⚗️ Digestion, Absorption and Metabolism

This lesson builds core elective concepts in BSc Agriculture with practical applications and exam-oriented clarity.

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Digestion, Absorption and Metabolism

Digestion is the process of breaking down complex food components into absorbable units through two mechanisms:

• Mechanical digestion: mastication (chewing), churning (stomach peristalsis), segmentation (intestinal mixing)
• Chemical digestion: enzymatic hydrolysis of macromolecules into monomers

The gastrointestinal (GI) tract provides distinct pH environments: mouth (pH 6.5–7), stomach (pH 1.5–3.5), small intestine (pH 6–7.5 after duodenum), colon (pH 5.5–7).

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Carbohydrate Digestion and Absorption

Digestion Pathway

1. Mouth: salivary amylase (ptyalin) → starch and dextrin → smaller dextrins and maltose
2. Stomach: no significant CHO digestion; salivary amylase inactivated by low pH after mixing
3. Small intestine (duodenum): pancreatic amylase → dextrins, maltose, maltotriose
4. Brush border enzymes (enterocyte surface): maltase → glucose; sucrase → glucose + fructose; lactase → glucose + galactose; isomaltase → glucose (from branch points)

Final products: monosaccharides — glucose, fructose, galactose

Lactose Intolerance

Lactase deficiency → unabsorbed lactose fermented by colonic bacteria → gas (bloating, flatulence), osmotic diarrhoea. Prevalence: very high in South and East Asia (up to 90% adults); North Europeans have higher lactase persistence. Managed by consuming small amounts, lactase supplements, or fermented dairy (yoghurt — lactose pre-digested by bacteria).

Absorption Mechanisms

• Glucose and galactose: absorbed via SGLT1 (sodium-glucose linked transporter 1) — secondary active transport (Na+ co-transport) in enterocytes; exits via GLUT2 into portal blood
• Fructose: absorbed via GLUT5 (facilitated diffusion); exits via GLUT2
• Route: portal vein → liver → glucose distributed to tissues

Insulin response: rising blood glucose → pancreatic beta cells release insulin → GLUT4-mediated glucose uptake in muscle and adipose; glycogen synthesis; lipogenesis.

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Protein Digestion and Absorption

Digestion Pathway

1. Stomach: pepsinogen activated to pepsin by HCl (pH <3.5) → endopeptidase; cleaves aromatic AA bonds; produces large peptides
2. Small intestine: pancreatic endopeptidases — trypsin (cleaves Lys, Arg bonds), chymotrypsin (Phe, Tyr, Trp), elastase (Ala, Gly, Ser); activated from zymogens by enteropeptidase (trypsinogen → trypsin)
3. Pancreatic exopeptidases: carboxypeptidase A (C-terminal neutral AA), carboxypeptidase B (C-terminal basic AA)
4. Brush border peptidases: aminopeptidases, dipeptidases → free amino acids and di/tripeptides

Absorption

• Amino acid transporters: multiple Na-dependent transporters (for neutral, basic, acidic, imino AAs) in enterocyte apical membrane
• Di/tripeptides: absorbed via PepT1 transporter (H+-dependent); hydrolysed inside enterocyte
• Exit via basolateral membrane → portal vein → liver
• First-pass hepatic extraction: liver takes 50–60% of absorbed AAs for protein synthesis and gluconeogenesis
• Nitrogen balance: positive (growth, pregnancy, recovery), negative (starvation, illness, trauma), zero (healthy adult)

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Fat Digestion and Absorption

Digestion Pathway

1. Stomach: lingual lipase and gastric lipase (minor); emulsification begins with churning
2. Small intestine: bile (from liver/gallbladder) → emulsifies fat → increases surface area → micelles formed (bile salts, fatty acids, monoglycerides, fat-soluble vitamins, cholesterol)
3. Pancreatic lipase (with colipase cofactor): triglyceride → 2 fatty acids + 2-monoglyceride
4. Phospholipase A2: phospholipids → lysophospholipids + fatty acids

Absorption and Transport

• Micelles diffuse to brush border; long-chain fatty acids (LCFA) and monoglycerides enter enterocytes by diffusion
• Inside enterocyte: re-esterification to triglycerides; packaged into chylomicrons (apoB-48, phospholipid coat) with cholesterol and fat-soluble vitamins
• Chylomicrons → lymph (lacteals) → thoracic duct → bloodstream
• Short and medium-chain fatty acids (SCFA/MCFA): absorbed directly into portal vein — used for quick energy; MCT (medium-chain triglycerides) oil used in clinical nutrition
• Fat-soluble vitamins (A, D, E, K): absorbed with dietary fat; steatorrhoea (fat malabsorption) → deficiency of these vitamins

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Carbohydrate Metabolism

Glycolysis (Embden-Meyerhof-Parnas Pathway)

• Glucose (6C) → pyruvate (3C); occurs in cytoplasm; net yield = 2 ATP + 2 NADH + 2 pyruvate
• Anaerobic: pyruvate → lactate (muscle during intense exercise); regenerates NAD+
• Aerobic: pyruvate → acetyl-CoA (via pyruvate dehydrogenase; requires B1, B2, B3, B5, lipoate)

TCA Cycle (Krebs Cycle / Citric Acid Cycle)

