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BiologyHuman Physiology
Match the digestive enzymes with their substrates:
A. Pepsin → I. Starch
B. Lipase → II. Triglycerides
C. Amylase → III. Dipeptides
D. Dipeptidase → IV. Proteins
Options
1
A-IV, B-II, C-I, D-III
2
A-I, B-III, C-II, D-IV
3
A-III, B-I, C-IV, D-II
4
A-II, B-IV, C-III, D-I
Correct Answer
A-IV, B-II, C-I, D-III
Solution
1

A. Pepsin: gastric enzyme, digests proteins = IV

B. Lipase: digests triglycerides (fats) = II

2

C. Amylase: digests starch = I

D. Dipeptidase: digests dipeptides = III

Answer: A-IV, B-II, C-I, D-III

Pepsin=proteins | Lipase=triglycerides | Amylase=starch | Dipeptidase=dipeptides
Theory: Human Physiology
1. Overview of Digestion

Digestion: breaking down large food molecules into absorbable units. Mechanical digestion: chewing, peristalsis. Chemical digestion: enzymes. Digestive system: mouth, esophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine (cecum, colon, rectum), accessory organs (liver, pancreas, gallbladder). Key principle: each enzyme is specific to substrate, requires optimal pH and temperature.

2. Salivary Digestion

Saliva: secreted by parotid, submandibular, sublingual glands. Composition: water (99%), mucin (lubrication), salivary amylase (ptyalin), lingual lipase, lysozyme (antibacterial), IgA, bicarbonate (pH 6.8-7.4). Salivary amylase: digests starch to maltose and dextrins. Inactivated by stomach acid. Lingual lipase: minor fat digestion, survives stomach acid better. Mucin: glycoprotein, lubricates food bolus.

3. Gastric Digestion

Stomach: HCl secreted by parietal cells (pH 1.5-2.0). Pepsinogen (from chief cells) activated by HCl to pepsin. Pepsin: endopeptidase, cleaves proteins at aromatic amino acids (Phe, Tyr, Trp). Optimum pH 1.5-2.5. Gastric lipase: minor lipid digestion. Mucus (from goblet cells): protects stomach lining. Intrinsic factor (from parietal cells): binds vitamin B12 for ileal absorption. Gastrin (G cells): stimulates HCl secretion. Peristalsis churns food + acid = chyme. Pyloric sphincter: regulates chyme entry into duodenum.

4. Pancreatic Enzymes

Pancreatic juice: secreted into duodenum via pancreatic duct. pH 7.5-8.8 (bicarbonate neutralises stomach acid). Proteases (secreted as zymogens): Trypsinogen → trypsin (activated by enterokinase/enteropeptidase). Trypsin activates other zymogens. Chymotrypsinogen → chymotrypsin. Proelastase → elastase. Procarboxypeptidase A and B → carboxypeptidase A and B. Pancreatic amylase: continues starch digestion. Pancreatic lipase: major fat-digesting enzyme. Requires bile salts + colipase. Phospholipase A2: digests phospholipids. RNase and DNase: digest nucleic acids.

5. Intestinal Enzymes (Brush Border)

Brush border enzymes of small intestinal epithelium (enterocytes): Disaccharidases: maltase (maltose → 2 glucose), sucrase (sucrose → glucose + fructose), lactase (lactose → glucose + galactose). Lactase deficiency: lactose intolerance (bloating, diarrhoea - common in adults, esp. Asian and African populations). Peptidases: aminopeptidase (N-terminal amino acids from oligopeptides), dipeptidase (dipeptides → amino acids), enterokinase/enteropeptidase (activates trypsinogen → trypsin). Alkaline phosphatase. Intestinal lipase. Final products: monosaccharides (glucose, fructose, galactose), amino acids, fatty acids + glycerol, nucleotides.

6. Absorption in Small Intestine

Glucose and galactose: Na+-glucose co-transporter (SGLT1) on apical membrane (secondary active transport). GLUT2 on basolateral membrane (facilitated diffusion). Fructose: GLUT5 on apical membrane (facilitated diffusion). Amino acids: Na+-amino acid co-transporters (several types). Di/tripeptides: PepT1 transporter. Fatty acids + glycerol: enter enterocytes by simple diffusion. Re-esterified to triglycerides. Packaged into chylomicrons with cholesterol and phospholipids (apolipoprotein coating). Secreted into lacteals (lymph capillaries) → lymph → thoracic duct → blood. Water-soluble vitamins (C, B): active transport. Fat-soluble vitamins (A, D, E, K): absorbed with fat into chylomicrons. Iron: Fe2+ absorbed by DMT1 (divalent metal transporter). Vitamin B12: bound to intrinsic factor, absorbed in ileum.

7. Liver Functions

Liver: largest gland. Functions: Bile production: ~600-1000 mL/day. Bile contains bile salts (cholate, deoxycholate), bilirubin (haem breakdown product), phospholipids, cholesterol. Bile salts emulsify fat for lipase. No digestive enzymes in bile. Metabolism: glucose homeostasis (glycogenesis, glycogenolysis, gluconeogenesis). Lipid metabolism (VLDL synthesis, fatty acid oxidation). Protein metabolism (albumin, clotting factors, urea cycle). Detoxification: cytochrome P450 enzymes metabolise drugs, alcohol, toxins. Kupffer cells: phagocytose bacteria and cell debris. Storage: glycogen, iron (ferritin), fat-soluble vitamins A, D, K, B12. Clotting factors: all (except factor VIII) synthesised by liver. Requires vitamin K for factors II, VII, IX, X. Bilirubin conjugation: unconjugated + glucuronic acid → conjugated bilirubin → excreted in bile.

