Hepatocyte membrane glucose transporter 2, GLUT2, transports glucose Keep intrahepatic cellular glucose concentration consistent with blood glucose concentration

Specific hexokinase isoenzyme IV, glucokinase Not inhibited by the product glucose-6-phosphate group, it is synthesized into liver glycogen for storage When blood sugar is high, it can also be converted into fat and used as very low-density lipoprotein VLDL is transported outside the liver

Glucose-6-phosphatase (not found in muscle tissue), liver glycogen → glucose-6-phosphate →glucose→blood sugar↑

Complete gluconeogenesis enzyme system, fasting for 12-18 hours Glucogenic amino acids, lactic acid, glycerol → glucose

Pentose phosphate pathway, provides NADPH Glucose → (Uronic acid pathway) UDP-glucuronic acid (UDPGA)

Endogenous triglyceride synthesis When full, liver, glucose and certain amino acids → acetyl CoA → fatty acids → triglycerides Exogenous fatty acids in the digestive tract are partially β-oxidized and partially synthesized into triglycerides. Endogenous TG and exogenous cholesterol and phospholipids synthesized in the liver →VLDL→extrahepatic tissue uptake and utilization.

During hunger, fat mobilization → fatty acids and glycerol → hepatic metabolism FA→β-oxidation→acetyl CoA→triccarboxylic acid cycle→oxidation energy supply FA is mostly → ketone bodies → oxidatively utilized by the brain and muscles. Brain energy supply (60-70%)

Regulate cholesterol metabolism balance

The liver synthesizes 90% of plasma proteins In addition to gamma globulin, albumin, prothrombin, fibrinogen, Ceruloplasmin, coagulation factor I II V VI IX

Various apolipoproteins: apoA B C E, some lipoprotein metabolic enzymes

In liver damage, prolonged clotting time and bleeding tendencies occur.

Plasma albumin is almost always synthesized by liver parenchymal cells Role: As a non-specific transport carrier of fat-soluble substances (FC, bilirubin) Maintain plasma osmotic pressure,

Alpha-fetoprotein, present in embryonic stage, inhibited after birth, important tumor marker for primary liver cancer

Important organ for the decomposition and transformation of amino acids except branched chain amino acids (leucine, isoleucine, valerian) Transamination, deamination, decarboxylation, transmethylation. ALT in the liver is helpful in the diagnosis of liver disease

Detoxify ammonia, ornithine cycle, ammonia → urea. Carbamoyl phosphate synthase I CPS-I, ornithine carbamoyltransferase OCT

Amine conversion: hepatic monoamine oxidase decarboxylates the aromatic amino acids phenylalanine and tyrosine into phenylethylamine and tyramine for oxidative elimination In case of severe liver disease → phenylethanolamine and octamine, similar to catecholamines, are abnormally suppressed. Hepatic encephalopathy.

The monooxygenase system is the most important enzyme for oxidizing xenobiotics Cytochrome P450, NADPH-cytochrome P450 reductase (Flavase with FAD as prosthetic group) RH+O2+NADPH+H+→ROH+NADP+➕H2O Increase water solubility, VD3 hydroxylation, bile acid and steroid hormone synthesis process hydroxylation Moldy grains and peanuts contain aflatoxin B1, → aflatoxin 2,3 epoxide, combined with guanine →DNA mutation→primary liver cancer.

2. Oxidation of aliphatic and aromatic amines Monoplus oxidase MAO in hepatocyte mitochondria Flavoenzymes Catalysis → Aliphatic and aromatic amines (Histamine, Tyramine, Tryptamine, Cadaverine, Putrescine) Serotonin, catecholamine oxidative deamination → aldehyde →Aldehyde dehydrogenase→Acid (inactivated) RCH2NH2+O2+H2O→RCHO+NH3+H2O2 RCHO＋NAD＋➕H2O→RCOOH＋NADH+H＋

