Gastrointestinal (GI) physiology encompasses motility, secretion, breakdown of

nutrients, absorption, and their regulation through hormonal and neural factors. Key
processes include swallowing, peristalsis, segmentation, and absorption, with regulatory
mechanisms involving enteric, autonomic, and hormonal controls.

1. Motility
A. Swallowing (Deglutition)

1. Phases:
o Oral Phase: Voluntary; involves forming a food bolus and pushing it into the
pharynx.
o Pharyngeal Phase: Involuntary; regulated by cranial nerves IX
(Glossopharyngeal) and X (Vagus). Breathing stops to prioritize swallowing.
o Esophageal Phase: Involuntary; involves peristalsis to move the bolus toward the
stomach.
2. Lower Esophageal Sphincter (LES):
o Open: Relaxed by vagal inhibitory fibers (VIP), nitric oxide.
o Closed: Maintained by acetylcholine and Substance P to prevent reflux of
stomach contents.

B. Peristalsis

1. Mechanism:
o Proximal Circular Muscles: Contract to push food forward.
o Distal Circular Muscles: Relax to allow passage.
o Longitudinal Muscles: Contract to shorten the canal.
2. Regulation:
o Hormonal: Motilin increases contractions.
o Neural: Parasympathetic system and enteric nervous system (ENS) via
acetylcholine and VIP.

C. Segmentation

1. Purpose: Mix and mechanically break down food, not move it.
2. Mechanism:
o Contraction of muscles in adjacent segments.
o Enhanced mixing with digestive secretions.
3. Regulation:
 o ENS and parasympathetic system play critical roles.

D. Stomach Motility

1. Churning:
o Oblique muscular layer mixes food with gastric juices, converting bolus into
chyme.
2. Pyloric Movements:
o Peristalsis moves chyme to the duodenum.
o Retropulsion: Reverse movement for further breakdown if particles are too large.

E. Small and Large Intestine Motility

1. Small Intestine:
o Segmentation for mixing.
o Peristalsis moves chyme to the ileocecal valve.
2. Large Intestine:
o Haustral contractions mix contents for water/ion absorption.
o Mass movements propel feces toward the rectum.

F. Defecation Reflex

1. Intrinsic Reflex: Mediated by ENS; weakly stimulates rectal contraction.

2. Extrinsic Reflex: Parasympathetic system strengthens rectal contraction and relaxes the
internal anal sphincter.
3. Voluntary Control: External anal sphincter remains closed until voluntary relaxation
occurs.

G. Migrating Motor Complex (MMC)

 Active during fasting; clears residual material.

 Cycle lasts ~90 minutes, comprising four phases.

2. Secretion
Major Players:

1. Salivary Glands: Produce saliva for lubrication and carbohydrate digestion (amylase).
2. Gastric Glands:
o Parietal cells (HCl, intrinsic factor).
o Chief cells (pepsinogen).
o Mucous cells (protective mucus).
3. Pancreas:
o Digestive enzymes (amylase, lipase, proteases).
o Bicarbonate for neutralizing stomach acid.
4. Liver and Gallbladder: Bile production and secretion for fat emulsification.

3. Breakdown of Nutrients
A. Carbohydrates:

 Enzymes: Salivary and pancreatic amylase.

 End Products: Monosaccharides (glucose, galactose, fructose).
 Transport: Sodium-glucose linked transporter (SGLT1).

B. Proteins:

 Enzymes: Pepsin (stomach), trypsin, chymotrypsin, carboxypeptidase (pancreas).

 End Products: Amino acids, dipeptides, tripeptides.
 Transport: Sodium-dependent cotransporters.

C. Lipids:

 Enzymes: Lipase (pancreas), bile salts (liver).

 End Products: Monoglycerides and free fatty acids.
 Transport: Formation of micelles for absorption into intestinal cells.

4. Absorption
Small Intestine:

1. Carbohydrates and Proteins:

o Sodium-linked absorption into epithelial cells.
2. Lipids:
o Passive diffusion after micelle formation.
 3. Vitamins and Minerals:
o Fat-soluble vitamins (A, D, E, K) absorbed with lipids.
o Water-soluble vitamins (e.g., B12 with intrinsic factor).

Large Intestine:

 Water and electrolytes are absorbed; residual material becomes feces.

5. Regulation of GI Function
A. Neural Control:

1. Enteric Nervous System (ENS):

o Independent “gut brain” with sensory, motor, and interneurons.
2. Parasympathetic System:
o Enhances motility and secretion via vagus and pelvic nerves.

