Digestive systems perform four basic digestive processes

Digestive systems perform four basic digestive processes
Motility Secretion Digestion Absorption

1. Motility *Muscular contractions within the gut tube and
move forward the contents of the digestive tract *smooth muscle in the digestive tract walls maintain a constant low level of contraction: tone *tone is important for: -maintaining a steady pressure on contents -preventing the walls from remaining permanently stretched

Two types of digestive motility
Propulsive movements: propel (push) the contents through digestive tract at varying speeds, with the rate of propulsion dependent on the functions of different regions Mixing movements: a. mix food with digestive juices b. facilitate absorption by increasing interactions between contents and surfaces of tract

Contraction sites and control
*smooth muscle: most of digestive tract skeletal muscle: ends of tract *acts of chewing, rumination, defecation: motor cortex control (“voluntary”) smooth muscle-contraction: complex autonomic (“involuntary”)

2. Secretion *a number of digestive juices are secreted into the digestive tract lumen by specific exocrine glands, after appropriate neuronal or hormonal stimulation *digestive secretion consists of water, electrolytes, and specific important organic constituents (enzymes, bile salts or mucus) *secretory cells extract materials from blood *secretion requires energy (active transport and synthesis) *digestive secretions are reabsorbed back into blood (may not be in original forms)

3. Digestion *carbohydrates, proteins, and fats are large molecules
unable to cross plasma membrane -> need to be broken down into smaller absorbable units by digestive enzymes before entering blood *digestion begins at anterior tracts and is accomplished by enzymatic hydrolysis *digestive enzymes are specific in the bonds they can hydrolyze

Figure 14–2 Structure and hydrolysis of common dietary carbohydrates
Figure 14–2 Structure and hydrolysis of common dietary carbohydrates. (a) An example of hydrolysis. In this example, the disaccharide maltose (the intermediate breakdown product of polysaccharides) is broken down into two glucose molecules by the addition of H2O at the bond site. Fig. 14-2a, p.615

stepwise enzymatic breakdown of foodstuffs Table 14-1, p.616

Dietary molecules Carbohydrates monosaccharides polysaccharides
starch: enzymes are most widely used cellulose: most abundant organic molecules in biosphere (major part of plant) chitin glycogen

Figure 14–2 Structure and hydrolysis of common dietary carbohydrates
Figure 14–2 Structure and hydrolysis of common dietary carbohydrates. (b) Hydrogen bonding relationships for glucose units in cellulose and starch. In cellulose, hydrogen bonds form between glucose chains. This pattern stabilizes the chains and permits them to become tightly bundled. In amylose, a form of starch, the bonds form between units within a chain, which permits the glucose units to coil. Fig. 14-2b, p.615

Table sugar Milk sugar Table 14-1a, p.616

Dietary molecules Neutral fats Also, nucleic acids -> pancreatic nucleases -> nucleotides Table 14-1b, p.616

4. Absorption *after digestion, absorption occurs in the middle to posterior sections of tracts *small units of nutrients, water, vitamins, and electrolytes are transferred from lumen into blood or body cavity *specialized transporters in epithelial cells carry hydrophilic units through membrane; surface area enhances absorption (ex. villi)

Digestive tract and accessory digestive organs
Digestive system: Digestive tract and accessory digestive organs *digestive (gastrointestinal) tract: mouth, pharynx (throat), esophagus, stomach, small intestine, large intestine, anus -> continuous tube but regional differences *accessory organs: salivary glands, exocrine pancreas, the biliary system (liver and gallbladder) -> connected with the digestive tract with ducts

Regulation of digestive function:
*digestive motility and secretion are carefully regulated to maximize digestion and absorption Autonomous smooth-muscle function *some smooth-muscle cells are “pacesetter” cells: interstitial cells of Cajal that display rhythmic, spontaneous variations in membrane potential *slow-wave potential, or basic electrical rhythm (BER), or pacesetter potential *slow-wave oscillations: cyclical variations in Ca2+ release from ER and Ca2+ uptake by mitochondria

*digestive motility and secretion are carefully regulated to maximize digestion and absorption Autonomous smooth-muscle function *rhythmic cycles of muscle contraction depends on mechanical, nervous, and hormonal factors *gap junctions: transmit electrical activity to contractile smooth muscle cells *rate of contraction: depends on pacesetter cells of each organ

Intrinsic nerve plexuses: digestive system’s “intramural” nervous sytem (enteric nervous system) a. myenteric plexus b. submucous plexus *located entirely within the digestive tract wall and run its entire length *influence all facets of digestive tract activity -> sensory neurons (input), neurons that innervate muscle or exocrine/endocrine cells (output), interneurons -> acetylcholine vs. NO and vasoactive intestinal peptide

3. Extrinsic nerves *nerve fibers from autonomic nervous system that innervate different digestive organs *influence digestive motility and secretion by: regulate intrinsic plexuses, gastrointestinal hormone secretion, smooth muscle and glands directly *“fight-or-flight” sympathetic system vs. “rest-and- digest” parasympathetic system *autonomic nervous system can modify only digestive system -> specific activation of extrinsic innervation leads to coordination of activity between dif. regions

4. Receptor activation *three different types sensory receptor: a. chemoreceptors b. mechanoreceptors (pressure receptors) c. osmoreceptors *receptors active through neural reflexes & hormone secretion *digestive system’s effector cells are activated: smooth muscle cells, exocrine gland cells, & endocrine gland cells