3. Alcohol dehydrogenase (NAD+ is a coenzyme, ADH) and aldehyde dehydrogenase ALDH, ethanol → acetic acid RCH2OH+NAD+→Enzyme-RCHO+NADH+H+ RCHO＋NAD＋➕H2O→RCOOH＋NADH+H＋ A 70Kg adult metabolizes 7-14g ethanol per hour, chronic ethanol poisoning from long-term drinking → hepatic microsomal ethanol oxidation system MEOS (functions with high ethanol content in blood) → consumption of O and NADPH can also catalyze lipid peroxidation to produce hydroxyethyl free radicals, Promote lipid peroxidation → oxidative damage to cells. The ALDH gene has normal homozygous, inactive homozygous and heterozygous types of both. On 45.10.45, this gene mutated and some ALDH activity was low. After drinking alcohol, the person's blood vessels expanded, his face flushed, his heart beat too fast, and his pulse accelerated. At the same time, ethanol oxidation leads to an increase in the NADH/NAD+ ratio in the cytoplasm of the liver, reducing pyruvate to lactate. Severe alcoholism → accumulation of ethanol, lactic acid, → acidosis and electrolyte balance disorders, blocked gluconeogenesis → hypoglycemia.

Nitro compounds: food preservatives, industrial reagents Azo compounds: food pigments, cosmetics, textile and printing industries (possible former carcinogens) Under the catalysis of liver microsomal nitroreductase and azoreductase, NADH or NADPH is used as a hydrogen donor carrier to reduce to amines. Then monooxygenase generates acid. Bailangduoxi → dapsamide with antibacterial activity.

Liver microsomes and cytoplasm contain a variety of hydrolases: esterase, amidase, glycosidase Catalyze ester bonds, amide bonds and glycosidic bonds in lipids, amides and glycosides compounds respectively Reduce or eliminate biological activity. Needs further transformation. Acetylsalicylic acid → salicylic acid → (hydroxysalicylic acid) → glucuronic acid conjugation conversion reaction.

1. Glucuronic acid conjugation is the most important and common conjugation reaction Uridine diphosphate glucuronic acid UDPG➕NAD+→ (UDDPG dehydrogenase) Uridine diphosphate glucuronic acid UDPGA+NADH+H+ As an active donor of glucuronic acid, UDPGA will have multiple functions under the catalysis of liver microsomal UDP-glucuronosyltransferase UGT. The glucuronic acid group of the hydroxyl group and the dissociable carboxyl group is transferred to the hydroxyl group, amino group and carboxyl group of the alcohol, phenol, amine, and carboxylic acid compound to form The corresponding β-D-glucuronide increases polarity and is easily excreted from the body. Thousands of lipophilic endogenous and xenobiotic substances can be combined with glucuronic acid, such as bilirubin, steroid hormones, morphine, and phenobarbital drugs, and converted and excreted from the body. Glucolactone (Gantyler) treats liver diseases as a glucuronic acid preparation to increase the liver's biotransformation of converted substances.

2. Sulfuric acid binding is also a common binding reaction. Sulfate transferase SLUT, 3·adenosine phosphate 5-phosphoryl sulfate PAPS serves as the active sulfate donor. Catalyzes the transfer of sulfate groups to steroids, phenols, aromatic amines → sulfate esters. Increased water solubility facilitates excretion and promotes its inactivation. Estrone → estrone sulfate.

3. Acetylation is an important transformation reaction for some amine-containing xenobiotics

4. Glutathione binding is an important defense response of cells against electrophilic xenobiotic substances.

5. Methylation reaction is an important reaction in metabolizing endogenous substances.

6. Glycine is mainly involved in the biotransformation of carboxyl-containing xenobiotics

1. Age has a significant impact on biotransformation

2. There are obvious gender differences in some biological transformation reactions.

3. Nutritional status also affects biotransformation.

4. Disease, especially severe liver disease, can significantly affect biotransformation

5. Genetic factors can also significantly affect the activity of biotransformation enzymes.

2. A small amount of cholinogen can be reabsorbed by the intestinal mucosa and enter the enterohepatic circulation of cholinogen.

3.4-17.1um/L

1. Physiological jaundice In prehepatic jaundice, the liver has insufficient ability to synthesize UDP-glucuronosyltransferase.

1. Pathological jaundice