B. Hormonal Control:

1. Gastrin: Stimulates gastric acid secretion and motility.

2. Cholecystokinin (CCK): Stimulates bile secretion and pancreatic enzymes.
3. Secretin: Promotes bicarbonate secretion.
4. Motilin: Stimulates MMC during fasting.
5. Serotonin (5-HT): Stimulates gut motility.

C. Reflex Pathways:

1. Enterogastric Reflex:
o Small intestine signals stomach to slow activity.
2. Gastrocolic Reflex:
o Stomach signals colon to promote defecation.
3. Gastroileal Reflex:
o Stomach signals ileum to relax ileocecal valve.

Key Highlights
 Motility and Secretion are tightly regulated by neural and hormonal factors to ensure
efficient digestion and absorption.
 Peristalsis and Segmentation work together for movement and mixing of contents.
 Nutrient absorption depends on specific transport mechanisms, with sodium playing a
central role in carbohydrate and protein absorption.
  Reflexes coordinate activity across GI regions for optimized function.

Carbohydrate Digestion and Transport

1. Digestion Pathway:
o Begins in the mouth with salivary amylase.
o Continues and finishes in the small intestine.
o No carbohydrate digestion occurs in the stomach.
2. Transporters on the Apical (Lumenal) Side:
o SGLT1 (Sodium-Glucose Linked Transporter 1): Transports glucose and
galactose using sodium as a co-transporter.
o GLUT5: Specific for fructose transport.
3. Basolateral (Interstitial) Transport:
o GLUT2: Moves glucose, galactose, and fructose into the interstitial space for
uptake by the portal circulation.

Protein Digestion and Absorption

1. Digestion Pathway:
o Begins in the stomach with pepsin activity.
o Continues in the small intestine with pancreatic enzymes (e.g., trypsin,
chymotrypsin).
2. Absorption Mechanisms:
o PEPT1 (Peptide Transporter 1): Transports dipeptides and tripeptides.
o Sodium-Linked Transporters: Handle single amino acids.

Fat Digestion and Absorption

1. Pre-digestion:
o Bile: Emulsifies fats into smaller particles for enzymatic access.
2. Enzymatic Breakdown:
o Lipase hydrolyzes triglycerides into monoacylglycerols, free fatty acids, and
glycerol.
3. Micelle Formation:
o Contains fat-soluble vitamins (A, D, E, K), monoacylglycerols, and fatty acids.
o Micelles facilitate fat transport to the intestinal mucosa.
4. Absorption Pathways:
o Small and Medium Chain Fatty Acids: Transported via simple diffusion.
o Long Chain Fatty Acids:
 Require incorporation into chylomicrons.
 Transported into lymphatics.
Iron Absorption

1. Heme Iron:
o Absorbed via endocytosis.
2. Non-Heme Iron:
o Requires DMT1 (Divalent Metal Transporter 1) for apical uptake.
o Involves ferritin and ferroportin for intracellular processing and transport.

Copper Absorption

1. Mechanisms:
o Uses DMT1 and Copper Transporter 1 (CTR1).
o Requires metallothionein and P-type ATPase for intracellular handling.
2. Regulation:
o High zinc levels inhibit copper absorption, and vice versa.

Zinc Absorption

1. Mechanism:
o Inhibited by high copper levels.

Manganese Absorption

1. Mechanisms:
o Utilizes DMT1 and is transported in blood via alpha-2-macroglobulin or albumin.
o High calcium levels reduce manganese absorption.

Gastrointestinal Blood Flow Regulation

1. Hyperemia:
o Blood flow increases in response to food intake.

Gastrointestinal Hormones and Regulation

 1. CCK (Cholecystokinin):
o Increases pancreatic exocrine secretion and gallbladder contraction.
o Relaxes the sphincter of Oddi.
2. Secretin:
o Stimulates bicarbonate release to buffer duodenal acidity.
3. Gastrin:
o Released in response to GRP (Gastrin-Releasing Peptide).
o Stimulates parietal cells to secrete gastric acid.
4. GIP (Gastric Inhibitory Polypeptide) and GLP-1 (Glucagon-Like Peptide-1):
o Incretins that enhance insulin release post-glucose intake.
5. Ghrelin:
o Appetite stimulant acting on the hypothalamus.
o Reduced in overweight individuals.
6. Leptin:
o Satiety signal that inhibits feeding behaviors.

