainder. Fatty acids from extrahepatic sources are stated to contribute substantially to hepatic steatosis. Implication: an intervention aimed only at de-novo lipogenesis is addressing the smaller share; the dominant inflow is fatty-acid delivery from adipose tissue, which is why adipose insulin resistance and weight sit upstream of liver fat. CD36 is one of several named uptake proteins (with SLC27A1 and FABP4) and is a PPAR target — this edge is the transport step, not the whole inflow. doi 10.2337/db07-0907
Alcohol metabolism increases it.
Ethanol-metabolism/FAO review 2024, Am J Physiol GI — alcohol dehydrogenase oxidizes ethanol to acetaldehyde and NADH, and the raised NADH/NAD+ ratio inhibits hepatic fatty-acid oxidation, driving alcoholic steatosis. PMC11901390
Ethanol-metabolizing enzyme increases it.
CYP2E1/NAFLD review 2011 — increased hepatic CYP2E1 generates ROS and lipid peroxidation, driving fatty-liver progression to steatohepatitis. PMID 21664213
Stops fat storage increases it.
Li 2011, Cell Metab 13:376 — SREBP-1c-driven de novo lipogenesis accumulates hepatic triglyceride; blocking it attenuates steatosis. Mouse. lipogenic gene expression did not correlate with intracellular triglyceride accumulation across AMPK activators (PMC5835560) -- the transcriptional step and the lipid outcome can dissociate. PMC5835560
Cellular cleanup reduces it.
Singh 2009, Nature 458:1131 — hepatic lipophagy degrades lipid droplets, clearing hepatic steatosis. doi 10.1038/nature07976
Insulin sensitivity reduces it.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
Fasting insulin increases it.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
Supports weight management increases it.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
Gut barrier reduces it.
Dysbiosis and increased intestinal permeability in the gut-liver axis worsen insulin resistance, leading to a vicious cycle of metabolic dysfunction. doi 10.1038/s41581-026-01066-0 · PMC11725408
Calms body-wide inflammation increases it.
heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. doi 10.1038/s41581-026-01066-0 · PMC11725408
Oxidative stress increases it.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. (doi 10.1038/s41581-026-01066-0; doi 10.3390/ijms26146962; PMC11725408; PMC11906131; PMC11764088; PMC12257864). Verbatim: “It is widely accepted that the excessive production of mitochondrial ROS is the main cause of the initiation and progression of hepatic steatosis”. doi 10.1038/s41581-026-01066-0 · PMID 36670871 · PMC11725408
Fatty-acid oxidation reduces it.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
What it drives
It reduces Kidney.
MAFLD requires hepatic steatosis combined with obesity, T2D OR other metabolic dysregulation, all of which significantly elevate the risk of chronic kidney disease. Scale: MAFLD affects approximately 1.27 billion people worldwide, 48.35 million incident cases, 3.67 million DALYs, risen more than 60 percent since 1990. doi 10.1038/s41581-026-01066-0 · PMC11725408
It increases PCOS.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
It reduces Liver.
Named across six gut-liver axis reviews. The main alteration is dysbiosis - A decrease in beneficial bacteria, an increase in potentially harmful microbes, and a loss of overall microbial diversity - with intestinal barrier integrity determining the levels of microbial metabolites, ENDOTOXINS and ammonia that reach the liver and systemic circulation. doi 10.1038/s41522-022-00352-6 · PMC11265038
It reduces Alcohol recovery.
Drawn from reviews of neighboring outcomes rather than from studies of this outcome itself, which is weaker evidence, and the map marks it so. Sources: PMC10132248; doi 10.1016/j.jhep.2023.03.017; PMC12673670. doi 10.1016/j.jhep.2023.03.017 · PMC10132248
It reduces Gut barrier.
dysbiosis and increased intestinal permeability in the gut-liver axis form a vicious cycle with hepatic steatosis. doi 10.1038/s41581-026-01066-0 · PMC11725408
It increases Galectin-3.
The metabolic trigger. Galectin-3 transcription is induced in hepatocytes 'by treatment with LPS plus free fatty acid (palmitate)' - endotoxin plus saturated fat - and that induction was suppressed by BRG1 depletion and abolished by TET1 silencing (PMC6901944). Separately, 'galectin-3 levels are up-regulated in the liver by a host of different injurious stimuli'. This link connects steatosis, lipogenesis, gut and insulin signaling to galectin-3. PMC6901944
It increases Liver inflammation.
10.3390/ijms15069924 — the stage boundary, stated by the trial that defined the field's endpoint. PIVENS design (S1551714408001146): 'Before and post-treatment liver biopsies ARE read centrally in a masked fashion for an assessment of steatohepatitis and a NAFLD activity score (NAS) consisting of steatosis, LOBULAR inflammation, and hepatocyte ballooning.' Steatosis is one of three components; NASH is the composite. The progression is not obligatory. The Mexican Ministry of Health guideline states, in Spanish, 'Esteatosis y hepatitis representan grados variables de lesión, PERO NO son REQUISITOS para EL DESARROLLO DE CIRROSIS.' The stages overlap rather than queue. doi 10.3390/ijms15069924
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.