GI Flashcards
Lumen
Cavity where food travels from mouth to anus and secretions from various organs drain
Blender
Stomach, stays for at least 4 hours
Reaction vessel
First part of small intestine, enzymes from pancreas neutralize acid, detergent is bile from liver
Residue combuster
Where feces are formed
Mouth
Mechanical shearing of ingested food, grinding to reduce size of food particles, saliva added
Saliva
Moistens to taste, signifiant amount of enzymes, lubricates food bolus to allow swallowing, begins digestion of carbohydrates and lipids
Esophagus
Transfers food to stomach by peristaltic waves, moves actively (without gravity), flexible tube with sphincter at each end
Lower esophageal sphincter
Opens as soon as food is swallowed, and opens until food enters your stomach
Begins stomach
Tonically contracted
Stomach
Begins with lower esophageal sphincter, 3 sections
1. Fundus
2. Body
3. Antrum
Exits antrum to small intestine through pyloric sphincter
Can also be divided into orad and caudad region
Stores food in upper stomach
Specialized cells secrete mucous, enzyme precursors, hydrochloric acid and hormones
Grinding occurs in lower stomach
Chyme
Enters small intestine from stomach, pretty liquid: delivered to duodenum
Small intestine
4-6 meters long 1. Duodenum 2. Jejunum 3. Ileum Absorption of nutrients occurs mostly in jejunum and ileum
Duodenum
Very short
Secretions from pancreas and liver via pancreatic and common bile ducts
Jejunum
40% of small gut
Larger diameter, thicker wall, more prominent circular folds, less fatty mesentery
Mesentery
Connects small intestine to wall and important in blood circulation
Ileum
60% of small gut
Empties into large intestine
Hard to say border between jejunum and ileum
Thinner than jejunum
Large intestine (colon)
Re-absorbs water used in digestion process, starts at cecum and ends at anus
Appendix
No function in humans
Villi
Fingerlike extensions that face lumen of tract, increase surface area of small intestine
Microvilli project outwards to form brush border
Crypt
Colon
Structurally and functionally different from villi
Three major salivary glands
- Parotid gland (large, behind ear)
- Submandibular gland
- Sublingual gland
Salivary glands
Units are called acini
Different types of cells producing enzymes and secretions
Produce large amount of saliva
Volume and amount of saliva under control of autonomic nervous system
Pancreas
Exocrine and endocrine functions
Exocrine functions of pancreas
Secretion of digestive enzymes and bicarbonate ions (HCO3) to the duodenum
Digestive enzymes break down nutrients
HCO3 neutralizes chyme
Endocrine functions of pancreas
Insulin and glucagon secretion
Liver
Storing and releasing nutrients that have been absorbed by the digestive tract
Produces and releases bile (fat digestion)
Gallbladder
Bile storage, concentrates, and pH changes, gets pushed down common bile duct to duodenum
Bile assists in fat digestion
Mucosa layer
Epithelium and lamina propria
Followed by submucosa
Submucosa
Contains many cells and glands that excrete into lumen
Muscular externa
Circular muscle contraction induces decrease in diameter of lumen
Longitudinal muscle contraction induces shortening of a segment of GI tract
Muscular muconsae
Innermost muscle layer that allows mucosa to fold and form ridges
Myenteric plexus
Outer nerve layer
Part of enteric nervous system
Between two muscle layers
Mainly controls motility of GI tract
Submucosal plexus
Inner nerve layer
Part of enteric nervous system
Located under mucosa
Control local secretion, absorption and submucosal muscle contraction
Receives sensory information from sensory neutrons in the GI tract
Epithelial cells in gut wall
Specialized in different parts of the GI tract for secretion or absorption, replaces al the time (every 5 days for total)
Includes secretory cells, endocrine cells and absorptive epithelial cells
Virtually all nutrients enter the body across the epithelium covering small intestinal villi
Central lacteal
Centre of villi, absorbs fat, lymphatic vessel, drains from intestine and rapidly flow into blood via thoracic duct