Neural Regulation of GI Functions

1. Parasympathetic Nervous System:

o Stimulates:
 Gastric secretion (via vagus nerve).
 Saliva secretion.
 Acid secretion from parietal cells.
o Inhibits somatostatin secretion.
2. Enteric Nervous System (ENS):
o Regulates motility and secretory activities through:
 Submucosal plexus.
 Myenteric plexus.

Saliva and Gastric Secretion

1. Saliva Composition:
o Hypotonic compared to plasma.
o Contains:
 Amylase (digestion).
 Haptocorrin, lysozyme, lactoferrin, and peroxidase (microbial control).
2. Gastric Secretion Components:
o Hydrogen Ions and Bicarbonate:
 Protect stomach lining.
o Pepsinogen:
 Converted to pepsin for protein digestion.
o Intrinsic Factor:
  Essential for vitamin B12 absorption.

Pancreatic Enzymes in Small Intestine

1. Enzymes include:
o Lipase.
o Trypsin.
o Chymotrypsin.
o Elastase.
o Carboxypeptidase.

Incretin Hormones

1. Released in response to dietary glucose.

2. Enhance insulin release from pancreatic beta cells

Gastrointestinal Motility

Deglutition (Swallowing)

Deglutition involves a combination of voluntary and involuntary processes requiring

coordination among 30 muscles and multiple cranial nerves.

Phases of Deglutition

1. Oral Phase (Voluntary)

o Mastication: Tongue prepares the food bolus for swallowing.
 Muscles of mastication are innervated by the mandibular branch of CN V.
o Tongue Action:
 Mylohyoid: Presses tongue against the hard palate.
 Hyoglossus & Styloglossus: Load the bolus into the oropharynx.
2. Pharyngeal Phase (Involuntary)
o Soft Palate Elevation:
 Tensor Palatini & Levator Palatini: Seal off the nasopharynx.
o Larynx Elevation:
 Stylopharyngeus, Palatopharyngeus, Salpingopharyngeus: Elevate the
larynx and close vocal cords.
o Upper Esophageal Sphincter (UES): Relaxes to receive the bolus.
o Cranial Nerves: IX (Glossopharyngeal) and X (Vagus) are involved.
3. Esophageal Phase (Involuntary)
 o Peristalsis: Movement of bolus by smooth muscle contraction under control of
the ENS (Enteric Nervous System).
 ENS Plexuses:
 Myenteric (Auerbach) and Submucosal (Meissner) plexuses
coordinate contractions.
o Bolus Movement:
 Stretch & Chemical Stimuli: Activate ENS to guide smooth muscle
activity.
 At the Lower Esophageal Sphincter (LES): Intraluminal pressure
overcomes LES resistance, allowing bolus entry into the stomach.

Lower Esophageal Sphincter (LES)

 Dual Control Systems: Inhibitory and excitatory mechanisms regulate the LES:
o Relaxation:
 Mediators: Vagal Inhibitory Fibers (VIFs), VIP, and Nitric Oxide.
 Occurs during swallowing.
o Contraction:
 Mediators: Vagal Excitatory Fibers (VEFs), Acetylcholine (ACh),
and Substance P.
 Maintains constant tone when not swallowing.
 Absence of inhibitory signals results in continuous contraction of the LES.

Peristalsis

Peristalsis propels contents through the GI tract, involving muscle contractions coordinated by
stretch, hormonal, and nervous stimuli.

Mechanisms

1. Stretch Response:
o Stretch Activation: Food stretches the gut, triggering smooth muscle contraction
via gap junctions.
o Depolarization Wave: Propagates signal to neighboring cells.
2. Hormonal Stimulation:
o Motilin (from M cells in the small intestine): Increases contractile waves.
3. Nervous Stimulation:
o Parasympathetic NS (PNS): ACh stimulates smooth muscle contraction (via M1
and M3 agonists).
o VIP: Induces smooth muscle relaxation.
4. Contraction and Relaxation Coordination:
o Above Bolus: Circular muscle contracts (via ACh and Substance P).
 o Below Bolus: Circular muscle relaxes (via VIP, Nitric Oxide, and ATP).
o Longitudinal Muscle: Contracts (via ACh and Substance P) to shorten the tube
for propulsion.

Segmentation

 Localized Circular Contractions:

o Form segments to move contents both forward and backward.
o Aids in mixing digestive enzymes, acids, and food for absorption.
 Unlike peristalsis, segmentation does not produce net forward movement.

