Class Notes (806,631)
Canada (492,365)
Physiology (244)
PHGY 214 (173)

PHGY214 - Digestion.docx

51 Pages
Unlock Document

Queen's University
PHGY 214
Alan Lomax

Lecture 1 - Overview of Gut Physiology 1. Understand the structure of the GI tract  Hollow tube stretching from mouth to anus, 4.5m long (9m in cadaver when smooth muscle is no longer contracting)  Accessory digestive organs: o Salivary glands o Exocrine pancreas o Liver (gall bladder) Oesophagus  Stomach  Small intestine (duodenum, jejunum, ileum)  Large intestine (ascending, transverse, descending and sigmoid colon)  Rectum  Mucosa o Innermost layer of GI tract, surrounding the lumen. o Divided into: epithelium, lamina propria, muscularis mucosae. o Structure of mucosa consists of invaginations of secretory glands or folded in order to increase surface area (i.e. villi).  Sub mucosa o Dense layer of irregular connective tissue with large blood vessels, lymphatics and nerves branching into mucosa and muscularis. o Contains submucosa plexus (Meissner’s), part of enteric nervous system, situated on the inner surface of muscularis externa.  Muscularis externa o Two layers of smooth muscle:  Inner circular layer squeezes the tract.  Outer longitudinal layer which shortens tract. o Coordinated contractions of the 2 smooth muscle layers is peristalsis. o Between the two muscle layers is the myenteric plexus (Auerbach’s).  Adventitia/serosa o Consists of several layers of connective tissue. o Covered by thin squamous epithelial cell layer, mesothelium. o Together forming a serosa (serous membrane). 2. Understand its basic digestive processes Note: The GIT is a major interface between microbes and the immune system. Primary function of the GI system is for the transfer of nutrients, water and electrolytes from the food we eat into the body’s internal environment.  Not regulated according to body homeostasis.  Maximizes absorption regardless of whether nutrients are needed. Four basic digestive processes:  Motility  Secretion  Digestion  Absorption 3. Identify the major cell types in the GI tract a. Muscle cells  Propulsion or mixing of contents  Two types of muscle cells in the gut o Skeletal muscle – oesophagus o Smooth muscle  Circular muscle, longitudinal muscle and muscularis mucosae.  Sphincters: valves that regulate emptying of organs.  Blood vessels b. Neurons  Afferent – sensory signals from the intestine.  Efferent – autonomic nervous system. o Parasympathetic o Sympathetic o Enteric Nervous System o Sympathetic inhibits motility and closes sphincters o Parasympathetic increases motility. c. Epithelial cells  A mucosal epithelium constitutes the physical barrier between the lumen and the body. Mucous secretions contribute to the barrier.  Functions include secretion, absorption, lubrication, protections. Also an important endocrine organ. Motility of the GIT  Contraction of the gastrointestinal smooth muscle is an involuntary process.  Movement of organ walls propels food/liquid along the GIT and mix contents.  Segmentation is the contraction of circular muscle in order to mix the food without propelling food along the GIT.  Peristalsis is the coordinated contraction of the circular and longitudinal muscle to propel food down the GIT. Motility – peristalsis The propulsive contractile movements of the oesophagus, stomach and intestine are called peristalsis.  The circular muscle produces a narrowing  The longitudinal muscle contracts, shortening the organ and moving the narrowed portion, and the food within, down the length of the organ. Gastrointestinal secretions  A total o 7L of secretions enter the GIT each day.  These secretions are produced by the: o Salivary glands o Stomach – gastric o Liver o Pancreas o Small intestine Mechanical and Chemical Digestion Digestion is the process where the food we ingest is converted by chemical and mechanical means into the nutrients required by the body to survive.  Mechanical: change in size and consistency of contents.  Chemical: enzymatic and chemical breakdown of food components into smaller units that can be absorbed across the GIT mucosa. Absorption – general The movement of small molecules across the wall of the small and large intestine through osmosis, active transport and diffusion.  