Figure 14–5 The enteric nervous system of a rat’s stomach
Figure 14–5 The enteric nervous system of a rat’s stomach. By injecting a tracer derived from a horseradish enzyme into the vagus nerve, which connects the brain to the esophagus and stomach, researchers were able to reveal the extent of the nerve network. As nerve fibers fray out into the tiny endings across the stomach, information concerning food volume, hunger, discomfort, and satiety are sent back the brain. Fig. 14-5, p.619

Mouth: obtaining and receiving food
*mouth, or oral cavity, is ringed by muscular lips -> prehension *palate: hard palate vs. soft palate -> separates mouth from nasal cavity *uvula: sealing off nasal passage during swallowing *tongue: floor of mouth, consists of voluntarily controlled skeletal muscle taste buds (also in soft palate, throat, linings of cheeks) *pharynx (throat): rear of oral cavity -> link between mouth and esophagus -> common passageway for both digestive system and the respiratory system

Mouth: mastication *motility of the mouth that involves slicing, tearing, grinding and mixing food by teeth *teeth: incisors, canines, molar *purposes of mastication: break food, mix food with saliva, stimulate taste buds *taste buds stimulation: reflexly increases salivary, gastric, pancreatic, and bile secretion *food in the mouth -> activates mechanoreceptors -> medullar oblongata has a chewing center -> activates motor neurons that open the oral cavity

Saliva aids in mastication & lubricates food
*saliva is secreted by salivary glands outside of mouth *salivary glands: produce serous product (water + enzyme) and mucus *saliva: 99.5% water and 0.5% electrolytes and protein *functions: a. facilitate swallowing: moistening and lubrication b. salivary amylase: starch -> maltose c. antibacterial action: lysozyme and rinsing away bacterial food source d. solvent for molecules that stimulate taste buds e. keeps oral cavity moist f. rich in bicarbonate buffers -> neutralization

Salivary secretion: simple and conditioned reflexes
*salivary secretion in vertebrates is the only digestive secretion entirely under neural control (all others also require hormones) *basal secretion: low level, stimulated by parasympathetic (0.5 ml/min, for moisture; max: 5 ml/min) *enhanced stimulation by two different salivary reflexes: 1. Simple (unconditioned) reflex 2. Acquired (conditioned) reflex learned response based on previous experience

+ + + + + Cerebral cortex Other inputs Salivary center in medulla
Conditioned reflex + + extrinsic Pressure receptors and chemoreceptors in mouth Autonomic nerves Simple reflex + Salivary glands Salivary secretion Fig. 14-6, p.622

Salivary secretion: simple and conditioned reflexes
*both sympathetic and parasympathetic stimulation (autonomic nervous system) increases salivary secretion, but quantity and consistency of saliva changes with food (sensory evaluation of food) *parasympathetic: increases blood flow, prompt and abundant flow of watery saliva rich in enzymes *sympathetic: reduces blood flow -> output of smaller volume but rich in mucus (stress situations) Mouth: digestion is minimal and no absorption

Pharynx, esophagus, and crop
*motility associated with the pharynx and esophagus is swallowing or deglutition (food from mouth to stomach) *swallowing begins when bolus is moved into esophagus *pharyngeal pressure receptors -> swallowing center in medulla -> muscles involved in swallowing *swallowing: a sequentially programmed all-or-none reflex highly coordinated activities are initiated in a regular pattern over a period of time

Swallowing: oropharyngeal & esophageal stages
*when in pharynx, bolus must be prevented from entering the mouth, nasal passages, and trachea a. tongue against hard palate b. uvula is elevated against the throat, sealing off nasal passages c. elevation of larynx and tight closure of glottis (vocal folds across the laryngeal opening) d. epiglottis e. respiration in humans is briefly inhibited during swallowing f. pharyngeal muscles contract to force bolus into esophagus

Figure 14–7 Oropharyngeal stage of swallowing in humans
Figure 14–7 Oropharyngeal stage of swallowing in humans. (a) Position of the oropharyngeal structures at rest. (b) Changes that occur during the oropharyngeal stage of swallowing to prevent the bolus of food from entering the wrong passageways. Fig. 14-7, p.624

Glottis at entrance of larynx (a)
Nasal passages Hard palate Soft palate Uvula Pharynx Epiglottis Esophagus Bolus Figure 14–7 Oropharyngeal stage of swallowing in humans. (a) Position of the oropharyngeal structures at rest. Trachea Tongue Glottis at entrance of larynx (a) Fig. 14-7a, p.624

Tight apposition of vocal folds across
Swallowing center inhibits respiratory center in brain stem Elevation of uvula prevents food from entering nasal passages Position of tongue prevents food from re-entering mouth Epiglottis is pressed down over closed glottis as auxiliary mechanism to prevent food from entering airways Figure 14–7 Oropharyngeal stage of swallowing in humans. (b) Changes that occur during the oropharyngeal stage of swallowing to prevent the bolus of food from entering the wrong passageways. Tight apposition of vocal folds across glottis prevents food from entering respiratory airways (viewed from above) (b) Fig. 14-7b, p.624

muscular tube guarded by sphincters at both ends
Esophagus: muscular tube guarded by sphincters at both ends *smooth muscle tube -> links pharynx and stomach *lies in thoracic cavity, penetrates diaphragm *guarded at both ends by sphincter valves: pharyngoesophageal sphincter gastroesophageal (cardiac) sphincter *the “oropharyngeal” stage of swallowing requires opening and closing of pharyngoesophageal sphincter *pharyngoesophageal sphincter prevents large volume of gas from entering digestive tract (called eructation or belching)