Intrinsic vs Extrinsic Control

1. Intrinsic System:
o Controlled by the ENS (myenteric and submucosal plexuses).
o Excitatory signals: ACh and Substance P.
o Inhibitory signals: VIP, Nitric Oxide.
2. Extrinsic System:
o Sympathetic NS: Inhibits via prevertebral ganglia and ENS.
o Parasympathetic NS (via CN X): Stimulates via ACh.

Role of Calcium in Smooth Muscle Contraction

 Ca2+ Influx: Essential for muscle contraction in smooth muscle.

 Smooth Muscle vs. Skeletal/Cardiac Muscle:
o Smooth muscle action potentials depend on Ca2+ (not Na+).
o Gap junctions facilitate depolarization across cells.

Interstitial Cells of Cajal (ICCs)

 Pacemaker cells generating slow waves in the stomach, small intestine, and large
intestine:
o Stomach: 3–4 waves/min.
o Small Intestine: 10–12 waves/min.
o Large Intestine: 3–7 waves/min.
 Link ENS plexuses to smooth muscle.
 Respond to PNS and SNS inputs.
Stomach Motility

1. Segmentation: Churning by the oblique muscle layer.

2. Peristalsis: Propulsion of chyme distally by circular and longitudinal layers.
o Controlled by myenteric plexus.
3. Upper Stomach: Reservoir for food; minimal electrical coordination.
4. Lower Stomach: Rhythmic contractions from ICCs concentrated along the greater
curvature.
5. Pyloric Sphincter: Filters food particles (1–3 mm); larger particles undergo retropulsion.

Small Intestine Motility

1. Segmental Contractions: Mix chyme with digestive enzymes.

2. Peristaltic Reflex: Propels chyme distally:
o Serotonin (5-HT) from ECCs activates ENS sensory cells.
3. Chyme Transfer:
o Moves from ileum to cecum through the ileocecal valve.

Fed vs. Fasting States

1. Fed State:
o Enterogastric Reflex: Fat in the intestine increases gastrin release.
o Gastrocolic Reflex: Stomach stretch signals colon to empty.
o Gastroileal Reflex: Stomach stretch opens ileocecal valve.
2. Fasting State:
o Migrating Motor Complex (MMC):
 Maintains GI tissue by clearing residual chyme.
 Four phases, with motilin peaking during phase 3.

Large Intestine Motility

1. Haustral Shuttling:
o Segmentation in haustra increases surface area for absorption.
2. Mass Movement:
o Powerful peristalsis moves hardened solids caudally (2–3 times/day).
o Propels material ~20 cm at a time.
Gastrointestinal Absorption

Carbohydrate Absorption and Transport

 Breakdown:
o Enzymes: Salivary and pancreatic amylase produce smaller sugars (α-dextrins,
maltose, sucrose).
o Brush border enzymes in the small intestine convert these into glucose, fructose,
and galactose.
 Transport:
o SGLT1 (Apical): Glucose & galactose with Na+ via secondary active transport.
o GLUT5 (Apical): Fructose via facilitated diffusion.
o GLUT2 (Basolateral): Glucose, galactose, and fructose into the bloodstream via
facilitated diffusion.

Protein Absorption and Transport

 Breakdown:
o Enzymes: Pancreatic and brush border peptidases produce single amino acids,
dipeptides, and tripeptides.
 Transport:
o Single Amino Acids: Sodium-linked transporters.
o Dipeptides/Tripeptides: PepT1 (proton-linked), digested to single amino acids
within enterocytes.
o Basolateral transporters export amino acids into the bloodstream.

Fat Absorption and Transport

 Breakdown:
o Bile emulsifies fats into micelles.
o Lipase digests fats into monoacylglycerols, fatty acids, and cholesteryl esters.
 Transport:
o Simple Diffusion: SCFAs & MCFAs diffuse into capillaries for portal
circulation.
o Carrier-Mediated: LCFAs and cholesterol form chylomicrons for lymphatic
transport.
o Chylomicrons: Packaged in the smooth ER, glycosylated in the Golgi, and
released into lacteals.
Iron Absorption and Transport

 Forms:
o Heme Iron: Absorbed by endocytosis (found in red meat).
o Nonheme Iron: Requires reduction to ferrous iron (Fe2+) via DcyB for
absorption by DMT1.
 Transport:
o Stored as ferritin in tissues or exported via ferroportin into the bloodstream.
o Ferrous iron binds transferrin for systemic circulation.
o Hepcidin: Regulates ferroportin, reducing iron release during high plasma iron
levels.