Splanchnic circulation
Blood supply to the intestine carries away absorbed water-soluble nutrients, flows to liver first via portal vein to be detoxified by hepatocytes
External anal sphincter
Under central control, skeletal muscle
there are two anal sphincters, internal anal sphincter is smooth muscle
Upper esophageal sphincter
Under central control, skeletal muscle
GI sphincters
Mainly smooth muscle, mainly positive resting pressure and regulate forwards and reverse movement
Enteric nervous system
Intrinsic innervation, mediated by nerve plexus in gut wall
Full length of GI system
Can and does function completely autonomously
Normal digestive function requires communicate between the intrinsic and CNS
100 million neurons (equal to spinal cord)
Extrinsic innervation
Autonomic nervous system, both parasympathetic and sympathetic systems
Sympathetic regulation
Inhibitory
Mainly postganglionic, connects directly to myenteric plexus (NE and rarely epinephrine), connects to submucosal for secretary processes, connects directly to epithelium
Pregangiolinc fibres arise from spinal cord (T5-L2) and terminate in pre vertebral ganglia (Ach)
Constant innervation
Sensory neurons
Monitor distension and inform enteric nervous system and brain
Stimulation of myenteric plexus
Increases tonic contraction of gut wall
Increased intensity and rate of contractions
Increased velocity of excretory waves along the gut causing more rapid peristaltic waves
Autonomic nervous system
Integrates activity of the enteric nervous system with the rest of the body
Do not directly innervate GI structure, but interact with ENS
Parasympathetic regulation
Excitatory
Mainly preganglionic and cholinergic, nerve fibres terminate on ganglion cells in enteric nerve plexuses and act on nicotinic ACH receptors
No direct innervation of the effector cells in gut wall
Vagal nerve fibres to basically all areas of the gut
Significant enervation in rectal column and anus via pelvic nerves
Afferent sensory nerve fibers
Strong afferent presence
Cell bodies either in ENS or dorsal root of ganglia in the spinal cord
Stimulated by irritation of the gut mucosa, distention of the gut, presence of chemical substances in the gut - sent to CNS
Activation can cause excitation or inhibition
Gastrocolic reflex
Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
If you start eating when colon is full: signals from stomach to evacuate colon
Enterogastic reflex
Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
Tells stomach that small intestine is still full, signals from colon and small intestine to inhibit stomach motility and secretion
Colonoileal reflex
Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
Signals from colon to inhibit stomach motility and secretion
Vagovagal reflex
Reflexes from gut to spinal cord or brain stem and back to GI tract
From stomach and duodenum to the brain stem and back to control gastric motor and secretory activity
Pain reflex
Reflexes from gut to spinal cord or brain stem and back to GI tract
Cause general inhibition of the gut
Defecation reflexes
Travel from colon and rectum to spinal cord and back to produce powerful colonic, rectal and abdominal contractions required for defecation
Gastrointestinal peptides
Regulate the functions of the GI tract
Contraction and relaxation of smooth muscle and the sphincters
Secretion for enzymes for digestion (peptides acting on pancreas)
Trophic (growth) effect on tissues
Can regulate secretion of other GI peptides
Somatostatin
Inhibits secretion of all GI hormones
Acetylcholine
Neurocrine
Contraction of smooth muscle, relaxation of sphincters, increased salivary, gastric and pancreatic secretions
Norepinephrine
Neurocrine
Limited function under normal circumstances, relaxation of smooth muscle, contraction of sphincters, increased saliva secretion
Vasoactive intestinal peptide
Neurocrine
Inhibits smooth muscle contraction, stimulates secretion and vasodilation
Serotonin (5-HT)
Diverse motor and sensory function in GI tract, 90% serotonin in GI tract