Esophagus: muscular tube guarded by sphincters at both ends *peristaltic waves push the food through esophagus *esophageal stage of swallowing -> swallowing center initiates a primary peristaltic wave that sweeps from the beginning to the end of esophagus *peristalsis: ringlike contractions of the circular smooth muscle that more progressively forward with a stripping motion *unsuccessful swallowing: bolus distends esophagus -> pressure receptors in the walls ->intrinsic nerve plexuses initiates a second, more forceful peristaltic wave (distension of esophagus also increases saliva secretion)

Esophagus: muscular tube guarded by sphincters at both ends *except during swallowing, gastroesophageal sphincter remains contracted, as a barrier between stomach and esophagus -> reducing reflux of acidic contents into esophagus (otherwise heartburn) *sphincter relaxes reflexly as the peristaltic wave sweeps down esophagus *achalasia: damage to the myenteric nerve plexus in the gastroesophageal sphincter -> failure to relax and delay in food passage to stomach *mucus is secreted throughout the length of the entire digestive tract: protective for esophagus

Food storage and nonsalivary digestion
Stomach or midgut: Food storage and nonsalivary digestion *initial digestion (after minor salivary digestion) of protein *stomach: muscular, saclike chamber *can be divided into three sections: fundus: food storage and adaptation to volume change corpus: food is mixed with gastric secretion antrum: mixing and expulsion of food into intestine *pyloric sphincter: barrier between stomach and duodenum

Esophagus Fundus Smooth muscle Gastroesophageal sphincter Body Stomach
folds Pyloric sphincter Figure 14–8 Anatomy of the stomach (mammalian). The stomach is divided into three sections based on structural and functional distinctions—the fundus, body, and antrum. The mucosal lining of the stomach is divided into the oxyntic mucosa and the pyloric gland area based on differences in glandular secretion. Oxyntic mucosa Pyloric gland area Antrum Duodenum Fig. 14-8, p.627

Stomach or midgut: Food storage and nonsalivary digestion *the stomach performs three main functions: 1. store food so the food can enter small intestine at a rate for optimal digestion and absorption 2. secretes HCl and enzymes for chemical digestion 3. through mixing, food is pulverized and mixed with gastric secretions to produce thick, liquid mixture called chyme

Stomach or midgut: Food storage and nonsalivary digestion *gastric filling: stomach can accommodate significant changes in volume (empty: 50 ml, after meal: 1 liter) *the interior of stomach has many deep folds -> during a meal, folds become smaller and flatten out as stomach relaxes *receptive relaxation: accommodate extra volume of food without rise in stomach pressure (triggered by eating)

Stomach or midgut: Food storage and nonsalivary digestion *pacesetter cells in the upper fundus generate slow-wave potentials -> peristaltic waves *peristaltic waves spread over the fundus and body to the antrum and pyloric sphincter (weaker to stronger) *food from esophagus is stored in the body without being mixed (the fundus area contains only gas)

Stomach or midgut: Food storage and nonsalivary digestion *gastric mixing takes place in the antrum, by strong peristaltic contractions -> producing chyme *tonic contraction of the pyloric sphincter keeps it almost, but not completely closed (for water and fluids passage) *chyme is pushed through the sphincter by strong antral peristaltic contractions *retropusion

Stomach or midgut: Food storage and nonsalivary digestion *antral peristaltic contractions drive gastric emptying *during digestive phase of gastric motility, only particles less than 2 mm in diameter can escape thru sphincter *intensity of antral peristalsis can be influenced by gastric and duodenal factors *housekeeping function of antrum: interdigestive motility complex (hourly interval), emptying remaining particles between meals

Figure 14–9 Gastric emptying and mixing as a result of antral peristaltic contractions (mammalian stomach). Fig. 14-9, p.629

Stomach 1 Esophagus Gastroesophageal sphincter Pyloric sphincter
Duodenum 3 4 Figure 14–9 Gastric emptying and mixing as a result of antral peristaltic contractions (mammalian stomach). Direction of movement of peristaltic contraction 2 Movement of chyme Peristaltic contraction Gastric emptying Fig. 14-9a, p.629

6 5 Peristaltic contraction Gastric mixing Fig. 14-9b, p.629
Figure 14–9 Gastric emptying and mixing as a result of antral peristaltic contractions (mammalian stomach). 5 Peristaltic contraction Gastric mixing Fig. 14-9b, p.629

Table 14-2, p.629

Duodenal factors that influence gastric emptying
*enterogastric reflex: neural response intrinsic nerve plexuses autonomic nerves *hormonal response: enterogastrones (endocrine) secretin: in response to acidity in dueodenum cholecystokinin (CCK) gastric inhibitory peptide *fat, acid, hypertonicity, distension

Other factors that influence gastric motility
*hunger may increase peristaltic contractions over stomach (parasympathetic) *emotions such as stress *intense pain: inhibit digestive tract motility (increased sympathetic activity)

Forceful expulsion of gastric contents though mouth
Vomiting: Forceful expulsion of gastric contents though mouth *caused by: irritation or distension of stomach and duodenum chemical agents, such as drugs toxins (either by acting in upper GI tract or chemoreceptor trigger zone in the brain) *stomach, esophagus (& sphincter), and pyloric sphincter are all relaxed *contraction of respiratory muscles (diaphragm and abdominal muscle -> stomach is squeezed *consequences?