Sugar – carbohydrate (monosaccharides) Small intestine  Fat – lipids (monoglycerides)  Protein (amino acids, small peptides)  Absorption of water and electrolytes Small & large  Absorption of minerals and vitamins intestine Gastrointestinal immune system  The largest component of the immune system o Eosinophils, neutrophils, macrophages, T calls, B-cells, mast cells o Gut exists in a state of physiological inflammation  Challenges include: o Antigens, bacteria, physical damage o Maintain protection while tolerating commensal microbes. Microbial flora of the gut Largest population of bacteria inhabit the gastrointestinal tract. Several factors determine the final composition of an individual’s microbiota:  Mother’s microbiota composition  Genetics  Diet Protection by commensal bacteria 1) Antagonism 2) Immunomodulation 3) Exclusion  Antibiotics may create a niche for enteric pathogens Balanced microbial community Antibiotics Increased species diversity Decreased species diversity Increased TLR signaling Altered TLR signaling Immune development and tolerance Immune dysregulation Clostridium difficile  Gram +ve, spore forming, toxin producing bacillus  20-50% carriage rate in hospital patients; 3% carriage rate in healthy individuals.  Antibiotic-associated colitis  16% mortality  Emerging treatments by stool sample transplant Lecture 2 – Swallowing and the events that follow 1. Learn about the swallowing reflex The Cephalic Phase  Preparation of GI tract for a meal  Stimuli – cognitive, olfactory, visual  Auditory – classic conditioning experiments e.g. Pavlov o Pairing auditory stimulus to presentation of food; auditiory stimulus along  salivary secretion.  Activaiton of dorsal motor nucleus of the vagus (DMV) in brainstem. Neural components of cephalic phase Activation of the DMV leads to increased activity in parasympathetic efferent innervation of the GI tract  Salivary secretion (cranial nerve IX/glossopharyngeal nerve)  Gastric acid secretion (cranial nerve X/vagus nerve)  Pancreatic enzyme secretion (cranial nerve X)  Gallbladder contraction and relaxation of sphincter of Oddi (cranial nerve X) Mastication – Chewing  Teeth o Incisors and canines exert a cutting/tearing action o Molars perform a grinding function  Chewing reflex o Food in the mouth causes a reflex relaxation and dropping of the jaw. o Initiates a stretch reflex and rebound closure of the jaw. o The food bolus again activates relaxation and the cycle repeats.  Neural control is largely from the motor branch of the 5 cranial nerve (trigeminal) controlled by areas of the brain stem. Salivary gland locations 1. Parotid (next to ear) 2. Submandibular (under jaw) 3. Sublingual (under tongue) Functions of secretions Secrete 1.5L /day of saliva. Responsible for:  Lubrication, oral hygiene, neutralize pH, initiate carbohydrate digestion.  Composition: mostly water (99.5%), 0.5% electrolytes and organic compounds. Organic Composition of Saliva  Two major proteins: o α-amylase initiates carbohydrate breakdown. o Mucin glycoproteins act as lubricant and barrier.  Also present in small amounts: o Lingual lipase – initiates lipid breakdown. o Lactoferrin (antibacterial actions) o Lysozyme (antibacterial actions) o Muramidase (antibacterial actions) o Immunoglobulins (IgA) Salivary gland acinar cells  Serous acinar cells: secrete a watery product containing α-amylase but lacking mucins.  Mucus acinar cells: secrete a viscous product containing mucin glycoproteins. Stimuli for salivation  Salivatory nuclei in the brain stem  Positive stimuli for the salivatory nuclei include: o Taste and tactile stimuli from the tonge o Sight and small of food  Parasympathetic fibres stimulate secretion from salivary glad via muscarinic receptors. Control of salivary secretion Secretion from salivary acinar cells is primary under control of the autonomic nervous system.  Parasympathetic: acetylcholine (Ach) acting on muscarinic M receptors. 3  Sympathetic: noradrenaline (norepinephrine) acting on α- and β- receptor subtypes.  