Nitric oxide
Relaxes smooth muscle activity
Gastrin
Produces by G-cells in the antrum, released in blood circulation to act on parietal cells to release HCl in the stomach
Also has affect on mucosal growth
Cholecystokinin
CCK
Secreted by I-cells in the duodenum and jejunum, homologous to gastrin
Tries to inhibit gastric emptying
Stimulates gallbladder contraction and relaxation of sphincter of Oddi
Secretin
Secreted by S-cells in duodenum
Homologous with glucagon, stimuli for release is gastric juice entering into small intestine, leads to neutralization of acidity in the small intestine
Glucose-Dependent Insulinotropic Peptide
Secreted by K-cells in the duodenum and jejunum
Homologous to secretin and glucagon
Stimulates insulin release and gastric acid secretion (unlikely during normal physiological conditions)
Motilin
Biology not fully understood, in humans: 22 amino acid linear peptide
Released cyclically from gut in fasting state
Responsible for stimulating a specific pattern of GI motility: migrating motor complex
Ghrelin
Mainly released from stomach and pancreas, a little along complete gut
Stimulates vagal afferents that triggers the release of signals in the solitary nucleus and hypothalamus that promote food intake (including orexin and neuropeptide Y)
Release normally suppressed by leptin
Leptin
Released from adipose tissue
Somatostatin
Secreted by D-cells in gastric mucosa
Acidity of astral region stimulates somatostatin release
Also released by neutrons in the enteric nervous system
Inhibits release of gastrin and histamine, inhibits gastric acid secretion from parietal cells
Histamine
Secreted from enterochromaffin cells in the stomach, acts on H2 receptors on parietal cells
With gastrin and Ach, stimulates acid secretion by the gastric parietal cells
Secreted from mucosal mast cells and has a role as an immune mediator
Peristalsis
Food moves forward along tract
Ring of contraction on oral side of bolus that moves towards the anus, as ring moves, muscle in front of food bolus relaxes
Completely enteric
Usual stimulus if distention of the gut
Chemical irritation of the gut and strong parasympathetic stimulation can also induce peristalsis
Mixing movements
Allow digestive enzymes to come in contact with chyme and for chyme to come in contact with intestinal walls
Segments of contraction
Similar to peristalsis but no net movement
Single-unit types smooth muscle
Depolarization of area spreads via gap junctions to result in well coordinated contraction: ring of smooth muscle
Slow waves
Cyclic variations in GI smooth muscle resting potential
Typical in each part of the gut (3/min stomach, 12/min in duodenum)
Depolarizing phase caused by calcium influx and depolarization by potassium efflux
Maximal frequency that muscle contractions can happen
Threshold for contraction
Slow waves above this threshold cause contraction
Electrical threshold
Cause action potentials, contractions become bigger as action potentials increase
Slow wave amplitude
Increases with parasympathetic stimulation
Decreases with sympathetic stimulation
Baseline tension
GI muscle does not relax completely, tonically contracted
Interstitial cells
Pacemaker activity and decide when contractions occur
Transfer signals from enteric motor nerves to muscle cells
Set smooth muscle membrane potential
Responsible for generating slow waves, peristalsis and segmentation
Mastication
Chewing
Both involuntary and voluntary reflexes are involved
Food in mouth activates mechanoreceptors which coordinate reflex activity
Breaks down and lubricates food, mixes it with salivary enzymes
Important in breaking down cellulose membrane of fruit and vegetables
Bolus
Moist, chopped up food
Oral phase (swallowing)
Voluntary
Tip of tongue pushes food towards pharynx
Pharyngeal phase (swallowing)
Involuntary control
Series of protective reflexes initiated by the stimulation of afferent fibres in the pharynx and organized in the swallowing centre
Close off nasal, oral and laryngeal cavities
Respiration in inhibited
Swallowing centre
Medulla and lower pons