Secretion of gastric juice
*rate and amount dependent on the frequency of feeding *cells are located in the gastric mucosa (lining of stomach) 1. oxyntic mucosa (body and fundus) 2. pyloric gland area (PGA, in antrum) *on luminal surface: there are deep pockets formed by infoldings of the gastric mucosa *the invaginations are called gastric pits, gastric glands lie at the base

Table 14-3, p.632

Oxyntic mucosa Stomach lumen Pyloric gland area Table 14-3a, p.632

Gastric pit Mucosa Submucosa Table 14-3b, p.632

Exocrine secretory cells in the oxyntic mucosa pits Mucous cells: secretes mucus Chief and parietal cells: enzyme precursor pepsinogen Parietal (or oxyntic) cells: HCl and intrinsic factor Also… Stem cells: parent cells of all new cells of gastric mucosa Surface epithelial cells: viscous, alkaline mucus on surface

Surface epithelial cells
In oxyntic mucosa Surface epithelial cells Gastric pit Mucous cells Chief cells Gastric gland Parietal cells Enterochromaffin- Like (ECL) cells Table 14-3c, p.632

Endocrine and paracrine secretory cells Enterochromaffin-like (ECL) cells: histamine G cells (of PGA): gastrin (into blood) D cells (pylorus and duodenum): somatostatin *the gastric glands of PGA primarily secret mucus and a small amount of pepsinogen

In pyloric gland area D cells G cells Table 14-3d, p.632

Table 14-3e, p.632

Exocrine products and role in digestion
Hydrochloric acid secretion *parietal cells actively transport H (and Cl) ions against huge concentration gradient into lumen -> requires energy, mitochondria *secreted H is not from plasma but metabolic process -> breakdown of water *transport: H-K ATPase in the luminal membrane *carbonic anhydrase: combine OH with CO2 ->HCO3 *basolateral border: HCO3-Cl carrier

Figure 14–10 Mechanism of HCI secretion (vertebrate)
Figure 14–10 Mechanism of HCI secretion (vertebrate). The stomach’s parietal cells actively secrete H+ and Cl- by the actions of two separate pumps. The secreted H+ is derived from the breakdown of H2O into H+ and OH-. Note that CA produces H+ and HCO3 - through two steps (see text). The secreted Cl- is transported into the parietal cell from the plasma. The HCO3 - generated from H2CO3 dissociation is transported into the plasma in exchange for the secreted Cl-. Fig , p.633

Hydrochloric acid secretion functions: *does not digest anything *activates pepsin *breakdown of large food particles *denatures protein *kills microorganisms

2. Pepsinogen/pepsin *stored in chief cell’s cytoplasm within secretory vesicles known as zymogen granules *released by exocytosis *HCl conversion into pepsin, pepsin also cleavages pepsinogen -> autocatalytic (“self-activating”) process *pepsin cleaves proteins into peptide fragments, works best at low pH *mucus protects gastric mucosa from: mechanical injury, pepsin digestion, low pH

Figure 14–11 Pepsinogen activation in the stomach lumen (vertebrate)
Figure 14–11 Pepsinogen activation in the stomach lumen (vertebrate). In the lumen, hydrochloric acid (HCl) activates pepsinogen to its active form, pepsin, by cleaving off a small fragment. Once activated, pepsin autocatalytically activates more pepsinogen and begins protein digestion. Secretion of pepsinogen in the inactive form prevents it from digesting the protein structures of the cells in which it is produced. Fig , p.634

Intrinsic factor *secretory product of parietal cells *important for vitamin B12 absorption (must be combined with intrinsic factor before being absorbed) *absorption: intrinsic factor-vit. B12 complex with a special receptor located in the terminal ileum (last portion of small intestine) -> receptor-mediated endocytosis *vitamin B12 is important for red blood cell formation

Regulation of parietal and chief cells
*4 chemical messengers influence gastric juice secretion: Ach, gastrin, histamine, and somatostatin *parietal cells have receptors for each messenger *Ach, gastrin, histamine: stimulatory on HCl secretion somatostatin: inhibit HCl secretion *Ach, gastrin: also increases pepsinogen secretion (effect on chief cells)

*Ach: neurotransmitter from intrinsic nerve plexus, acts on parietal, chief, G, and ECL cells *gastrin: from G cells, into blood in response to protein products in stomach and to Ach, major gastrointestinal hormone, main factor for HCl secretion -> parietal and chief cells: acidic gastric juice -> stimulate ECL cells to release histamine -> HCl -> trophic (growth promoting) to mucosa of stomach and small intestine

*histamine: a paracrine released from ECL cells in response to gastrin and Ach -> parietal cells for HCl secretion *somatostatin: a paracrine released from D cells in response to acid -> inhibit secretion by parietal, G and ECL cells -> negative feedback effect to turn off HCl secretion

Table 14-3e, p.632

Control of gastric secretion involves three phases
*rate of gastric secretion can be increased by: 1. Factors arising before food reaches stomach -> cephalic phase 2. Factors due to presence of food in stomach -> gastric phase 3. Factors originating in the duodenum after food has left stomach -> intestinal phase

Cephalic phase: *gastric secretion occurs in response to food-related stimuli acting in the brain -> feedforward activation *vagal stimulation of intrinsic plexuses and G cells in PGA 2. Gastric phase: *may be independent from the cephalic phase *stimuli acting in the stomach (peptide fragments) can trigger release of gastrin