Copper Transport

1. Absorption: Copper enters duodenal enterocytes via Ctr1 and DMT1.

2. Intracellular Regulation: Binds to metallothionein (MT).
3. Export: Transported to blood by ATP7A at the basolateral membrane.
4. In the Blood: Binds to albumin and ceruloplasmin, then travels to the liver.
5. Regulation: Primarily controlled by hepatic metabolism and excretion (not absorption).
6. Inhibition: High fiber and zinc reduce copper absorption.

Zinc Transport

1. Absorption: Zinc enters duodenal enterocytes via DMT1.

2. Intracellular Handling: Binds to MT, which regulates its storage or export.
3. Regulation: Controlled by MT levels in enterocytes.
4. Inhibition: Absorption decreases with high levels of copper and iron.

Manganese Transport

1. Absorption: Via DMT1 in duodenal enterocytes.

2. In the Blood: Binds to albumin or α-2 macroglobulin for transport to the liver.
3. Regulation: Absorption is reduced by high fiber, calcium, and high serum iron.

Hyperemic Response

 Definition: Increased intestinal blood flow during digestion.

 Mechanism: Triggered by fat micelles, glucose, and water, causing local vasodilation in
the intestinal mucosa and smooth muscle.
 Purpose: Facilitates nutrient transport to the liver and throughout the body.
Gastrointestinal Regulatory Hormones

1. Secretin

 Stimulus: Low pH (acidic chyme) in the duodenum.

 Source: S cells in the duodenum.
 Functions:
o ↑ Pancreatic bicarbonate (HCO₃⁻) secretion.
o ↑ Bile secretion (via CCK).
o ↓ Gastric acid secretion (via somatostatin).

2. Cholecystokinin (CCK)

 Stimulus: Fatty acids and amino acids in the duodenum.

 Source: I cells in the duodenum and jejunum.
 Functions:
o ↑ Pancreatic enzyme and HCO₃⁻ secretion.
o ↑ Gallbladder contraction and bile release.
o ↓ Gastric motility.
o Signals satiety to the brain.

3. Gastrin

 Stimulus: Stomach distention, peptides, and vagal stimulation.

 Source: G cells in the stomach antrum and duodenum.
 Functions:
o ↑ Gastric acid (H⁺) secretion.
o Maintains gastric mucosa.
o Promotes gastric motility.

4. Vasoactive Intestinal Polypeptide (VIP)

 Stimulus: Small intestinal distention and vagal stimulation.

 Source: Parasympathetic ganglia in the GI tract.
 Functions:
o ↑ Relaxation of intestinal smooth muscles and sphincters.
o ↑ Secretion of water and electrolytes.

Transport Summary Table

 Substance Absorption Site Key Transporters
Carbohydrates Small intestine SGLT1, GLUT5, GLUT2
Proteins Small intestine PepT1
Fats Small intestine FATP4, Caveolin-1
Iron Duodenum DMT1, DcyB, Ferroportin
Copper Duodenum DMT1, Ctr1, MT, ATP7A
Zinc Duodenum DMT1, MT
Manganese Duodenum DMT1

Hormones and Their Functions

1. Bombesin (Gastrin-Releasing Peptide, GRP)

 Stimuli: Parasympathetic vagal nerve stimulation.

 Functions:
o Acts on nearby G cells to release gastrin.
o Plays a role in satiety via neuromodulation.

2. Glucagon-Like Peptides (GLP)

 GLP-1:
o Source: L cells of intestines.
o Stimuli: Fatty acids, amino acids, oral glucose.
o Functions:
 Potentiates insulin secretion.
 Decreases gastric acid secretion.
 GLP-2:
o Source: CNS neurons and intestinal L cells.
o Stimuli: Similar to GLP-1.
o Functions:
 Enhances mucosal growth.
 Protects myenteric plexus neurons.

3. Motilin

 Source: Duodenal enteroendocrine cells.

 Stimuli: Fasting states.
 Functions:
o Triggers migrating motor complex (MMC).
o Generates borborygmi (rumbling sounds).
4. Ghrelin

 Source: Parietal cells in stomach fundus.

 Stimuli: Fasting.
 Functions:
o Stimulates appetite and food intake.
o Increases gastric motility and acid secretion.
o Decreases insulin secretion.

5. Leptin

 Source: Adipose tissue.