Esophageal phase (swallowing)
Food enters esophagus and upper sphincter closes, primary peristaltic contract moves and pushes food bolus down, lower esophageal sphincter relaxes and food bolus enters the stomach
Second peristaltic contraction clears esophagus of remaining food
Dysphagia
Difficulty in swallowing
Can result in abnormalities in any components of swallowing reflex or anatomical structures
Common, especially in elderly (stroke, ALS, Parkinsons)
Risk of malnutrition, aspiration, choking
Achalasia
Failure to relax
LES does not relax and open
Problem with myenteric ganglion nerves
GERD
Gastrointestinal reflux disease
Acid gastric contents reflux to the distal esophagus
Very common, severity varies
May result in inflammation, ulcers
Orad region
Stomach
Main area of reception and storage
Caudad region
Main region of propulsion in stomach
Stomach muscles
Longitudinal, middle circular, inner oblique
Body and fundus are thin walled, antrum is thicker with more muscle
Pyloric sphincter
End of antrum entering into duodenum, prevents bolus from entering duodenum, causes mixing of food
Gastric contractions
Allow stomach to grind, crush and mix ingested food
Lower part of stomach contracts to propel liquid chyme into duodenum in spurts
Retropulsion
Lower and body and antrum contracts and propels food bolus to fundus
Gastric emptying
Takes about three hours, liquids empty more rapidly than solids (less than 1 mm diameter), isotonic liquids empty faster, nature of contents affect emptying
Migrating Myoelectric Complex
Empties non digestible material during inter digestive period
Gastoparesis
Disorder where gastric emptying is delayed without evidence of obstruction
Symptoms: early satiety, nausea, vomiting, bloating and upper abdominal discomfort
Causes: system disease affecting neuromuscular function, education, injury to vagus nerve
Pyloric stenosis
Congenital condition usually present infancy
Pyloric muscle thickens and pylorus fails to relax after a meal, leading to regurgitation and vomiting
Infants develop malnutrition and dehydration
Cured by surgical myotomey: longitudinal incision to muscle surrounding pyloric region
Segmented contractions
Small intestine muscle contraction
Squirt luminal contents bidirectionally
Contractions increase resistance to flow, and there are more contractions upstream causing overall aborad movement
Aborad
Away from the stomach
Peristaltic contractions
Entry of chyme into duodenum causes peristaltic wave: travels only a few centimetres before dying out
Intestinal contents are slowly mixed and chyme is steadily moved
Ileocecal valve
Prevents back flow from colon to ileum
Ileocecal sphincter is normally constricted, but strong peristaltic activity immediately after a meal relaxes the sphincter
Colon storage
Mainly in distal colon
Sigmoidscopy
Colonoscopy to sigmoid colon
Hautrations
Circular and longitudinal muscles of colon contract simultaneously to form haustra, move back and forth to move contents
Mass movements
1-3 times a day, move colonic contents over long distances
Final mass movement propels faces to rectum where they are stored until defecation
Defecation
Involved both reflexes and voluntary actions
Upper portion of rectum relaxes to permit entry of faces
Rectal distention relaxes the internal anal sphincter
External sphincter is contracted until it is convenient to defecate (then voluntary)
Smooth muscle of rectum contracts and faces are forced out of body
Hirschsprung’s Disease
Congenital megacolon, developmental abnormality where the ENS fails to develop
Segment of internal anal sphincter and upwards remains permanently contracted causing obstruction
Symptoms can be completely alleviated by surgical excision of diseased segment
Irritable Bowel Syndrome
Motility disorder caused by visceral hypersensitivity, very common (10-30% of people)
Causes cramping, abdominal pain, bloating, gas, diarrhea, constipation
Partially due to dysmotility (consistent motor abnormalities have not been seen)