Intestinal phase: *occurs with the entry of food enter small intestine *excitatory component: products of protein digestion in the duodenum triggers release of intestinal gastrin -> stomach *inhibitory component: enteroglucagon is released into blood when the pH of intestine is too low -> shut off gastric secretion

Table 14-4, p.635

Gradual inhibition of gastric secretion
*as food enters duodenum, stimuli for enhanced gastric secretion (protein) is withdrawn *in response to low gastric pH after food leaves stomach, somatostatin is released -> gastric secretion lowers *same stimuli that inhibit gastric motility also inhibit gastric secretion

Table 14-5, p.636

Gastric mucosal barrier of stomach
*mucosal linings provide barriers a. luminal membranes of mucosal cells are impermeable to H (acid can’t enter cells) b. lateral edges of these cells are joined near luminal borders by tight junctions -> gastric mucosal barrier *the entire stomach lining is replaced every three days *peptide ulcer: protective mechanisms fail

Two separate digestive processes in stomach
*food in the body of stomach: still semi-solid due to weak mixing -> very little protein digestion (only on then surface *carbohydrates digestion continues in the interior of food mass (by salivary amylase) *digestion by gastric juice is done in the antrum, due to mixing with HCl and pepsin *fat digestion has not begun in the stomach

mixture of exocrine and endocrine tissue
Pancreas: mixture of exocrine and endocrine tissue *~98% of the pancreas has exocrine function *acini (exocrine) secrete pancreatic juice: enzymatic secretion and aqueous alkaline secretion *islets of Langerhans (endocrine) *most important pancreatic hormones are insulin and glucagon

(islets of Langerhans)
Bile duct from liver Stomach Duodenum Hormones (insulin, glucagon) Blood Figure 14–12 Schematic representation of the exocrine and endocrine portions of the mammalian pancreas. The exocrine pancreas secretes into the duodenal lumen a digestive juice composed of digestive enzymes secreted by the acinar cells and an aqueous NaHCO3 solution secreted by the duct cells. The endocrine pancreas secretes the hormones insulin and glucagon into the blood. Duct cells secrete aqueous NaHCO3 solution Acinar cells secrete digestive enzymes Endocrine portion of pancreas (islets of Langerhans) Exocrine portion of pancreas (acinar and duct cells) The glandular portions of the pancreas are grossly exaggerated. Fig , p.638

Exocrine pancreatic secretion
Proteolytic enzymes (for protein digestion): *trypsinogen: activates by enterokinase in the luminal border of mucosal cells (autocatalytic activation) *chymotrypsinogen and procarboxypeptidase: activated by trypsin *protein can be digested into amino acids or peptides 2. Pancreatic amylase polysaccharides to disaccharides

Pancreatic chitinase: chitin: chains of glucose molecules Pancreatic lipase: *principal enzyme that digests fat *hydrolyzes dietary triglycerides into monoglycerides and free fatty acids (absorbable) *pancreas is the only significant source of lipase *steatorrhea: excessive undigested fat in the feces

Pancreatic aqueous alkaline secretion *pancreatic enzymes function best in neutral or slightly alkaline condition *acidic chyme from stomach must be neutralized -> allow optimal digestion and prevent acid damage *alkaline (NaHCO3-rich) fluid: largest component of pancreatic secretion

Hormonal regulation of pancreatic secretion
*parasympathetic stimulated pancreatic secretion occurs during the cephalic and gastric phases *major stimulation occurs during intestinal phase, when chyme is in the small intestine -> enterogastrones are released Secretin: *stimulated by acid in the duodenum *secretin stimulates duct cells in pancreas *a mechanism for maintaining neutrality of chyme

Hormonal regulation of pancreatic secretion
2. CCK (cholecystokinin) *regulates pancreatic digestive enzyme secretion *released from duodenal mucosa in response to nutrients in the lumen (fat) *CCK stimulates pancreatic acinar cells *all three types of pancreatic enzymes are packaged together in the zymogen granules -> released together (adaptive response?) Both secretin and CCK exert trophic effects on exocrine pancreas

+ Acid in duodenal lumen Fat and protein products in duodenal lumen
Neutralizes Digests Secretin release from duodenal mucosa CCK release + (secretin carried by blood) (CCK carried by blood) Pancreatic duct cells Pancreatic acinar Secretion of aqueous NaHCO3 solution into duodenal lumen Secretion of pancreatic digestive enzymes into Fig , p.640

Biliary system: liver and gallbladder
*liver is the largest and most important metabolic organ in vertebrates -> biochemical factory *perform a wide variety of functions: a. bile salts secretion b. metabolic processing of major nutrients after absorption c. detoxification or degradation of body wastes and foreign compounds d. synthesis of plasma proteins: for blood clotting or transport of hormones and cholesterol e. storage of glycogen, fats, iron, copper, and many vitamins

Biliary system: liver and gallbladder
*perform a wide variety of functions: f. activation of vitamin D (with kidneys) g. removal of bacteria and worn-out RBC (macrophages) h. excretion of cholesterol and bilirubin (breakdown product of RBC) i. gluconeogenesis (converting noncarbohydrates into glucose) *hepatocyte: single cell type for the wide variety of jobs

Liver blood flow Hepatic portal system Fig. 14-14, p.641
Figure 14–14 Schematic representation of liver blood flow (mammal). Fig , p.641

Liver lobules *liver is organized into functional units: lobules
(hexagonal arrangements of tissue with a central vein) *channels: a. vessels: hepatic artery, branch of portal vein, & bile duct b. sinusoids: capillary network c. hepatic vein d. bile canaliculs -> bile duct *each hepatocyte is in contact with a sinusoid and a bile canaliculus