 Stimuli: Increased energy stores (e.g., post-meal).
 Functions:
o Reduces appetite (satiety signal).
o Inhibits neuropeptide Y (feeding behavior promoter).

6. Somatostatin

 Source: D cells in stomach/pancreas.

 Stimuli: Low pH, high pepsinogen.
 Functions:
o Inhibits gastrin, insulin, and glucagon.
o Reduces exocrine secretions and motility.

7. Gastric Inhibitory Polypeptide (GIP)

 Source: K cells in duodenum/jejunum.

 Stimuli: Glucose, fatty acids, amino acids.
 Functions:
o Enhances insulin release.
o Lowers gastric acid secretion.

Enteroendocrine Cells and Their Roles

 G Cells (Stomach, Duodenum):

 o Release gastrin upon stimulation by amino acids, calcium, or low pH.
 I Cells (Small Intestine):
o Triggered by fatty acids/amino acids to release CCK.
 S Cells (Duodenum):
o Respond to luminal nutrients to release secretin.

Neural Factors

 Physical Distention:
o Activates the vagus nerve, prompting:
 GRP Release: Stimulates gastrin (G cells).
 Inhibition of Somatostatin: Enhances digestion.
 Pepsin Secretion: From chief cells.
 VIP (Vasoactive Intestinal Peptide):
o Released during stomach/duodenal distention.
o Relaxes pyloric sphincter for chyme movement.
o Increases fluid/electrolyte secretion in intestines

Enteric Nervous System (ENS)

 Autonomous Function: ENS operates independently of the PNS and SNS and is often
called the "second brain."
 Components: Afferent neurons (sense stimuli), interneurons (process information), and
efferent neurons (execute responses).
 Submucosal Plexus: Controls enzyme secretion.
 Myenteric Plexus: Regulates peristalsis.
 Signaling Molecules: Includes acetylcholine (ACh), vasoactive intestinal peptide (VIP),
serotonin, and dopamine.

Parasympathetic and Sympathetic Effects

 Parasympathetic (PNS):
o Enhances digestion by increasing acid and fluid secretion.
o Promotes smooth muscle contraction (proximal to bolus) and relaxation (distal to
bolus).
 Sympathetic (SNS):
o Releases catecholamines, inhibiting parasympathetic action and slowing
digestion.

Gastric Secretion Regulation

1. Stimulators:
o ACh (Vagal Input): Directly acts on parietal cells (HCl secretion) and indirectly
stimulates histamine and gastrin release.
 o Histamine: Binds H2 receptors on parietal cells, increasing H+ secretion.
o Gastrin: Stimulates histamine release and parietal cell H+ secretion.
2. Inhibitors:
o Somatostatin: Directly inhibits parietal, ECL, and G cells.
o Prostaglandins: Inhibit parietal cell acid secretion.

Gastrointestinal Secretions

 Saliva:
o Volume: ~1500 mL/day.
o Components: Enzymes (amylase, lipase), glycoproteins (haptocorrin), and
immune factors (lysozyme, lactoferrin).
o Regulation: Parasympathetic (increases secretion, watery saliva) vs. sympathetic
(viscous, mucin-rich saliva).
 Gastric Secretions:
o Volume: ~2500 mL/day.
o Components: HCl, bicarbonate, intrinsic factor (B12 absorption), pepsinogen.
o Functions: Digestion (acid denatures food), pepsinogen activation, B12 protection
(intrinsic factor).
 Pancreatic Secretions:
o Volume: ~1500 mL/day.
o High in bicarbonate (neutralizes stomach acid) and enzymes (amylase, lipases,
proteases).
 Intestinal Secretions:
o Volume: ~1000 mL/day.
o Components: Brush border enzymes (sucrase, lactase), bile, and hormones (GIP).
o Functions: Neutralize acid (HCO3-), digest macronutrients (enzymes), emulsify
fats (bile).

Incretins and Hormonal Regulation

 Incretins (e.g., GIP, GLP-1):

o Released by K cells in the duodenum/jejunum.
o Enhance insulin release in response to glucose.
o Effects: Reduce H+ secretion, slow gastric emptying, and stimulate insulin
release.

Key Enzymatic Processes

 Amylase: Starts carbohydrate digestion.

 Pepsin: Activated in low pH, breaks proteins into peptides.
 Trypsin: Activated by enterokinase in the intestine, it activates other proteases.
 Lipase: Crucial for fat digestion in the duodenum.