Patients with diarrhea have shortened transit times though intestines and increase in propulsive contractions in the colon
Patients with constipation-predominant disorders have slowed transit of intestinal contents
Vomiting
Always centrally controlled, many triggers
Usually good to vomit
1. Hypersalivation
2. Fundus becomes flaccid
3. Sold palate rises, glottis closes, larynx moves forward, esophagus dilates, LES relaxes and moves upward
4. Diaphragm contracts, abdominal muscle contracts, gastric contents forced upwards
Vomit control centre
Vomiting centre and nuclease tracts solitaires
Parotid glands
Big, by ear
Serous glands
Submandibular glands
Close to jaw bone
Mixed mucous and serous glands
Serous acinar cells secrete salivary amylase
Mucous cells secrete mucins
Intercalated duct drains into salivary duct which has striated and excretory ducts
Sublingual glands
Under bottom teeth
Mixed mucous and serous glands
Buccal glands
Smaller glands present in oral cavity, only secrete mucous
Serous acinar cells
Secrete salivary amylase
Two state model of saliva secretion
Primary secretion
Secondary secretion
Primary secretion
Nearly isotonic, levels of Na, K, Cl and HCO3 are similar to plasma
Secondary secretion
Ductal cells reabsorb Na and Cl ions from the saliva and secrete K and HCO3 into the saliva
Water does not follow ions but remains so saliva becomes more watery
Saliva composition
Function of flow rate, the faster the flow rate the less time there is for ductal cells to act: saliva is closer to isotonic
~1L/day, pH 6-7
Parasympathetic regulation of saliva secretion
Autonomic nervous system
Messages from tongue and other parts of oral cavity, stimulated by taste and pressure
Otic ganglion stimulation increases Ach and stimulates parotid gland
Submandibular ganglion stimulation increases Ach and stimulates submandibular gland
Sympathetic regulation of saliva
Changes composition of saliva but no affect on volume
Xerostomia
Dry mouth
Several different conditions cause decreases saliva secretion
Sjorgrens syndrome, side effects of many drugs, secondary to head and neck radiation
Decreased pH in mouth leads to tooth decays and esophageal erosions
Difficulty swallowing
Gastric secretions
Mixture of secretions of the surface epithelial cells, mucous neck cells and gastric glands
1.5-2L/day
Largest volume is contributed by parietal cells
pH 1-3.5
Mucous cells
All parts of gastric mucosa
Secrete mucus that coats and lubricates the gastric surface and protects epithelium
Parietal cells
Body of stomach
Secrete HCl and intrinsic factor
Chief (peptic) cells
Body of stomach Secrete pepsinogen (pepsin precursor)
G-cells
Antrum of stomach
Secrete gastrin hormone
Gastric oxyntic gland
Located on body of stomach
Contains: epithelial cells, mucous neck cells, parietal cells, and chief cells
Gastric acid secretion
- H/K pumps H into lumen
- Cl ions flow via Cl ion channels into lumen
- HCO3 is absorbed into the blood stream in exchange for Cl
Pepsinogen
Inactive precursor of pepsin
Secreted by chief cells
Vagovagal reflex and gastrin release stimulates acid and pepsinogen release
Intrinsic factor
Secreted by gastric parietal cells
Essential for absorption of vitamin B12 in the ileum
Secretion is only gastric function that is essential for human life
Vitamin B12
Cobalamin
Involved in synthesis of all cells, affects DNA synthesis
Couples with R protein in small intestine, and breaks down from component R in alkaline conditions and binds to intrinsic factor
Absorbed when complex interacts with receptors in final parts of small intestine
Pernicious anemia
Red blood cells fail to mature because of problem in intrinsic factor production and B12 absorption
Regulating HCl secretion
Vagus nerves stimulate G-cells to release gastrin and parietal cells to release HCl
Distension on the antrum stimulates G cells to release gastrin
Ulcer disease
Breaks in the stomach or in the duodenal mucosa
Corrosive action of pepsin and HCl on supper gastrointestinal tract mucosa
Caused be excess secretion of acid and pepsin by mucosa or diminished protective abilities of gastric mucosal barrier: Helicobacter pylori, non steroidal anti-inflammatories, alcohol, smoking, gastrinoma
