Digestive Enzymes
Amylase, Lipase, Pepsin, Collapse, Phospholipase, Trypsin, Chymotrypsin, Enterokinase, Disaccharides, Dipeptidases
Salivary Glands
Enzymes: amylase, lipase
Targets: starch, TGLs
Stomach
Enzymes: pepsin, lipase
Targets: proteins, TGLs
Pancreas
Enzymes: amylase, lipase/colipase, phospholipase, trypsin, chymotrypsin
Targets: starch, TGLs, phospholipids, peptides,
Intestine
Enzymes: enterokinase, disaccharides, dipeptides
Targets: activates trypsin, complex sugars, peptides
“entero”
= gut
enterocyte: absorbs nutrients - lipids in the SI
GI tract anatomy
Mesentery - OUTER layer containing blood vessels
Mucosa - Epithelial, lamina propria, muscularis mucosa
Submucosa - Meisseners plexus
Muscular Propria - circular muscle (auerbachs myenteric plexus), longitudinal muscle
Serosa - cell lining around the mesentery
Trypsin
attracts:
lys (+) - aromatic won’t fit
arg (+) - activates chymotrypsin & collapse
Epithelial vs. Endothelial
Epithelial - in contact with outside world
Endothelial - inside only (i.e.: blood vessels)
How to make food usable?
1) Mechanical disruption (mastication in mouth and churning in stomach)
2) Chemical digestion (lipids, aa, carbs)
Pepsin
ONLY zygomen that is is not activated by cleavage - activated by LOW pH
Enterokinase
enteropeptidase that activates trypsinogen by converting it to trypsin
GI peptides/modulators
1) Endocrine - SLOW
- ALL GI endocrine hormones are peptides
2) Paracrine
- peptides: somatostatin
- non-peptides: histamine
3) Neurocrine - FAST
- peptides: VIP
- non-peptides: ACh, NE
- nerve release diffuse to target cells
GI Hormones
Secretin Gastrin Cholecystokinin (CCK) Glucose-Dependent Insulinotropic Peptide Motilin
Hormonal Control of Digestion
1) Physiological even in one part that alters activity in another
2) Effect persists after denervation
3) Eliminating source tissue prevents response
4) Isolated substance produces response when injected into blood at proper dose
Gastrin
ANTRUM! (duodenum & jejunum too)
- related to CCK (Trp-Met-Asp-Phe-NH3)
- G cells
- gastric acid secretion is 1,500x MORE potent than histamine
- trophic activity: stimulates growth of oxyntic mucosa of stomach, duodenal mucosa, and colon mucosa
- surgical removal of antrum causes atrophy
- patients with gastrin-secreting tumors have mucosal hyperplasia and hypertrophy
Tyrosine
MUST be sulfated in Gastrin & CCK
CCK
- related to Gastrin (Trp-Met-Asp-Phe-NH3)
- digests fat and slows down chyme to slow gastric emptying
- emptying of gallbladder
- pancreatic exocrine enzymatic secretion
- inhibits gastric emptying
- delivery of pancreatic enzymes and bile into small intestine
- trophic effects: exocrine pancreas and gallbladder mucosa
Secretin
- natures antacid
- requires ALL 27 AA for activity
- released from S cells of duodenal mucosa
- stimulates bicarb and pepsin to inhibit gastric secretion
- acid (less than 4.5pH) and fatty acids cause release
- trophic effect on exocrine pancreas
GIP (gastric inhibitory polypeptide)
- released from K cells of the duodenum and proximal jejunum
- oral glucose
- all food (protein, carb, fat)
- fat MUST be hydrolyzed
- stimulates insulin release
- inhibits gastric acid secretion
Motilin
- released from M cells of duodenum and proximal jejunum during FASTING (100+ min)
- peptide family
- Neural controls release
- stimulates upper GI motility
- “housekeeping contractions”
Hypertrophy vs. Hyperplasia
trophy - cell size
plasia - replication
Zollinger-Ellison Syndrome
Gastrinoma!!!
- ChiRhoStim (synthetic secretin) used to inhibit gastric secretions! if gastrin production doesn’t stop, indicative of a gastrinoma (NOT a peptic ulcer)
- Loss of K+ in stool
- increase in parietal cell mass: increase acid production
- intestinal hyperacidity leads to peptic ulcer
- decrease in bile salts and lipase activity
= diarrhea, steatorrhea, hypokalemia
Low pH
- inactivates pancreatic lipase
- bile salts precipitate
= steatorrhea
