Portal blood enters sinusoids
Absorbed water-soluble nutrients and gut-derived molecules reach hepatocytes through a fenestrated exchange bed.
DIGESTIVE / LIVER METABOLISM
The liver receives portal nutrients, buffers glucose, handles amino nitrogen, packages lipid, produces bile and transforms many endogenous molecules, medicines and toxicants. Transformation can inactivate, activate, or create reactive intermediates.
12-STAGE MAP
“Detoxification” is not one pathway and does not imply that a product can cleanse the liver. Dose, route, enzymes, transport, genetics, interactions and liver health change handling.
Absorbed water-soluble nutrients and gut-derived molecules reach hepatocytes through a fenestrated exchange bed.
Glycogen synthesis, glycolysis and reduced glucose output coordinate the fed state; fasting reverses key fluxes.
Fatty-acid oxidation, triglyceride storage, de novo synthesis and VLDL export compete according to substrate and signals.
Hepatic pathways capture ammonia and amino nitrogen for urea-cycle disposal.
Oxidation, reduction or hydrolysis—often involving CYP enzymes—can expose functional groups or form active intermediates.
Glucuronidation, sulfation, glutathione and other reactions often increase water compatibility.
Metabolites may enter bile or blood for fecal or renal elimination; some compounds recirculate.
Reactive metabolites, immune responses, mitochondrial stress and dose can produce drug-induced liver injury in susceptible people.
Alcohol dehydrogenase oxidizes ethanol, producing toxic acetaldehyde and NADH.
Aldehyde dehydrogenase oxidizes acetaldehyde and generates more NADH.
A higher NADH/NAD+ ratio alters lactate/pyruvate balance, gluconeogenesis and lipid oxidation.
Steatosis, inflammation and fibrosis are distinct, non-inevitable stages influenced by dose pattern and susceptibility.