Gastric ulcers
Breaks in the stomach mucosa
Duodenal ulcers
Breaks in the duodenal mucosa
Helicobacter pylori
Bacteria that colonizes in the gut
Main cause for ulcers
Gastrinoma
Zollinger-Ellison Syndrome
Rare tumour that releases gastrin hormone leading to excess HCl secretion
Ductal cells
In pancreas
Secrete bicarbonate
Stimulated by secretin, CCK and Ach
Aqueous component of pancreatic secretion
High bicarbonate concentration that neutralizes chyme in duodenum
pH ~8, isotonic with plasm
About 1L/day
Enzyme components of pancreatic secretion
Proteases - proteins
Amylases - carbohydrates
Lipases - lipids
Anicar cells in pancreas
Secrete enzyme components
Stimulated by CCK and Ach
Pancreatic secretion and flow rate
Na remains constant
Bicarbonate increases with flow rate
Cl decreases with flow rate
Pancreatic insufficiency
Rare
Secretion can drop down to 10% of normal without an effect on nutrient absorption: pancreatic enzymes are secreted in excess
Pancreatitis
Inflammation of the pancreas
Auto digestion of pancreatic tissue due to enzyme retention
Can be caused by gallstones in ducts, malignancy, alcohol abuse
Medical emergency
Cystic fibrosis
Pancreatic ducts are inefficient to secrete bicarbonate and water
Enzymes cannot be flushed properly from pancreas and limited quantities reach the intestinal lumen
Enzymes that reach lumen are inactive because of failure to neutralize gastric acid
Enzymes provided as supplements
Bile
Secreted by liver continuously, 1L/day pH 7.8-8.6 Isotonic Flow into duodenum is intermittent Diverted to gallbladder for concentration, acidification and increase in viscosity during inter digestive periods
Bile acids
Synthesized from cholesterol in liver
In small intestine, bile salts that are more soluble
Phospholipids (bile)
Lecithins: major
Bile pigments
Bilrubin: major
Sphincter of Oddi
Allows entry to duodenum from gallbladder
Closed while gallbladder is filled with bile
Relaxes shortly after eating (CCK induced gallbladder contraction)
Primary bile acids
Chalice acid
Chenodeoxycholic acid
>90% of bile salts are reabsorbed from ileum not portal blood and resecreted by liver
Secondary bile ducts
Deoxycholic acid
Lithocholic acid
Small amount of bile salts dehydroxylated by colonic bacteria, reabsorbed, returned to liver to be resecreted
Gallstones
Collection of solid material, mainly cholesterol, in gallbladder
Often asymptomatic
Abdominal pain (upper middle, right), nausea, jaundice, fever
Hyper secretion of cholesterol
Caused by obesity, oral use of contraceptives, estrogen, old age, sudden weight loss and genetic factors
Diminished bile acid pool
Enterohepatic circulation is interrupted
Cholecystectomy
Gallbladder removal
Gallbladder is not essential for normal digestive function: removal has no effect on life expectancy or metabolic status
Balance of specific bile acids may change, but no change on cholesterol
Inability to form concentrated bile and to secrete in coordinated fashion: patients have a harder time tolerating large fatty meals
Can have diarrhea
Crohn’s disease
Inflammation that affects the full thickness of the bowel wall
Early onset, usually teens to early twenties
Abdominal cramps, diarrhea, weight loss, fever, anemia, ulcers, fistulae, abscess
Abnormal immune response to intestinal bacteria, mutations in NOD2 gene
No cure, but symptoms can be alleviated using medication, surgery, dietary adjustments ileal resection
Ileal resection
40% resection is tolerated well
More causes bile salts to not be recirculated but secreted in diarrhea: causes depletion of bile salt, and fat absorption is impaired, also affects absorption of some vitamins, iron and calcium
Transcellular route (epithelial cells)
Through epithelial cells from lumen to blood circulation
Large molecules only go via transcellular route
Paracellular route
Between tight junctions
Apical membrane
Lumen
Basolateral membrane
Blood
Sucrose
Cane sugar
Disaccharide
Glucose + fructose
Lactose
Milk sugar
Disaccharide