8. Large Intestine

Large intestine: 1.5 m long. Parts: cecum (appendix attached), ascending colon, transverse colon, descending colon, sigmoid colon, rectum, anus. Functions: Water absorption: ~90% of remaining water reabsorbed. Electrolyte absorption: Na+, K+, Cl-, HCO3-. Bacterial fermentation: gut microbiome (trillions of bacteria) ferment indigestible fibre (cellulose, pectin): produce short-chain fatty acids (SCFA: butyrate, propionate, acetate). Butyrate: preferred energy source for colonocytes. Vitamin synthesis: gut bacteria synthesise vitamin K, biotin, B12 (limited absorption). Gas production: CO2, methane, hydrogen from fermentation. Defecation reflex: mass movements of colon → rectum fills → distension → urge to defecate. Internal anal sphincter: smooth muscle, involuntary. External anal sphincter: skeletal muscle, voluntary control.

Frequently Asked Questions
1. What are the zymogens and why are digestive enzymes secreted in inactive form? ⌄
Zymogens (proenzymes): inactive precursors of digestive enzymes. Examples: Pepsinogen → pepsin (by HCl, then autocatalysis). Trypsinogen → trypsin (by enterokinase in duodenum). Chymotrypsinogen → chymotrypsin (by trypsin). Proelastase → elastase (by trypsin). Procarboxypeptidase → carboxypeptidase (by trypsin). Why inactive precursors? If proteases were secreted in active form, they would digest the cells that made them! Autodigestion would destroy the pancreas (as happens in acute pancreatitis when zymogens are prematurely activated inside the pancreas - medical emergency). Safety mechanism: zymogens only activate in the correct location (stomach, duodenum). The pancreas is protected by: trypsin inhibitor proteins in pancreatic juice (suppress any prematurely activated trypsin), alkaline mucus coating. Acute pancreatitis: blockage of pancreatic duct or alcohol abuse causes premature zymogen activation inside pancreas → pancreatic self-digestion → severe abdominal pain, potentially fatal.
2. How is fat digested and why are bile salts needed? ⌄
Fat digestion challenges: fat is hydrophobic, cannot mix with watery digestive fluids. Lipase is water-soluble but fat is not. Solution: emulsification by bile salts. Bile salts (cholate, deoxycholate): amphipathic molecules (hydrophilic + hydrophobic portions). In small intestine: surround fat droplets → break large droplets into tiny micelles (emulsification). Dramatically increases surface area available for lipase. Pancreatic lipase: requires colipase (protein co-factor that anchors lipase to fat-water interface). Digests triglycerides → 2 fatty acids + monoglyceride. Products: free fatty acids + monoglycerides + lysolecithin enter mixed micelles with bile salts. Micelles carry lipid products to brush border of enterocytes. Lipids diffuse from micelles into enterocytes. Bile salts recycled: reabsorbed in ileum → enterohepatic circulation → back to liver. ~95% of bile salts recycled (only ~5% lost in faeces). Malabsorption syndromes: bile salt deficiency (liver disease, ileal disease) causes fat malabsorption → steatorrhoea (fatty, foul-smelling stools).
3. What is the role of the pancreas in digestion? ⌄
Exocrine pancreas (99% of pancreatic tissue): secretes pancreatic juice into duodenum. Acinar cells: synthesise and secrete digestive enzymes (zymogens). Ductal cells: secrete bicarbonate-rich fluid. Triggers for pancreatic secretion: Secretin: released by S cells in duodenum when acid chyme enters. Stimulates ductal cells to secrete bicarbonate. Neutralises stomach acid. CCK (cholecystokinin): released by I cells in duodenum when fat and protein enter. Stimulates acinar cells to release enzymes. Also causes gallbladder contraction (releases bile). Acetylcholine: vagal stimulation during cephalic phase. Pancreatic juice composition: ~1.5 L/day. pH 7.5-8.8 (bicarbonate neutralises stomach acid pH 1.5-2 in duodenum to safe ~pH 6-7 for enzyme activity). Contains: all major digestive enzymes (proteases, lipases, amylase, nucleases). Endocrine pancreas (islets of Langerhans, 1%): insulin (beta cells), glucagon (alpha cells), somatostatin (delta cells).
4. Describe the absorption of carbohydrates in the small intestine? ⌄
Final products of carbohydrate digestion: monosaccharides (glucose, galactose, fructose). All absorption occurs in small intestine, mainly jejunum. Glucose and galactose: absorbed by SGLT1 (sodium-glucose linked transporter 1) on brush border (apical membrane). Na+ enters with glucose (symport, secondary active transport - Na+ gradient maintained by Na+/K+ ATPase). Glucose exits enterocyte basolaterally via GLUT2 (facilitated diffusion into capillary). Fructose: GLUT5 on apical membrane (facilitated diffusion). GLUT2 on basolateral membrane. Slower absorption than glucose/galactose. Absorbed monosaccharides → portal vein → liver → blood glucose. GLUT2 also acts as glucose sensor (triggers insulin secretion when glucose rises in portal blood). Brush border disaccharidases complete digestion: maltase splits maltose, sucrase splits sucrose, lactase splits lactose. Lactase deficiency: lactose reaches colon undigested → bacterial fermentation → gas, bloating, osmotic diarrhoea. Prevalent in adults (70% of world population). Most common in East Asian and African populations.
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