Figure 14–15 Anatomy of the mammalian liver. (a) Hepatic lobule
Figure 14–15 Anatomy of the mammalian liver. (a) Hepatic lobule. (b) Wedge of a hepatic lobule. Fig , p.642

Branch of hepatic portal Central vein vein Bile canaliculi Cords of
hepatocytes (liver cells) Bile duct Branch of hepatic artery Figure 14–15 Anatomy of the mammalian liver. (a) Hepatic lobule. Hepatic portal vein To hepatic duct Sinusoids Hepatic artery (a) Fig a, p.642

Branch of hepatic portal vein Branch of Bile hepatic artery duct
Connective tissue Kupffer cell Bile canaliculi Sinusoids Figure 14–15 Anatomy of the mammalian liver. (b) Wedge of a hepatic lobule. Cords of hepatocytes (liver cells) Hepatic plate Central vein Fig b, p.642

Bile secretion *sphincter of Oddi: bile duct-duodenum junction
prevents bile from entering until during digestion *when closed, bile is diverted back to gallbaldder *gallbladder can concentrate bile 10-to-20-fold *gallbladder: storage and concentration of bile between meals

Figure 14–16 Enterohepatic circulation of bile salts (mammal)
Figure 14–16 Enterohepatic circulation of bile salts (mammal). The majority of bile salts are recycled between the liver and small intestine through the enterohepatic circulation, designated by the blue arrows. After participating in fat digestion and absorption, most bile salts are reabsorbed by active transport in the terminal ileum and returned through the hepatic portal vein to the liver, which resecretes them in the bile. Fig , p.642

Bile secretion: enterohepatic circulation
*bile consists of an aqueous alkaline fluid (similar to pancreatic NaHCO3 secretion, by duct cells) and other organic constituents: bile salts, cholesterol, lecithin, bilirubin (from liver) *bile is important for digestion and absorption of fats, through emulsification effect of the bile salts *bile salts: derivatives of cholesterol (conjugated with taurine or glycine) *bile salts are reabsorbed back into blood by active- transport in terminal ileum -> hepatic portal system -> liver (enterohepatic circulation)

Bile salts aid fat digestion and absorption:
Detergent action of bile salts *detergent action: convert large fat globules into a lipid emulsion that consists of small fat droplets -> increase surface area for pancreatic lipase attack *bile salts emulsify large fat droplets for better digestion *bile salts molecule *large fat droplets -> intestinal mixing -> small droplets -> lipid emulsion -> lipase and colipase *food in duodenum triggers release of CCK -> contraction of gallbladder & relaxation of sphincter of Oddi

Lipid-soluble portion (derived from cholesterol)
Negatively charged H2O-soluble portion (a carboxyl group at the end of a glycine or taurine chain) Small lipid (fat) droplet with bile salt molecules adsorbed on its surface Large fat droplet Through action of bile salts Lipid emulsion Fig , p.644

Bile salts aid fat digestion and absorption:
Micellar formation *bile salts (and cholesterol and lecithin) are important for fat absorption through micellar formation *in micelle, both bile salts and lecithin aggregate in small clusters (1/106 the size of emulsified lipid droplet) *micelles provide a vehicle for carrying water-insoluble substances through the watery luminal contents: products of fat digestion and fat-soluble vitamins

Figure 14–18 Schematic representation of a micelle
Figure 14–18 Schematic representation of a micelle. Bile constituents (bile salts, lecithin, and cholesterol) aggregate to form micelles that consist of a hydrophilic (water-soluble) shell and a hydrophobic (lipid-soluble) core. Because the outer shell of a micelle is water soluble, the products of fat digestion, which are not water soluble, can be carried through the watery luminal contents to the absorptive surface of the small intestine by dissolving in the micelle’s lipid-soluble core. Fig , p.645

Bile secretion: bilirubin
*waste product excreted by by the liver: breakdown of worn out RBC *RBC -> removed from blood by macrophages -> degraded by Kupffer cells to yield heme -> converted into biliverdin -> transformed into bilirubin -> released into lobule sinusoid -> extracted from blood by hepatocytes -> excreted into bile *small amount of bilirubin is absorbed by the small intestine and exreted in the urine *jaundice: accumulation of bilirubin

Small intestine *site where most digest and absorption of nutrients takes place in vertebrates *a coiled tube that lies within the abdominal cavity, divided into three segments: duodenum, jejunum, and ileum *digestive tract wall has four layers: a. mucosa b. submucosa c. muscularis externa d. serosa

Figure 14–19 Structure of the vertebrate digestive tract
Figure 14–19 Structure of the vertebrate digestive tract. (a) Generalized layers of the vertebrate digestive tract wall, consisting of four major layers: from innermost out, the mucosa, submucosa, muscularis externa, and serosa. (b–d) The mammalian small intestine: (b) One of the circular folds of the small-intestine mucosa, which collectively increase the absorptive surface area threefold. (c) Microscopic fingerlike projection known as a villus. Collectively, the villi increase the surface area another 10-fold. (d) Electron microscope view of a villus epithelial cell, depicting the presence of microvilli on its luminal border; the microvilli increase the surface area another 20-fold. Altogether, these surface modifications increase the small intestine’s absorptive surface area 600-fold. Fig , p.646