Glucose + galactose
Starches
Large polysaccharides present in almost all non-animal foods
Glycogen
Small amounts
Animal polysaccharides
Cellulose
Large amount
Cannot digested and contributes to dietary fiber
Amylase
Salivary and pancreatic alpha-amylases partially break down glucose polymers (alpha 1,4 bonds of amylose and amylopectin)
Not necessary for healthy humans, important in infants and pancreatic insufficiency
Inactivated by acidic pH in stomach
Isomaltase
Only enzyme that an break down alpha 1,6 bonds of alpha-limit dextrins
Sucrase-isomaltase
Brush border enzyme that binds sucrose
Lactase
Brush border enzyme
Especially important in infants
If it is lacking, milk sugar does not break down and causes diarrhea
GLUT5
Fructose transporter
Fructose is not natural product from corn
Excess amount can overwhelm transporter
Apical membrane
SGLT1
Na-glucose transporter
Active transport
Apical membrane
GLUT2
Transports glucose, galactose, fructose over basolateral membrane
Facilitated diffusion
Essential amino acids
Many need to be obtained from dietary sources
Pepsins
Inactive in the duodenum (pH >5)
Max, pepsin digests 15% of dietary proteins to small peptides and amino acids
Not necessary for protein digestion
Enteropeptidase
Absolutely necessary to activate trypsinogen to trypsin and activate other pancreatic enzymes
PEPT1
Absorbs peptides with a proton
Apical membrane
Cytosolic proteases
Digests peptides absorbed into cells
Amino acids are secreted over basolateral side using transport proteins
Most are Na dependent
Vitamin A
Retinoid acid
Regulates gene transcription
Fat soluble
Vitamin D
Important in Ca absorption
Supplements: Cholecalciferol, ergocalciferol
Fat soluble
Vitamin E
Tocopherol
Important antioxidant
Fat soluble
Vitamin K
Important in blood clotting
Fat soluble
Gastric lipase
pH optimum of 4-5.5 Resistant to pepsin Hydrolyzes fatty acid linked to first position of triglyceride Does not fully break down triglyceride Inhibited by bile acids
Pancreatic lipase
Acts on 1 and 3 positions of glycerol molecule to liberate esterified fatty acids
Neutral pH optimum
Inhibited by bile acids
Lipase
Can absorb on the surface of fat droplet
Displaced by bile acids
Colipse binds both bile acids and lipase
Phospholipase A2
Breaks down dietary phospholipids
Cholesterol esterase
Degrades cholesterol esters derived form dietary sources and esters of vitamins A, D and E
Breaks down position 2 in triglycerides
Emulsifiation
Large fat aggregate is exposed to bile, and non polar portions of bile salts and lecithin intercalate into the lipid
Polar parts demain at the surface
Bile sat/lecithin coat makes fat droplets easily fragmentable causing increased surface area
Micelles
Formed from lipids breakdown products and bile acids
Transport lipids to brush border
Not necessary for triglycerides or glycerol
Necessary for cholesterol, plant sterols and fat soluble vitamins
Apolipoproteins
Synthesized in rough ER and glycosylated, then coated in lipid cores to form chylomicrons
Chylomicrons
Secreted from basolateral side of enterocyte via exocytosis and enter central lacteal
Vitamins
Act as cofactors for many metabolic reactions
Must be acquired from diet
Vitamin B9
Folate
Absorbed by at least three different transport mechanisms
Water-soluble vitamins
B1, B2, B6, C, biotin, nicotinic acid, pantothenic acid
Absorbed by sodium dependent cotransport
Sodium-coupled nutrient transport in intestines
Glucose transport is coupled to Na transport
Na absorption in colon
ENaC
No glucose absorption
K absorbed with lumen concentration is high, or secreted if lumen concentration is low
NHE3 and DRA
Na/H exchanger and Cl/HCO3 exchanger transport NaCl into epithelial cells
KCC1
Transports Cl out of epithelial cells
CFTR
Cl exists epithelial cells via cystic fibrosis transmembrane regulators
Phosphorylated by PKA, which is activated by cAMP (Gs protein, VIP and PGE2)
HCO3 also exits, either coupled with Cl or by itself
Cholera toxin
Activates Gs protein, which leads to cAMP increase, activating CFTR, Cl efflux and watery diarrhea