Digestion

bicarbonate

bicarbonate neutralizes acidic chyme, we do not want to injure the cells that make up our small intestine due to the acidic chyme . . . bicarbonate is secreted by pancreatic duct cells, once bicarbonate reaches the pancreatic duct it will travel until it reaches the common bile duct, where it will then empty into the duodenum through the sphincter of Oddi (where acidic chyme needs to be neutralized)

chief cell

chief cell - epithelial cell part of gastric gland of stomach, secrete pepsinogen (pepsin precursor, breakdown of protein), secrete lipase (breakdown of fats) . . . pepsinogen secretion occurs during both cephalic and gastric phases (enteric input) and works in conjunction with parietal cells . . . chief cells are found associated with parietal cells (numerous in the fundus and body regions of the stomach, not so much in antrum)

G-cell

G-cell - enteroendocrine cell part of gastric gland of stomach, responsible for release of gastrin (hormone) . . . G-cells are numerous in antrum region of stomach (especially near pyloric sphincter) as well as the duodenum, stimulated by enteric input GRP

bicarbonate

bicarbonate secretion (pancreatic duct cell): 1.) carbon dioxide and water combine to form carbonic acid, catalyzed by carbonic anhydrase . . . 2.) carbonic acid will disassociate into H+ and bicarbonate . . . 3.) lumenal Cl/bicarbonate exchanger will move bicarbonate into pancreatic duct and Cl- back into cell . . . 4.) the cAMP-dependent CFTR transporter allows the facilitated diffusion of Cl- back into the pancreatic duct . . . 5.) basolateral H/Na exchanger will move H+ out of cell (into interstitial fluid --> capillary network) and move Na into cell . . . 6.) basolateral Na/K-ATPase pump keeps intracellular Na levels low to allow for continued use of exchanger (by pumping out Na, pumping in K) . . . 7.) basolateral K-leak channel restocks extracellular K

somatostatin

somatostatin = inhibitory (decrease number of H/K-ATPase pumps), works by way of blocking production of cAMP . . . somatostatin is released by D-cells in response to increased H+, duodenum stretching, and presence of nutrients in duodenum: 1.) somatostatin will directly decrease acid secretion of parietal cells (by work of decreasing number of H/K-ATPase pumps) . . . 2.) somatostatin also inhibits G-cells, which will decrease their release of gastrin (indirectly decreasing acid secretion)

D-cell

D-cell - enteroendocrine cell part of gastric gland of stomach, responsible for release of somatostatin (in this case, acts as paracrine molecule) . . . D-cells are numerous in antrum region of stomach (especially near pyloric sphincter) as well as the duodenum, they are closely associated with G-cells because paracrine agent somatostatin acts locally

lipid digestion

lipid digestion (small intestine): 1.) large, insoluble fat droplets enter small intestine from stomach . . . 2.) gallbladder will begin to release bile . . . 3.) bile will help break up and emulsify fat droplets . . . 4.) lipase will then begin to work on the fringes of the emulsified fat droplets (break down triglycerides) . . . 5.) as monoglycerides and free fatty acids are spit out, they will form very small micelles . . . 6.) lipase will continue to act on micelles to assure that all triglycerides are broken up (can't be absorbed until triglyceride is broken up) . . . 7.) cholesterol is also released as lipase is doing its job on emulsified fat droplets . . . 8.) monoglycerides, free fatty acids, and cholesterol move into cell (cholesterol needs channel, while both monoglycerides and free fatty acids diffuse across membrane) . . . 9.) smooth ER recombines monoglyceride and two fatty acid tails into triglyceride, also aids in the creation of the chylomicron (triglycerides, cholesterol, and protein) . . . 10.) chylomicrons are put into vesicles within Golgi . . . 11.) chylomicrons will undergo exocytosis into interstitial fluid, where they enter lacteal-component of lymphatic system . . . 12.) lymph will re-enter bloodstream carrying chylomicrons . . . 13.) chylomicrons will be broken down by into components by lipases within bloodstream

lipid digestion

lipid digestion - the smooth ER will recombine the monoglyceride and two fatty acid tails into triglyceride, and aid in the creation of the chylomicron (triglycerides, cholesterol, and protein) . . . the Golgi will put chylomicrons into vesicles so that they can undergo exocytosis out of cell - chylomicrons are large, they cannot diffuse into capillary but rather they'll enter lacteal (portion of lymphatic system) . . . eventually chylomicrons will be deposited into circulatory system, where they will be broken back down into monoglycerides, fatty acids, and cholesterol (lipases in bloodstream break down chylomicron)

