The functions of liver in human body are given below:

1. Carbohydrate Metabolism

• Storage of glycogen: Excess glucose in the body is converted by the liver into glycogen, and the liver stores this glycogen. Normally, the liver contains about 5–6% glycogen. By converting glucose to glycogen, the liver prevents the occurrence of hyperglycemia after a carbohydrate meal, which could result in glucosuria. (This acts like a “glucose buffer” after meals.)
• Conversion of glycogen to glucose: When blood glucose levels fall during prolonged fasting, the liver converts stored glycogen back into glucose to maintain normal blood glucose levels. (This helps prevent hypoglycemia between meals.)
• Gluconeogenesis (formation of glucose from non-carbohydrate compounds, e.g., lactic acid and amino acids): When glycogen stores are depleted, the liver performs gluconeogenesis, during which it forms glucose from non-carbohydrate precursors such as lactate, glycerol, and amino acids. (Important during long fasting or starvation.)
• Conversion of monosaccharides, e.g., fructose and galactose to glucose. (So that all sugars can enter normal glucose metabolism.)
• Regulation of blood glucose by hormonal control: The liver responds to insulin (promotes glycogenesis) and glucagon (promotes glycogenolysis and gluconeogenesis), thereby maintaining glucose homeostasis. (Acts as a central “glucose control organ”.)
• The removal of the liver results in severe hypoglycemia (not hyperglycemia), and death occurs within a short time due to failure of metabolic homeostasis. (Because glucose cannot be maintained.)

2. Protein Metabolism

• Formation of plasma proteins such as albumin (the liver is the only site of synthesis of albumin), alpha and beta globulins, and many clotting factors including fibrinogen, prothrombin, and factors V, VII, IX, and X. (These are essential for fluid balance and clotting.)
• Deamination of amino acids (breakdown of amino acids with removal of amino groups). (Helps remove excess nitrogen.)
• Formation of urea: Ammonia produced from amino acid metabolism and intestinal bacterial action (putrefaction) is transported via the portal circulation to the liver, where it is converted into urea via the urea cycle. This is an important detoxification function of the liver. (Prevents ammonia toxicity in blood.)
• Transamination, transpeptidation, etc. (Amino acid interconversion for protein synthesis.)
• Synthesis of transport and acute-phase proteins such as transferrin, ceruloplasmin, C-reactive protein, and complement proteins. (Important in immunity and inflammation.)

3. Fat Metabolism

• Formation of ketone bodies: The liver produces ketone bodies; however, it does not utilize them (extrahepatic tissues utilize them). (Used by brain and muscles during fasting.)
• Formation of lipoproteins. (For fat transport in blood.)
• Synthesis and regulation of plasma lipid transport (VLDL assembly and secretion). (Helps distribute triglycerides.)
• Synthesis of cholesterol and its esters; cholesterol is also excreted in bile. (Important for membranes and hormones.)
• Conversion of cholesterol into bile acids (primary step in bile acid synthesis). (First step in fat digestion system.)
• Formation of phospholipids such as lecithins and cephalins. (Structural lipids of membranes.)
• Saturation, desaturation, shortening, and lengthening of fatty acids. (Fat modification for body needs.)

4. Secretion of Bile

Bile is formed continuously at a rate of about 0.5–1 mL/min (approximately 30–60 mL/hour). It is secreted from bile canaliculi into bile ducts and then into larger bile passages. (Bile flows even when not eating.)

Bile formation also plays an important role in excretion of cholesterol, bilirubin, drugs, and xenobiotics. (Acts as a waste disposal route.)

5. Metabolism of Bile Pigments

Bilirubin is transported to the liver bound to albumin (as unconjugated bilirubin). Hepatocytes release bilirubin from albumin and conjugate it with glucuronic acid to form bilirubin diglucuronide (conjugated bilirubin), which is water soluble and excreted in bile. (Conjugation makes bilirubin water-soluble for excretion.)

In the intestinal lumen, urobilinogen is formed by bacterial reduction of bilirubin. About half of this is reabsorbed into portal circulation (enterohepatic circulation), returned to the liver, and re-excreted in bile. A small fraction enters systemic circulation and is excreted in urine as urobilinogen (and oxidized to urobilin). (This cycle helps recycling and pigment formation.)

In clinical physiology, serum bilirubin levels reflect hepatic conjugation and excretory capacity, and their elevation leads to jaundice. (Yellow discoloration of skin/eyes.)

6. Metabolism of Bile Salts

Bile salts are derived from cholesterol. Cholic acid and chenodeoxycholic acid are the primary bile acids. They are conjugated with glycine or taurine in hepatocytes to form bile salts (e.g., glycocholate, taurocholate). (Conjugation improves solubility.)