Some medications of anti-cholinergic actions that can block stimulation of saliva secretion leading to dry mouth (side effect). SWALLOWING Complex mechanism involving voluntary and involuntary phases as well as sharing of the upper airways. Phases of swallowing  Voluntary phase: oral – food moved by tongue pushing upwards and backwards towards pharynx.  Involuntary phases: o Pharyngeal – mechanoreceptors initiate closure of the trachea, relaxation of the upper esophageal sphincter (UES) and initiation of a primary peristaltic wave. Involves swallowing centre in medulla (brain stem) and several cranial nerves (vagus, trigeminal and glossopharyngeal). o Esophageal – conduction of food to the stomach is assisted by gravity, primary and secondary peristaltic waves, opening of the LES and receptive relaxation of the stomach. All of this involves local enteric neural reflexes and extrinsic parasympathetic reflexes. Step by step: 1) Swallowing centre inhibits respiratory centre in brain stem. 2) Elevation of uvula prevents food from entering nasal passages. 3) Position of tongue prevents food from re-entering mouth. 4) Epiglottis is pressed down over closed glottis as auxiliary mechanism to prevent food from entering airways. Regions of the stomach  Fundus: near the gastro-esophageal junction, mainly for storage.  Body: larges portion of the stomach and contains parietal and chief cells.  Antrum: most distal portion of the stomach, most endocrine cells are found in the antrum. Stomach anatomy  Surface area of the stomach increased by folds in wall – rugae.  Folds in the mucosa – glands and pits.  Glands contain several cell types: o Mucosa – mucus secreting o Parietal – acid secreting o Chief – pepsinogen secreting o Endocrine cells – hormone secreting Functional anatomy of the stomach  Oxyntic gland area o Body and fundus, upper 80% o Acid secreting parietal cells  Pyloric gland area o Atral region, lower 20% o Gastrin secreting G cells Mucous neck cells  Mucous neck cells secrete mucins – viscous and sticky glycoproteins.  Mucins are stored in large granulaes in the apical cytoplasm of the mucous neck cells.  Maintenance of the protective mucus layer requires continuous secretion of mucins. Surface epithelial cells  The surface epithelial cells are tall columnar epithelial cells.  Gastric epithelial cells secrete a watery fluid containing a high concnetraion of HCO .3-  The high HCO concnetration helps buffer the pH of the mucus layer. 3 -  Mucins and HCO tog3ther form a protective barrier that prevents acid and pepsins from damaging the gastric mucosa. Lecture 3 – The gastric phase of digestion Gastric mucosa Oxyntic mucosa  Lines the body and fundus of the stomach. These glands constitue 80% of the stomach and secret:  Acid (H , proton)  Pepsin (as pepsinogen) -  Mucus (and HCO ) 3  Intrinsic factor Pyloric mucosa  Lines the antrum of the stomach and secretes:  Mucus  Pepsinogen  Gastrin  Not acid Functions of Gastric Secretions  Acid (proton) o Required to convert pepsinogen to pepsin. o Bacteriostatic (stops bacterial growth) o Initiates digestion of protein together with pepsin.  Mucus lubricates and protects against physical damage.  Mucus plus HCO ma3ntains a near neutral pH at the lining of the stomach.  Intrinsic factor (IF) is critical for the absorption of vitamin B12 in the terminal small intestine (ileum). Parietal Cells  Parietal cells secrete both acid and intrinsic factor (required for absorption of Vit B12).  Parietal cells have a distinct triangular morphology with an abundance of mitochondria, intracellular vesicles and canalicular structures. Control of intrinsic factor secretion  Required for transport of vitamin B12. Uptake takes place in terminal ileum.  Lack of B12 leads to pernicious anemia.  Failure to secrete IF is associated with a lack ofk parietal cells and chlorydia (lack of acid secretion). Parietal cell acid production 1) Vesicles with proton pumps (H+/K+ ATPase) waiting for stimulation. 2) Mitochondria provide energy for active transport. 3) Proton pumps relocate to the cell membrane and pump H+ into lumen. 4) K+ channels exist in the apical membrane to return K+ to the lumen. 