lipids

lipids - 30% caloric intake, lipids are completely insoluble in water thus lipids aggregate into large insoluble droplets . . . lipase is water soluble and can only act upon the surface of lipid droplets = VERY SLOW digestion . . . bile is solution to lipid digestion - it increases surface area of lipid droplets, increasing the effectiveness of lipase

gastric emptying

regulating gastric emptying - long neural reflex sends signals to brain that we need to slow down gastric emptying, which will in turn increase the activity of sympathetic efferent neurons while decreasing activity of parasympathetic efferent neurons (increasing sympathetic neurotransmitter output while decreasing parasympathetic neurotransmitter output) . . . sympathetic input to enteric nervous system is inhibitory, while parasympathetic input to enteric nervous system is excitatory

gastric emptying

regulating gastric emptying - short neural reflex sends signals directly to stomach via the enteric nervous system, these signals culminate in inhibitory transmitters that will reduce contractile force of stomach

gastric emptying

regulating gastric emptying - when there is the presence of chyme within the duodenum, not only will factors activate neural receptors but these factors will also activate the secretion of enterogastrones . . . enterogastrones are hormones secreted by enteroendocrine cells of the mucosa of the duodenum, they enter bloodstream and will target smooth muscle cells of stomach, tell stomach to slow down digestion by slowing down gastric emptying (decrease gastric motility)

gastric emptying

regulating gastric emptying - when we slow digestion by decreasing gastric emptying, we maximize the time that chyme is spent within the duodenum so we have plenty of time to neutralize that acid . . . this also increases time to allow for breakdown of amino acids, fats, sugars (give digestive enzymes times to do their jobs) - this maximizes intestinal digestion

bicarbonate

regulation of bicarbonate secretion (pancreatic duct cell) - presence of acid in duodenum is primary trigger for secretion: 1.) increased acidic chyme output from stomach . . . 2.) increased H+ is detected by S-cells of duodenum . . . 3.) S-cells secrete secretin in response . . . 4.) secretin will travel through bloodstream and target smooth muscle cells of stomach (decrease gastric motility = decrease gastric emptying) . . . 5.) secretin will also target pancreas and induce the increased secretion of bicarbonate

carbohydrate digestion

carbohydrate digestion - occur in ileum and jejunum of small intestine, epithelial cells have transporters that readily absorb monosaccharides from lumen: 1.) fructose = GLUT-5 unitransporter within lumenal membrane, fructose will utilize GLUT-2 unitransporter in basolateral membrane to be transported into interstitial fluid and taken-up by capillary network surrounding small intestine . . . 2.) glucose, galactose = SGLT (sodium-glucose cotransporter), both sugar and Na pumped into epithelial cells (basolateral Na/K-ATPase pump keeps intracellular Na levels low, keep the SGLT cotransporter active), both galactose and glucose will utilize GLUT-2 unitransporter in basolateral membrane to be transported into interstitial fluid and taken-up by capillary network surrounding small intestine

carbohydrate digestion

carbohydrate digestion: 1.) ingestion of polysaccharide . . . 2.) pancreatic amylase (via common bile duct) within lumen of small intestine will break down polysaccharide into disaccheride maltose . . . 3.) ingestion of other disaccherides like sucrose and lactose (also include maltose) . . . 4.) brush border enzymes, bound to lumenal membrane of epithelial cells, will breakdown any disaccheride within lumen of small intestine (maltase = maltose, sucrose = sucrase, lactose = lactase) . . . 5.) brush border enzymes convert disaccharides into absorbable monosaccharides . . . 6.) fructose will utilize lumenal GLUT-5 unitransporter to get into intestinal epithelial cell, glucose and galactose will utilize lumenal Na-glucose cotransporter (SGLT - both sugar and Na pumped into epithelial cells) . . . 7.) basolateral Na/K-ATPase pumps remove intracellular Na, basolateral K-leak channel facilitates diffusion of K out of cell . . . 8.) all three monosaccharides utilize basolateral GLUT-2 unitransporter (interstitial fluid --> capillaries)

retropulsion

retropulsion = gastric emptying - pyloric sphincter valve opens due to vigorous peristaltic muscle contractions reaching muscular antrum, some chyme is projected into duodenum while other chyme is projected backwards (stimulates mixing) . . . beginning of intestinal phase, mechanisms following gastric emptying inhibit further muscle contractions and close pyloric sphincter