These conjugates are secreted into bile as sodium salts. Most bile salts are reabsorbed in the terminal ileum and returned to the liver via enterohepatic circulation. The liver synthesizes approximately 0.2–0.6 g of bile salts per day (value varies in modern texts). (They are recycled efficiently.)

Bile salts aid in digestion and absorption of fats and fat-soluble vitamins (A, D, E, and K). (Essential for vitamin absorption.)

They also play a key role in emulsification of dietary fats and formation of micelles, which is essential for lipid absorption. (Micelles help fat digestion in intestine.)

7. Formation of Blood Cells

In intrauterine life, the liver is a major site of hematopoiesis, including red blood cell formation. This function ceases at birth, but the liver may regain limited hematopoietic activity in pathological conditions (extramedullary hematopoiesis). (Seen in severe anemia or disease.)

8. Destruction of Blood Cells

Kupffer cells (hepatic macrophages) are responsible for phagocytosis of aged erythrocytes and contribute to bilirubin formation. Iron released from hemoglobin breakdown is stored in the liver as ferritin and hemosiderin. (Iron is recycled for new RBCs.)

The liver also plays a role in recycling amino acids from hemoglobin degradation. (Reuses protein components efficiently.)

9. Formation of Heparin

The liver is not a major source of heparin in the body. Heparin is primarily produced by mast cells in connective tissue and basophils. The historical association with liver is due to its early extraction source. (So liver is not the main producer.)

10. Storage Function

The liver stores important substances such as iron, and vitamins A, D, E, K, and B12. It also serves as a blood reservoir and helps regulate blood volume by accommodating fluctuations in circulatory volume. (Acts like a storage tank.)

It also stores glycogen as a rapidly mobilizable energy reserve and maintains short-term glucose availability between meals. (Quick energy backup system.)

11. Detoxification Function

Detoxification refers to biochemical processes that convert toxic substances into less toxic or more excretable forms. In many cases, toxicity is reduced rather than completely eliminated. (Main protective function of liver.)

Foreign compounds may enter the body via:

• Intestinal bacterial putrefaction products
• Drugs and food preservatives
• Environmental toxins and xenobiotics

Detoxification reactions are classified into four major types: conjugation, hydrolysis, oxidation, and reduction. (Phase I and II metabolism systems.)

1. Conjugation:

• Glucuronidation is the most common pathway. Glucuronic acid (derived from glucose via UDP-glucuronic acid) conjugates with compounds such as bilirubin, steroids, chloramphenicol, morphine, and trichloroethanol. (Major detox pathway in liver.)
• Glycine conjugation occurs with benzoic acid (forming hippuric acid), nicotinic acid, and p-aminobenzoic acid. (Helps remove aromatic acids.)
• Sulfation: Indole and skatole (from tryptophan) form indoxyl sulfate and skatoxyl sulfate. Phenol and p-cresol are also excreted as sulfate conjugates. (Important for gut-derived toxins.)
• Methylation: Examples include methylation of pyridine, catecholamines, and nicotinic acid derivatives. (Regulates hormone/inactive forms.)
• Acetylation: Sulfonamide drugs are detoxified by acetylation. (Drug metabolism pathway.)
• Glutathione conjugation: Reactive electrophilic compounds and oxidative metabolites are detoxified by conjugation with glutathione, an important protective mechanism against oxidative stress. (Key antioxidant defense system.)

2. Hydrolysis:

• Acetylsalicylic acid (aspirin) is hydrolyzed to acetic acid and salicylic acid. (Breakdown of drugs.)
• Diisopropyl fluorophosphate (DFP) and atropine undergo hydrolysis.
• Ester and amide bonds of many drugs are hydrolyzed by hepatic esterases and amidases. (Simple breakdown reactions.)

3. Reduction:

• Picric acid is reduced to picramic acid (conversion of nitro to amino group).
• Trinitrotoluene (TNT) undergoes reduction of nitro groups to amino derivatives.
• Chloral hydrate is reduced to trichloroethanol.
• Azo and nitro reduction reactions occur for certain dyes and xenobiotics under hepatic and intestinal microbial enzymes. (Often gut bacteria assist here.)

4. Oxidation:

• Oxidation of amines such as tyramine, histamine, cadaverine, and putrescine (via monoamine oxidase pathways). (Prevents toxic buildup.)
• Methanol is oxidized to formaldehyde and then formic acid, which is highly toxic and slowly eliminated. (Important clinical toxicity pathway.)
• Meprobamate is metabolized by oxidation to hydroxymeprobamate.
• Sulfur-containing amino acids (methionine and cysteine) are oxidized to sulfates for urinary excretion.
• Phase I oxidation reactions are mainly mediated by cytochrome P450 enzyme system in hepatocytes. (Main drug-metabolizing enzyme system.)