Place · Level 3
1.5 kg · 500+ 化学反应 · 双血供 · Phase I 拆分子 + Phase II 装把手 · NAFLD 全球第一肝病 · 排毒99% 是营销
synergy · 1
Drug metabolism: liver Phase I/II metabolites are mostly renally excreted. Hepatic or renal impairment burdens the other — combined pharmacokinetics is the core risk in polypharmacy.
cofactor · 1
Glutathione only neutralises peroxides through glutathione peroxidase (GPx), whose catalytic centre is a selenocysteine — there is a selenium atom embedded in the liver's busiest detox line.
regulates · 7
The liver produces ~600 mL bile daily; gut FXR receptors feed bile-acid reabsorption signals back. In NASH, disrupted enterohepatic signaling is the key second hit.
Liver is the lipid hub: VLDL export → peripheral fat deposition; NASH patients carry 2-3× CVD risk. 'Fatty liver is not just a liver problem' has a molecular basis.
Taylor twin cycle: NAFLD (hepatic TG >5%) → VLDL output ↑ → ectopic lipid deposition in pancreatic islets → β-cell decline → T2D. DiRECT reverses in this order: hepatic TG drops 30% in week 1, normalises by week 8; pancreatic TG normalises by week 12.
Portal blood feeds liver directly → gut-microbial products (LPS, SCFA, secondary bile acids) are major hepatic metabolic + inflammatory signals. NAFLD two-hit model: hepatic fat + gut-derived LPS → NASH progression.
Chronic drinking induces CYP2E1. That route generates ROS which keeps damaging the liver, and it pushes acetaminophen toward its toxic metabolite — so a chronic drinker can reach acute liver failure on a normal dose of the painkiller.
Liver converts T4→T3, produces IGF-1 (GH downstream), and is the first site of insulin resistance — 'obesity + fatty liver + hormone dysregulation' are three chapters of one metabolic story.
Liver-resident Kupffer cells are the body's largest fixed macrophage pool — in NASH, gut-derived LPS activates Kupffer → NF-κB → inflammatory liver injury. The liver also produces CRP and acute-phase proteins amplifying systemic inflammation.
contrast · 1
Milk thistle is the commonest ingredient on the liver-pill shelf, yet the liver's own phase I/II clearance workshop already runs continuously, and pooled randomized trials show no effect on mortality or complications of liver disease.