secretin

secretin - enterogastrone, hormone secreted by enteroendocrine S-cells of duodenum, S-cells are responsible for detecting decreases in pH (increases in amount of hydrogen ions) - presence of acidic chyme in duodenum via gastric emptying . . . secretin will: 1.) inhibit gastric motility, 2.) stimulate production and secretion of bicarbonate from pancreatic duct cells (regulate pH of duodenum)

carbohydrates

carbohydrates - represent 50-60% of caloric intake, the larger the sugar molecule the increased need for its digestion . . . monosaccharides can be absorbed by epithelium cells without their breakdown (include glucose, galactose, and fructose) . . . disaccharides - must be broken down by brush border enzymes into monosaccharide units before being absorbed, include sucrose (fructose-glucose), maltose (glucose-glucose), lactose (galactose-glucose) . . . polysaccharides - must be broken down via pancreatic amylases, include starch (plants) and glycogen (glucose storage units), but cellulose cannot be digested

cephalic phase

cephalic phase - begins when you smell, taste, think, see food (any external stimuli that tells system to prepare of food) . . . response is the secretion of gastric juices in preparation for digestion (secretion of mucus, acid, pepsinogen, and hormones/paracrines that promote acid secretion like gastrin and histamine) = feed forward (positive feedback) . . . strictly neural control (parasympathetic --> enteric nervous systems)

CCK

cholecystokinin (CCK) - enterogastrone, hormone secreted by enteroendocrine I-cells of duodenum, I-cells are responsible for detecting the increasing presence of fats and amino acids - signifies presence of chyme in duodenum . . . CCK will: 1.) inhibit gastric motility, 2.) increase pancreatic enzyme secretion, 3.) increase bile secretion

vitamin absorption

vitamin absorption - most vitamins will be readily absorbed with lipids (they are lipid soluble, so they'll be packed into chylomicrons) . . . vitamin-B12 is exception - it is water soluble, cannot be dissolved inside chylomicron (it is also fairly large) . . . you get B12 from animal products (always associated with proteins) . . . vitamin-C is other exception, because it is hydrophilic - on ileal cells, there are Na/vitamin-C cotransporters

vitamin-B12 absorption

vitamin-B12 absorption (components): 1.) R-binder - secreted by salivary glands, binds to B12 within stomach to protect it from acid degradation . . . 2.) intrinsic factor - released by parietal cells of stomach, will bind to free B12 within duodenum after R-binder has been degraded by pancreatic proteases . . . 3.) transcobalamin-2 - protein associated with B12 when in bloodstream, cells that need B12 have transcobalamin-2 receptors to recognize B12

digestion

digestion - three phases, include cephalic, gastric, and intestinal . . . each phase is named where stimuli is initiated (neural regulation - inputs from both parasympathetic and sympathetic nervous systems, as well as enteric nervous system)

digestive enzyme regulation

digestive enzyme regulation: 1.) increases in fatty acids and amino acids within duodenum . . . 2.) increased secretion of CCK from I-cells (circulating hormone) . . . 3.) increases in plasma CCK . . . 4.) CCK will bind to pancreatic duct cells . . . 5.) increased pancreatic secretion of digestive enzymes . . . 6.) CCK will also target sphincter of Oddi (opening of common bile duct into duodenum) - CCK will induce relaxation of this sphincter = decreasing resistance to flow of bile into duodenum . . . 7.) relaxation of the sphincter of Oddi makes it easier for pancreatic enzymes and other secretions to reach duodenum . . . 8.) increased digestion within small intestine

ECL cell

enterochromaffin-like cell (ECL) - enteroendocrine cell part of gastric gland of stomach, secrete histamine that acts as paracrine agent . . . they are found near parietal cells (fundus and body portions of stomach) because histamine acts as a paracrine agent for parietal cells, inducing their secretion of acid . . . they are stimulated by both enteric input acetylcholine and gastrin

mucus cell

foveolar (mucus) cell - epithelial cell part of gastric gland of stomach (distinguishable from goblet cells of intestine), secrete mucus to protect stomach from acid . . . whenever stomach is secreting acid, it will also secrete mucus (numerous in every region of stomach)