5) Carbonic anhydrase converts water and CO to H2and HCO 3- 6) HCO i3 exchanged for Cl- at the basal membrane. 7) Cl- leaves the cell through apical Cl- channels. Stimulation of gastric acid secretion Secretion of acid by parietal cells is stimulated by:  Acetylcholine released from the vagus nerve and enteric neurons acting through muscarinic M re3eptors o Can stimulate acid release directly or via gastrin and histamine release.  Gastrin is released from G cells in the antrum in response to acetylcholine. o Gastrin acts via gastrin-cholecystokinin receptors.  Histamine released from enterochromaffin-like cells acts through histamine H 2eceptors. o Histamine release can be stimulated by both gastrin and ACh. Digestive phases and regulation of gastric secretion 1) Cephalic phase via vagus 2) Parasympathetics excite pepsin and acid production 3) Gastric phase: a. Locat nervous ENS secretory reflexes. b. Vagal reflexes. c. Gastrin-histamine stimulation. 4) Intestinal phase: a. Nervous mechanisms b. Hormonal mechanisms Cephalic phase of acid secretion  20-30% of maximal secretory response to a meal  Occurs before food reaches the stomach  Driven by taste and smell through mechano- and chemoreceptors and by sight.  Mediated by branches of the Vagus o Parasympathetic nerve  Ach  gastrin  increased acid secretion  Has be studied by sham feeding (via oesophageal and gastric fistulas) Gastric phase of acid secretion  Greater than 50 of maximal secretory response  Food enters the stomach buffering the pH to approx. 6 which dis-inhibits gastring release (the brake is off).  Distension of the stomach walls via mechanoreceptors initiate short (ENS) and long (vago-vagal) reflexes.  G cells are also directly stimulated by digested protein (amino acids), calcium and caffeine (not blocked by vagotomy).  Gastrin release is: o Increased by gastrin-releasing peptide (GRP) from the ENS o Inhibited by release of somatostatin (SS) from the D cells Intestinal phase of acid secretion  Approx. 5% of maximal secretory response  There is evidence that amino acids contribute to gastrin release (from the intestinal mucosa) and possible a role for other unidentified hormones.  The intestinal phase is more important in inhibiting acid secretion and gastric emptying. Interdigestive phase of acid secretion  Acid secretion rate is approximate 10% of maximal secretory response.  Stomach contains a low volume of gastric juice at pH less than 2.0.  A low pH inhibits gastrin release from the G cells and thus limits excessive acid production. Inhibition of gastric secretion  Gastric luminal pH  Acid solutions in the duodenum  Digestive products in the duodenum  Hyperosmotic solutions in the duodenum  Secretion of acid by parietal cells is inhibited by the hormone somatostatin:  Somatostatin released from endocrine “D cells” in both the antrum and body regions of the stomach o Antral D cells are stimulated by low luminal pH o Antral somatostatin inhibits release of gastrin from G cells o Body D cells are stimulated by neural and hormonal mechanisms o Somatostatin can act on enterochromaffin like cells (ECL) to block histamine release or directly on parietal cells to block acid release. Chief Cells  Secrete pepsinogen but not acid.  Pepsinogen is activated by low pH (less than 3) and converted to pepsin.  Pepsins are endopeptidases that initiate protein digestion by hydrolysis. Control of pepsinogen secretion  Pro-enzyme released from peptic (chief) cells.  Strongest stimulus is vagally-mediated (via ENS and Ach release). Release will occur in the cephalic and gastric phases.  H+ stimulates a local enteric (ENS) cholinergic reflex to release pepsinogen.  Low pH 3-5 is required to activate pepsin (and pepsin will activate pepsin) and greater than pH 5 is inhibitory. Motor functions of the stomach 4 events in the process of gastric filling and emptying: 1) Receiving and providing temporary storage of foods and liquids. 2) Mixing of food and liquid with gastric secretory products including pepsin and acid. 3) Grinding of food to reduce particle size to enhance digestion and permit passage through the pylorus. 