Digestive tract wall *mucosa has three layers:
1. Mucous membrane, inner epithelial layer that is a surface for protection and secretion/absorption (exocrine, endocrine, and epithelial cells) 2. Lamina propria: thin middle layer of connective tissue (contains small blood vessels, lymph vessels and nerve fibers, and gut-associated lymphoid tissue, or GALT) 3. Muscularis mucosa: outer layer of smooth muscles

Outer longitudinal muscle Muscularis externa Serosa
Body wall Peritoneum Mesentery Outer longitudinal muscle Muscularis externa Serosa Inner circular muscle Mucous membrane Lamina propria Mucosa Submucosa Muscularis mucosa Lumen Duct of large accessory digestive gland (i.e., liver or pancreas) emptying into digestive tract lumen Figure 14–19 Structure of the vertebrate digestive tract. (a) Generalized layers of the vertebrate digestive tract wall, consisting of four major layers: from innermost out, the mucosa, submucosa, muscularis externa, and serosa. (b–d) The mammalian small intestine: (b) One of the circular folds of the small-intestine mucosa, which collectively increase the absorptive surface area threefold. (c) Microscopic fingerlike projection known as a villus. Collectively, the villi increase the surface area another 10-fold. (d) Electron microscope view of a villus epithelial cell, depicting the presence of microvilli on its luminal border; the microvilli increase the surface area another 20-fold. Altogether, these surface modifications increase the small intestine’s absorptive surface area 600-fold. Myenteric plexus Submucous plexus (a) Fig a, p.646

Digestive tract wall *submucosa: thick layer of connective tissue that
provides distensibility and elasticity -> contains large blood and lymph vessels -> nerve network called submucous plexus *muscularis externa: major smooth muscle coat of digestive tube -> inner circular layer: constricts tube -> outer longitudinal layer: shortens the tube -> contraction: propulsive and mixing movements -> nerve network between the two layers: myenteric plexus

Outer longitudinal muscle Muscularis externa Serosa
Body wall Peritoneum Mesentery Outer longitudinal muscle Muscularis externa Serosa Inner circular muscle Mucous membrane Lamina propria Mucosa Submucosa Muscularis mucosa Lumen Duct of large accessory digestive gland (i.e., liver or pancreas) emptying into digestive tract lumen Figure 14–19 Structure of the vertebrate digestive tract. (a) Generalized layers of the vertebrate digestive tract wall, consisting of four major layers: from innermost out, the mucosa, submucosa, muscularis externa, and serosa. (b–d) The mammalian small intestine: (b) One of the circular folds of the small-intestine mucosa, which collectively increase the absorptive surface area threefold. (c) Microscopic fingerlike projection known as a villus. Collectively, the villi increase the surface area another 10-fold. (d) Electron microscope view of a villus epithelial cell, depicting the presence of microvilli on its luminal border; the microvilli increase the surface area another 20-fold. Altogether, these surface modifications increase the small intestine’s absorptive surface area 600-fold. Myenteric plexus Submucous plexus (a) Fig a, p.646

Digestive tract wall *serosa: outer connective tissue covering the tract *function: secretes a watery serous fluid that lubricates and prevents friction between the digestive organs and surrounding vscera *serosa is continuous with the mesentery throughout the tract -> fixation and position support, freedom for mixing and propulsive movements

Mucous lining of small intestine:
Well adapted to its absorptive functions Surface area of mucosa: *inner surface is arranged in circular folds: increase area 3x *microscopic projection from this folded surface: villi (increase another 10x) -> surface of villi: epithelial and mucous cells -> villi are dynamic and can change dimension *microvilli (or brush border) of epithelial cells: increase area another 20x -> each cell has 3k-6k microvilli, longest in jejunum -> membrane space within microvilli, called glycocalyx (carbohydrate filaments with enzymes)

Villus Figure 14–19 Structure of the vertebrate digestive tract. (a) Generalized layers of the vertebrate digestive tract wall, consisting of four major layers: from innermost out, the mucosa, submucosa, muscularis externa, and serosa. (b–d) The mammalian small intestine: (b) One of the circular folds of the small-intestine mucosa, which collectively increase the absorptive surface area threefold. (c) Microscopic fingerlike projection known as a villus. Collectively, the villi increase the surface area another 10-fold. (d) Electron microscope view of a villus epithelial cell, depicting the presence of microvilli on its luminal border; the microvilli increase the surface area another 20-fold. Altogether, these surface modifications increase the small intestine’s absorptive surface area 600-fold. (b) Fig b, p.646

Epithelial cell Capillaries Mucous cell Central lacteal Crypt of
Figure 14–19 Structure of the vertebrate digestive tract. (c) Microscopic fingerlike projection known as a villus. Collectively, the villi increase the surface area another 10-fold. Crypt of Lieberkühn Arteriole Venule Lymphatic vessel (c) Fig c, p.646

Microvilli Figure 14–19 Structure of the vertebrate digestive tract. (d) Electron microscope view of a villus epithelial cell, depicting the presence of microvilli on its luminal border; the microvilli increase the surface area another 20-fold. Altogether, these surface modifications increase the small intestine’s absorptive surface area 600-fold. (d) Fig d, p.646

Mucous lining of small intestine:
Well adapted to its absorptive functions 2. Structure of a villi *epithelial cells on the villi surface: tight junctions at lateral borders (leakier than those in stomach) *carriers at the brush borders for nutrients and electrolytes; digestive enzymes at brush borders *capillary network: each villus is supplied by an arteriole *terminal lymphatic vessel: each villus is supplied by a lymphatic vessel (central lacteal) -> transepithelial transport of nutrients