gastric emptying

gastric emptying - cells within duodenum are capable of detecting hydrogen ions, fats, amino acids, osmolarity (glucose), and stretch (any of these factors will stimulate entergasterone secretions and neural receptors) . . . all these factors tell system that there's food entering duodenum (small intestine) = we need to slow down digestion by slowing down gastric emptying

gastric emptying

gastric emptying - moving chyme into duodenum during the intestinal phase of digestion, coincides with retropulsion (when peristalsis reaches muscular antrum and pyloric sphincter is forced open)

gastric gland

gastric gland of stomach - made up of two cell types: 1.) epithelial cells - parietal, mucus, and chief cells . . . 2.) enteroendocrine cells - ECL-, G-, and D-cells . . . includes two types of glands: fundus (upper portion of stomach) and pyloric (lower portion of stomach)

GIP

gastric inhibitory peptide (GIP) - enterogastrone, hormone secreted by enteroendocrine K-cells, K-cells are responsible for detecting increasing osmolarity of fluid within lumen of duodenum (increasing osmolarity is caused by increases in glucose), K-cells are also capable of directly detecting carbohydrates . . . GIP will inhibit gastric motility (target smooth muscle cells of stomach)

gastric motility

gastric motility - peristaltic gastric contractions, driven by muscular antrum, allow for the: 1.) crushing, grinding, and mixing of food into chyme, 2.) movement of chyme into duodenum (gastric emptying) . . . occurs in three phases: propulsion, grinding, and retropulsion

gastric phase

gastric phase - when food enters stomach, two things will happen to stimulate this phase: 1.) stretch of the stomach, 2.) increase in pH of stomach (food neutralizes acid) . . . acid and enzyme secretion, and gastric mixing (mechanical digestion) . . . neural control, endocrine control (gastrin), and paracrine control (histamine)

gastrin

gastrin = stimulatory (increase number of H/K-ATPase pumps), work by way of IP3 pathway . . . release of gastrin-releasing peptide (GRP) via enteric nervous system during cephalic and gastric phases onto G-cell induces release of gastrin, gastrin will first circulate through bloodstream before targeting and activating parietal cells . . . G-cells are also stimulated by the decreasing concentration of H+ (due to food neutralizing stomach acid) and by increasing nutrient concentrations - both situations during gastric phases

grinding

grinding - vigorous peristalsis mixes food inside stomach if pyloric sphincter is closed (peristalsis waves reach antrum, very muscular portion of stomach) . . . mechanical digestion, also aids chemical digestion by mixing concoction of enzymes and food up = increases surface area for reactions

histamine

histamine = stimulatory (increase number of H/K-ATPase pumps), work by way of cAMP pathway . . . release of acetylcholine via enteric nervous system onto ECL-cells induce release of histamine, histamine remains local and acts as paracrine agent (ECL cells are closely associated with parietal cells within gastric glands)

intestinal phase

intestinal phase - when food (chyme) starts to leave stomach and enter duodenum, characterized by secretion of bile and secretion of enzymes from pancreas . . . controlling how fast food will leave stomach and enter duodenum . . . neural control, endocrine control, paracrine control

lipase

lipase - can only do its job if it is in the same compartment as the fat droplet (lipase is soluble in aqueous, so bile makes fat droplets soluble in aqueous environment as well) . . . lipase comes from pancreas, it converts triglycerides into monoglycerides and two fatty acids (in turn form little micelles) - we can absorb these two broken-down components . . . colipase is an enzyme that helps lipase find and bind with emulsified fat droplets

vitamin-B12 absorption

vitamin-B12 absorption: 1.) B12 enters system attached to proteins . . . 2.) R-binder, produced by salivary glands, follows B12 protein-complex into stomach . . . 3.) pepsin will break bond between B12 and protein (breaks down protein) . . . 4.) R-binder will then find and bind B12 (protects it from degradation from stomach acids) . . . 5.) intrinsic factor is released by parietal cells, both intrinsic factor and R-B12 complex will travel out of stomach and into duodenum . . . 6.) proteases secreted by pancreas will break down R-binder, thus B12 will be released within duodenum . . . 7.) intrinsic factor will then bind to B12 within the small intestine . . . 8.) IF-B12 complex will be recognized by ileal cells (of ileum), binding of intrinsic factor complex to receptors will induce endocytosis of the entire IF-B12 complex . . . 9.) lysozymes within ileal cell will separate intrinsic factor from B12 . . . 10.) B12 will then be transported into bloodstream, where it will be found associated with protein transcobalamin-2 (80%) . . . 11.) cells that need B12 will have receptors for transcobalamin-2