4) Regulating the exit of material from the stomach into the duodenum. Neurally-mediated relaxation of (upper) stomach  Accommodation: food volume increases without pressure increases.  Depends on parasympathetic input to enteric nerves.  Vagotomy was used as a weight loss strategy. Pyloric region of the stomach  Contributes to the mechanical reduction of particle size and mixing  Movements have three stages o Propulsion: bolus is pushed toward the pylorus. o Grinding: the antrum churns the trapped material. o Retropulsion: bolus is pushed back into the proximal stomach.  All together this is called the “pyloric pump” Content of meal influences rate of gastric emptying The rate is greater if the meal is: -Liquid, non-nutrient, carbohdrate > protein > fat, neutral > acid. Regulation of gastric emptying Promotes Emptying Inhibits emptying -Gastric chyme volume Cholecystokini (CCK) Enterogastric reflexes Distension or irritation of duodenum, protein and fat digestion products. Protective mechanisms Esophageal protective mechanisms for resisting the corrosive effects of acid:  A certain amount of acid reflux is normal while excess exposure can be damaging.  Saliva acts to neurtralize acid.  Protective action of mucus.  Barrier function of the lower esophageal sphincter. Helicobacter pylori and gastric ulcers  Only known bacteria that can thrive in acidic environment of the stomach.  Estimated 66% of worlds population are infected with H. pyloria. o 70% are asymptomatic. o Symptomatic people develop stomach ulcers.  H. pylori excretes the enzyme urease o Urea ---urease---> (NH3 + HCO3-)  A ‘basic cloud’ protects the bacteria from the acidic stomach environment but the ammonia is toxic to the gastric epithelial cells.  H. pylori also produces other enzymes including protease, catalase and phospholipases - damage gastric cells initiating an inflammatory response. Helicobacter pylori and gastric ulcers  Antibiotic therapy now common.  Standard ulcer therapy is triply therapy: o Amoxocillin o Clarithromycin o Omeprazole (proton pump inhibitor to reduce acid damage during healing)  Other treatments include histamine (H2) receptor antagonists. Lecture 4: Small Intestinal Physiology 1 Objectives  Understand how structure and function of the small intestine are linked.  Appreciate the different type of small intestinal motility.  Understand the roles of the pancreas in nutrient digestion. Major functions of the small intestines  Movement of food (mixing and propulsion)  Absorption of nutrients is the main function of the small intestine.  The small intestine absorbs nutrients after extensive digestion by luminal and brush border enzymes. Anatomical divisions of the small intestine  The small intestine (bowel) o Duodenum (first 5%) o Jejunum (middle 40%) o Ileum (final 55%)  The bile and pancreatic ducts enter the small intestine in the duodenum (ampulla of Vater)  Absorption of nutrients is the major function of the small intestine (mostly in jejunum and ileum) Surface are for nutrient digestion and absorption is maximized  Inner surface contains folds (plicae circulares) on which villi are positioned.  Each enterocyte is lined by a “brush border” containing microvilli.  Actin filaments allow for movement. What determines the movement patterns of the GI tract?  Optimal time of exposure to various segments of the GI tract is essential for effective digestion and absorption.  Motility provides both mixing and propulsion.  GIT function is highly regulated by neural, hormonal, local chemical and physical factors. ‘Slow waves’ in smooth muscle  Smooth muscle shows continual oscillations in membrane potential called “slow waves”. o Frequency decreases down the intestine:  3/min in stomach  12/min in duodenum, 8/min in ileum, 3/min in colon  Thus there is a gradient from top of the small I. to large I. o Peridically the slow waves give rise to “spike potentials”  These are slow Ca++ mediated action potentials (APs). o This increases cytoplasmic Ca++ and gives rise to smooth muscle contraction. Generation of slow waves  Interstitial cells of Cajal (ICC) o Contained within the smooth muscle layers. o Some ICC act as pacemakers.  