• Acetyl-CoA (2C) + oxaloacetate → citrate cycle in mitochondria
• Per acetyl-CoA: 3 NADH + 1 FADH2 + 1 GTP + 2 CO2
• Requires coenzymes from B vitamins: thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5)

Oxidative Phosphorylation (Electron Transport Chain)

• NADH and FADH2 donate electrons to ETC on inner mitochondrial membrane
• O2 is final electron acceptor → H2O
• ATP synthase (chemiosmosis): ~30–32 ATP per glucose (aerobic complete oxidation)

Gluconeogenesis

• Synthesis of glucose from non-carbohydrate precursors; primarily in liver (also kidney)
• Substrates: amino acids (glucogenic AA — all except Leu, Lys), glycerol (from fat catabolism), lactate (Cori cycle), propionate
• Activated during fasting, starvation, prolonged exercise

Glycogen Metabolism

• Glycogenesis: glucose → glycogen (liver and muscle); insulin stimulates
• Glycogenolysis: glycogen → glucose-1-phosphate → glucose; glucagon and adrenaline stimulate
• Liver glycogen (~100 g): maintains blood glucose during fasting (depleted in 12–18 hours)
• Muscle glycogen (~400 g): fuels muscle contraction; cannot directly raise blood glucose

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Fat Metabolism

Beta-Oxidation of Fatty Acids

• Fatty acids activated to acyl-CoA (cytoplasm) → transported into mitochondria via carnitine shuttle
• Sequential removal of 2-carbon units as acetyl-CoA; generates NADH + FADH2
• Palmitic acid (C16): 8 acetyl-CoA + 7 FADH2 + 7 NADH = 129 ATP net
• Ketogenesis: during starvation/uncontrolled diabetes, excess acetyl-CoA → ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) in liver; used by brain and heart

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Protein Metabolism

Catabolism

• Transamination: amino group transferred to alpha-ketoglutarate → glutamate (requires B6/PLP as coenzyme); deamination → NH3
• Urea cycle: liver; NH3 → urea (CO(NH2)2) → excreted in urine; 2 ATP consumed per urea
• Carbon skeletons: glucogenic AAs → glucose; ketogenic AAs (Leu, Lys) → ketone bodies; most AAs are both

Metabolic Interconversions

• Excess carbohydrate → fat (de novo lipogenesis): acetyl-CoA → fatty acids → triglycerides (stored in adipose)
• Protein → glucose (gluconeogenesis): important in starvation
• Fat cannot convert to glucose in humans (no net gluconeogenesis from acetyl-CoA)

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Hormonal Control of Metabolism

Hormone	Source	Triggers	Metabolic Actions
Insulin	Pancreas (beta cells)	High blood glucose (post-meal)	Glucose uptake (GLUT4), glycogen synthesis, lipogenesis, protein synthesis — anabolic
Glucagon	Pancreas (alpha cells)	Low blood glucose (fasting)	Glycogenolysis, gluconeogenesis, lipolysis — catabolic
Cortisol	Adrenal cortex	Stress, fasting	Gluconeogenesis, protein catabolism, lipolysis
Thyroid hormones (T3/T4)	Thyroid gland	Always present	Set BMR (basal metabolic rate); protein synthesis; mitochondrial biogenesis
Adrenaline (epinephrine)	Adrenal medulla	Acute stress, exercise	Glycogenolysis, lipolysis — "fight or flight"

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Basal Metabolic Rate (BMR)

BMR = energy expenditure at complete rest (thermoneutral environment, post-absorptive state; 12-hour fast). Represents ~60–70% of total daily energy expenditure in sedentary individuals.

Factors increasing BMR: male sex, younger age, larger body size, greater muscle mass, fever, hyperthyroidism, cold climate.

Harris-Benedict equation (revised 1984):

• Men: BMR = 88.36 + (13.40 × weight kg) + (4.80 × height cm) − (5.68 × age years)
• Women: BMR = 447.59 + (9.25 × weight kg) + (3.10 × height cm) − (4.33 × age years)

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Digestive Enzymes — Summary Table

Enzyme	Site of Secretion	Site of Action	Substrate	Products
Salivary amylase	Salivary glands	Mouth	Starch	Dextrins, maltose
Pepsin	Stomach (chief cells)	Stomach	Proteins	Large peptides
Pancreatic amylase	Pancreas	Small intestine	Dextrins	Maltose, glucose
Pancreatic lipase	Pancreas	Small intestine	Triglycerides	Fatty acids + 2-MG
Trypsin	Pancreas (zymogen)	Small intestine	Peptides (Lys, Arg bonds)	Smaller peptides
Chymotrypsin	Pancreas (zymogen)	Small intestine	Peptides (aromatic AA bonds)	Smaller peptides
Maltase	Brush border	Small intestine	Maltose	Glucose + Glucose
Sucrase	Brush border	Small intestine	Sucrose	Glucose + Fructose
Lactase	Brush border	Small intestine	Lactose	Glucose + Galactose
Bile (not enzyme)	Liver/Gallbladder	Small intestine	Fat	Emulsification → micelles

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Summary Cheat Sheet

Topic	Key takeaway
Main focus	Digestive enzymes, absorption mechanisms, and metabolic pathways for carbohydrates, proteins, and fats including glycolysis, TCA cycle, beta-oxidation, and hormonal control.
Section context	Revise this lesson with the rest of Human Nutrition for stronger conceptual continuity.