propulsion

propulsion - peristaltic waves move food from esophagus into fundus and then into body of stomach and then into the antrum and then up against the pyloric sphincter (the pyloric valve is closed) . . . rhythmic peristalsis is set by pacemaker (Cajal) cells of the longitudinal muscles lining the stomach

acetylcholine

acetylcholine = stimulatory (increase number of H/K-ATPase pumps), work by way of IP3 pathway . . . dumped directly onto parietal cell from enteric nervous system (enteric nervous system is active by way of parasympathetic input)

acid regulation

acid regulation - parietal cells have many receptors: 1.) gastrin = stimulatory (increase number of H/K-ATPase pumps), work by way of IP3 pathway . . . 2.) histamine = stimulatory (increase number of H/K-ATPase pumps), work by way of cAMP pathway . . . 3.) acetylcholine = stimulatory (increase number of H/K-ATPase pumps), work by way of IP3 pathway . . . 4.) somatostatin - inhibitory (decrease number of H/K-ATPase pumps), work by way of blocking production of cAMP

acid regulation

acid regulation - the number of parietal H/K-ATPase pumps is the best way to regulate acid production and secretion (parietal cells house vesicles with large number of H/K-ATPase pumps) . . . to increase acid secretion we want to induce fusion of vesicle with lumenal membrane of parietal cell / to reduce acid secretion we want to make sure fusion of vesicle with lumenal membrane never happens

acid secretion

acid secretion (parietal cell): 1.) carbon dioxide and water combine to form carbonic acid catalyzed by carbonic anhydrase (carbon dioxide can diffuse from bloodstream into parietal cell, or carbon dioxide results from breakdown of amino acid arginine within cell) . . . 2.) carbonic acid disassociates rapidly to generate H+ and bicarbonate . . . 3.) cytosolic H+ will be moved into lumen of stomach by way of H/K-ATPase pump (hydrolysis of ATP is coupled with anti-transport of H+ out of cell and K+ into cell) . . . 4.) lumenal K-leak channel allows K+ to get back to lumen of stomach so that we can continue to utilize pump . . . 5.) basolateral Cl/bicarbonate exchanger will move bicarbonate out of cell and Cl- into cell (local blood will become more basic = alkaline tide) . . . 6.) lumenal Cl-leak channel will facilitate diffusion of Cl- into lumen of stomach

acid secretion

acid secretion - cephalic and gastric phases of digestion via parietal cell (goal of system is to get HCl into lumen of stomach) . . . good source of bicarbonate is reaction catalyzed by carbonic anhydrase, basolateral Cl-/bicarbonate exchanger can be utilized to couple movement of bicarbonate out of cell and movement of Cl- into cell (local blood will become more basic = alkaline tide) . . . once Cl- is inside cell, it can be transported into lumen of stomach driven by facilitated diffusion offered by Cl-leak channels (H+ is being transported into lumen of stomach as well = HCl)

acid secretion

acid secretion - we want it when we are expecting food (cephalic phase), when we are digesting food (stretching of stomach during gastric phase), and when there's a decrease in lumenal H+ content (presence of food in stomach during gastric phase) . . . cephalic and gastric phases

acid secretion

acid secretion: we want to inhibit acid secretion during the intestinal phase - we are trying to neutralize chyme, so as food is entering duodenum we want to stop acid secretion (when duodenum begins to stretch, that will send signals to block enteric nervous system and strangle release of stimulatory signals onto parietal cells) . . . with the passage of acidic chyme into duodenum, if a decrease in pH is observed than that will serve as signal to halt acid secretion, presence of fats and amino acids within duodenum is also detected and used as indicator to halt acid secretion (slows down gastric emptying)

bicarbonate

bicarbonate production in pancreatic duct cells counter the alkaline tide generated by the parietal cells - parietal cells generate bicarbonate and H+, and transport H+ into lumen of stomach while transporting bicarbonate into interstitial fluid --> capillaries (local basicity) . . . blood that has undergone alkaline tide will be basic, this is neutralized by basolateral H/Na exchanger of pancreatic duct cells (pump H+ into interstitial fluid --> capillaries)

bile

bile - made in liver and stored in gallbladder, composed of bile salts and phospholipids . . . bile will emulsify lipid droplets, breaking them down into smaller units and increasing surface area available for water soluble lipases to act on them (bile salts have both polar and nonpolar sides, allow emulsified droplets to be soluble in water -nonpolar side associates with lipid droplet, polar side faces outward) . . . association of bile salts with lipid droplets allow little droplets to be present in water without reforming huge aggregations (increasing surface area for lipase to do its job)