Contain specialized ion channels that underlie this activity. o Other ICC transfers excitability to the smooth muscle cells.  Act through gap junctions.  Spread the excitation more widely. Tonic contractions  Suited to the function of sphincters  Underlying electrical activity can be either: o Repetitive spike potentials o Sustained depolarization o “Latching”  May need inhibitory transmission (ATP, NO, VIP) to relax some smooth muscle. Ileocacal sphincter controls movement of chyme from small to large intestines 1) Pressure and chemical irritation relax sphincter and excite peristalsis 2) Fluidity of contents promotes emptying 3) Pressure or chemical irritation in cecum inhibits peristalsis of elium and excites sphincter. Peristalsis A wave-like movement of muscles in the GI tract, characterized by the alternate contraction and relaxation of the muscles that propel the contents downward.  Mediated by the local, intrinsic enteric nerves (ENS) and is not affected by vagotomy or sympathectomy.  Moves contents down the GIT. Segmentation contractions A non-propulsive mixing motility seen especially in the small intestine. Segmental rings of contraction chop and mix the ingested materials to enhance digestion. Fasting patterns of motility: MMC  Fasting state exhibits the Migrating Motility Complex (MMC).  Contractile wave periodically moving down the GI tract from the mid- stomach to the ileum and on to the colon.  Housekeeper function.  Associated with increased levels of the motilin.  Interrupted by feeding. Digestion in the small intestine  Breakdown of nutrients/macromolecules to enable transport to bloodstream. o Enzymatic digestion o Sugar, protein and fats o Pancreatic enzymes are key Functional roles of the pancreas  Pancreas has both endocrine and exocrine functions  Endocrine functions: important for metabolic control (insulin production)  Exocrine functions: important for gastrointestinal function. Pancreatic digestive enzyme secretion  Pancreas has the highest rate of protein secretion of any organ.  Each day the pancreas delivers 5-15g of protein to the small intestine.  The pancreas secretes over 20 proteins.  Most of these proteins are digestive enzymes secreted in an inactive form. Secretin and the birth of endocrinology  Pavlov believed that the pancreas was exclusively regulated by the nervous system.  Bayless and Starling denervated the pancreas and still observed pancreatic secretions in response to acid.  Removed mucosa, stimulated with acid, collected supernatant o Supernatant caused pancreatic secretion o Active ingredient “secretin”, the first hormone.  The lesson, as always: beware dogma. Structure of pancreatic exocrine glands  Exocrine glands are made up of acini which are clusters of cells that synthesize and secrete protein (e.g. enzymes) into the ducts.  The acini contain secretory acinar cells while the ducts contain duct epithelial cells which secrete bicarbonate. - Pancreatic HCO sec3etion 1. H 2 diffuses across the cell membrane, CO is 2ormed as a by-product of cellular metabolism. 2. Cytoplasmic carbonic anhydrase (CA) catalyses the conversion of CO and 2 - - + OH to HCO an3 H . 3. H leaves the cell via the basal Na /H exchanger. 4. HCO se3retion into the duct lumen occurs via the Cl /HCO exchanger3- - - 5. Outward rectifying Cl channels in the apical membrane return the Cl into the lumen. 6. Na /K ATPase removes the accumulating Na +. Composition of pancreatic juice  Two distinct components of pancreatic juice: o Duct cells: watery alkaline secretion rich in HCO . 3- o Acinar cells: digestive enzymes.  Pancreatic HCO ac3s to neutralize the acidic stomach contents as they enter the small intestine.  