bile secretion regulation

bile secretion regulation: 1.) increases in fatty acids and amino acids within duodenum . . . 2.) increased secretion of CCK from I-cells (circulating hormone) . . . 3.) increases in plasma CCK . . . 4.) CCK will target and induce contraction of the gallbladder = squeezing out bile . . . 5.) CCK will also target sphincter of Oddi (opening of common bile duct into duodenum) - CCK will induce relaxation of this sphincter = decreasing resistance to flow of bile into duodenum . . . 6.) relaxation of the sphincter of Oddi makes it easier for pancreatic enzymes and other secretions to reach duodenum . . . 7.) increased bile within small intestine (facilitated by gallbladder contractions and sphincter of Oddi relaxation) allows for lipid digestion

nucleic acid digestion

nucleic acid digestion - pancreatic nucleases break up RNA and DNA into nucleotides, this nucleotides are further broken up into their respective components (nitrogenous bases, sugars, phosphates) . . . products are recycled for reuse rather than utilized for energy

protein digestion

protein digestion: 1.) proteins are ingested . . . 2.) pancreas secretes trypsinogen . . . 3.) trypsinogen is cleaved into active protease enzymes trypsin and chymotrypsin by lumenal brush border peptidases . . . 4.) active proteases break down proteins into amino acids and small peptides . . . 5.) small peptides are either cotransported into cell with H+ or cleaved into single amino acids by lumenal brush border peptidases (basolateral Na/H exchanger keeps intracellular H+ low) . . . 6.) single amino acids are cotransported into cell with Na+ (basolateral Na/K ATPase pumps keep intracellular Na+ low) . . . 7.) intracellular small peptides are cleaved into single amino acids by peptidases . . . 8.) basolateral amino acid unitransporters facilitate diffusion of single amino acids out of cell (interstitial fluid --> capillaries)

proteins

proteins - 15-20% caloric intake, occur in ileum and jejunum of small intestine, epithelial cells have variety of basolateral amino acid transporters facilitate diffusion into interstitial fluid, taken up by capillaries (only single amino acids can leave epithelial cells) . . . 1.) single amino acids can be readily absorbed by intestinal epithelial cells (cotransported into cell from lumen with Na = Peptide type-1, Na driven down concentration gradient generated by basolateral Na/K ATPase pumps) . . . 2.) small peptides can also be cotransported into epithelial cells alongside H+ and then broken down into amino acids by intracellular peptidases (basolateral Na/H exchanger keeps intracellular H+ concentration low)

gastric emptying

regulating gastric emptying - cells of duodenum stimulate neural receptors, receptors can send signals either directly to the stomach via the enteric nervous system or to the central nervous system (short vs. long neural reflexes), which will in turn alters signals to stomach . . . both reflexes culminate in telling stomach to slow down digestion by slowing down gastric emptying (slow down muscular contractions in stomach by decreasing gastric motility, prevent pyloric valve from opening)

protein digestion

pancreatic proteases in lumen of small intestine breakdown proteins: 1.) trypsin - cleave proteins at arginine and lysine sites, 2.) chymotrypsin - cleaves proteins wherever there's an aromatic ring . . . pancreas secretes trypsinogen, precursor enzyme will be cleaved into active trypsin and chymotrypsin proteases by brush border peptidases (bound to lumenal membrane of small intestinal epithelial cells)

parietal cell

parietal cell - epithelial cell part of gastric gland of stomach, produce and secrete acid, also responsible for intrinsic factor (absorption of vitamin B12) . . . numerous in the fundus and body regions of the stomach, not so much in antrum (highly regulated - inputs from paracrine substances, hormones, and enteric input)

pepsinogen

pepsinogen - released by chief cells during cephalic and gastric phases, important for breakdown of proteins into peptides (pepsinogen does not have enzymatic activity itself, it must be cleaved into pepsin which in turn has enzymatic activity to break proteins down - once pepsin is in system, it will break pepsinogen down into pepsin = positive feedback loop) . . . release governed primarily by stimulation with enteric nervous system (dumping of acetylcholine) . . . pepsinogen will be converted to pepsin in the presence of HCl - same things that stimulate release of acid are same things that stimulate release of pepsinogen