Pancreatic digestive enzymes complete the digestion of protein, carbohydrates and fats o Broken down into small constituent molecules that can be absorbed. Pancreatic digestive enzymes  Protein digestion o Trypisonigen enteropeptidase Trypsin o Chymotrypsinogen trypsin Chymotrypsin o Procarboxypeptidase trypsin Carboxypeptidase  Carbohydrate digestion o Pancreatic amylase  Fat digestion o Pancreatic lipases Proenzyme/active Activating agent Product enzyme TRYPSINogen Enteropeptidase Peptides CHYMOTRYPSINogen Trypsin Peptides ProELASTASE Trypsin Peptides ProCARBOXYPEPTIDASE B Trypsin Amino acids Phase Stimulant Regulatory Pathway % of max secretion Cephalic Sight, small, taste,Parasympathetic 25 (head) mastication Gastric Distension Parasympathetic, hormones, H + 10-20 (stomach) Intestinal Amino acids, fatty Intestinal hormones (e.g. secretin 50-80 acids, H & cholecystokinin) Digestive Enzymes Lecture 5 Small Intestinal Physiology II – Nutrient digestion/absorption Objective: Understand how nutrient components of a meal are digested/absorbed. Carbohydrates in the diet  60% complex carbohydrates – starch  30% disaccharides – sucrose and lactose  10% monosaccharides – glucose and fructose Monosaccharides can be absorbed across the small intestine epithelium therefore for most of the carbohydrate in the diet digestion has to take place first. Digestion of carbohydrate  Takes place in the lumen of the gut.  Luminal digestion of starch to disaccharide by salivary and pancreatic amylases.  Further broken down by the action of amylases that are expressed by the cells themselves. Brush border digestion of disaccharides to monosaccharides by  Sucrose  sucrase  glucose  fructose  Lactose  lactase  glucose  galactose  Maltose  maltase  2 glucose Enzymes for CHO digestion Absorption of carbohydrates The monosaccharide products of carbohydrate digestion (glucose, fructose, galactose) are absorbed by the small intestine in a two-step process. 1) Across the apical cell membrane a. Glucose and galactose i. Na+/glucose co-transporter (SGLT1) b. Fructose facilitated sugar transporter (GLUT5) 2) Across the basal cell membrane Monosaccharide absorption Abnormalities of CHO digestion or absorption Lactose intolerance: genetic or acquired conditions where the enzyme lactase is deficient. NOT an allergy. Controlled by dietary modification or exogenous enzymes.  Lactose = “milk sugar” o o  Lactose accumulates in the gut o Acts as an osmolyte (osmotic laxative – traps water in lumen) o Acts as nutrient for bacteria o Accumulation of gas and water lead to irritation, bloating, diarrhea. Lactose intolerance is actually a deficiency of the enzyme lactase. ot enough lactase to break lactose into glucose and galactose. The excess lactose then acts as an osmotic stimulant. It can also act as a substrate for bacterial growth leading to bacterial overgrowth that can produce gas. This leads to feelings of bloating and diarrhea. Protein in the diet  The protein requirements of the body o Adult 0.6g/kg body weight per day; child 3-4g/kg body weight/day  Average diet – 90g protein per day o 10-30g from gastrointestinal secretions including proteases produced by pancreas. o 3g albumin. o Stomach production of pepsin.  During first six months of life some protein uptake by phagocytosis (passive immunity from mother to child). Digestion of protein 4 major pathways: 1) Luminal proteases from the stomach and small intestines can hydrolyse proteins to peptides and amino acids (30%). 2) Brush border enteropeptidase digest the peptides to amino acids. 3) Peptides are absorbed and broken down to individual amino acids by cytoplasmic peptidase. 4) Peptides are absorbed and cross directly into the blood stream. Absorption of amino acids 1) Across apical cell membrane a. Na+ dependent amino acid co-transporter b. H+ dependent peptide co-transporter 2) Across basal cell membrane a. Mainly an amino acid co-transporter which is Na+ INdependent Apical transport of amino acids Amino acids  At lease 7 transport systems in the apical membrane. o For groups of amino acids (e.g. acidic/basic amino acids).  The pre-dominant amino acid transporter is the Na+-dependent amino acid co-transporter. o Driven by the inward directed Na+ gradient. Small peptides (3-6 amino acids)  Small peptide uptake occurs via the H+/peptide co-transporter (Pept1) o An active process driven by the H+ gradient. o Most small peptides are broken down in the enterocyte by cytoplasmic peptidases to single amino acids. Basal transport of amino acids o 90% of absorbed amino acids
More Less

Related notes for PHGY 214

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.