Small intestine: segmentation contractions
*segmention: small intestine’s primary method of motility *consists of oscillating, ringlike contractions *contractile rings do not sweep like peristaltic waves *serves the dual functions of mixing chyme and enzymes and exposing chyme to the mucosa surface *initiation and control *pacesetter cells produce BER *smooth muscle’s responsiveness and intensity of segmentation contractions are influenced by: distension of intestine, gastrin, and extrinsic nerve

Small intestine: segmentation contractions
*initiation and control *when food enters, both duodenum and ileum segment simultaneously: duodenum (local distension) ileum (gastrin): gastroileal reflex *extrinsic nerves modify strength of contractions *chyme progress forward slowly by segmentation, but segmentation frequency declines along the length of small intestine (12/min vs. 9/min) -> slow progress allows time for mixing and absorption (3-6 hours to move through small intestine)

Small intestine motility between meals
*migrating motility complex, or intestinal housekeeper: weak, repetitive peristaltic waves *short peristaltic waves take about mins to migrate from from stomach to end of small intestine *sweeping residual chyme, mucosal debris, and bacteria towward colon *hormone called motilin may play a role in regulation *ceases when next meal arrives

Figure 14–20 Segmentation. Segmentation consists of ringlike contractions along the length of the vertebrate small intestine. Within a matter of seconds, the contracted segments relax and the previously relaxed areas contract. These oscillating contractions thoroughly mix the chyme within the smallintestine lumen. Fig , p.647

Ileocecal juncture *juncture between small and large intestines:
*valvelike folds of tissue protrude from ileum into the lumen of cecum -> ileocecal valve *the smooth muscle within the last centimeters of ileal wall is thickened, forming a sphincter -> ileocecal sphincter *the sphincter is under neuronal control (intrinsic plexuses) and hormonal control (gastrin)

Figure 14–21 Control of the ileocecal valve/sphincter (shown for a human). The juncture between the ileum and large intestine consists of the ileocecal valve, which is surrounded by thickened smooth muscle, the ileocecal sphincter. Pressure on the cecal side pushes the valve closed and contracts the sphincter, preventing the bacteria-laden colonic contents from contaminating the nutrient-rich small intestine. The valve/sphincter opens and allows ileal contents to enter the large intestine in response to pressure on the ileal side of the valve and to the hormone gastrin secreted as a new meal enters the stomach. Fig , p.648

Small intestine secretions
*exocrine glands in small intestine mucosa secrete 1.5L/day of succus entericus: aqueous salt and mucus *digestive enzymes function within the borders of epithelial cells *succus entericus: protection and lubrication; H2O for enzymatic digestion (hydrolysis) *regulation of this secretion (after a meal) is not clear, probably by the presence of chyme

Small intestine enzymes
*digestion in small intestine lumen is done by pancreatic enzymes, with fat digestion enhanced by bile *fat digestion is complete in small intestine lumen, but not protein and carbohydrate *epitheial cell brush border: *enterokinase: activates pancreatic trypsinogen *disaccharidases *aminopeptidases

Table 14-6, p.649

Small intestine: primary role in absorption
*normally, all products of carbo, protein, and fat digestion, and most of electrolytes, vitamins and water are absorbed by small intestine (except calcium and iron) *length of small intestine and the types and density of its transporters are matched to typical diets of species *most absorption occurs in the duodenum and jejunum (very little in ileum) *small intestine has an abundant reserve absorptive capacity *vitamin B12 and bile salts are absorbed only in terminal ileum (all others throughout length of small intestine)

Small intestine: rapid turnover of mucosal lining
*crypts of Lieberkuhn: secrete water and electolytes for the succus entericus *also functions as nurseries: new cells at bottom of crypts migrate up the villi and replace turnover cells on the top (100 million intestinal cells are shed per minute) *migration takes about three days in human, cells also undergo changes during migration *Paneth cells in the crypts: defensive function for safe- guarding the stem cells -> produce lysozyme and defensins (anti-microbial)

Small intestine: water and electrolytes absorption
*sodium: active and passive absorption *passive diffusion through tight junctions *movement through cells involves two different carriers *entering epithelial cells: passive, or co-transported with glucose, amino acids, or other nutrients *actively pumped out at basolateral border *finally diffuse into the capillaries

Small intestine: water and electrolytes absorption
*aborption of Cl, H2O, glucose and amino acids from small intestine is linked to the energy-dependent Na absorption *H2O absorption in the digestive tract depends on active carrier that pumps Na into lateral space -> osmotic pressure

Small intestine: carbohydrate absorption
*glucose and galactose are both absorbed by secondary active transport (co-transport with Na at lumine border) *co-transport depends on Na concentration gradient created by energy-dep. basolateral Na-K pump *glucose leaves cells through passive carrier in the basolateral border (by concentration gradient) *fructose: into blood by facilitated diffusion (passive carrier-mediated transport)

Figure 14–22 Carbohydrate digestion and absorption (vertebrate small intestine).
Fig , p.652

Small intestine: protein absorption
*both ingested and endogenous proteins are absorbed *amino acids: secondary active transport (with Na) (like monosaccharides, enter capillary in villi) *neonatal mammals: active process of endocytosis for uptake of whole proteins (IgA class of antibodies) *some large protein molecules can be absorbed intact into blood through a process called persorption

Figure 14–23 Protein digestion and absorption(vertebrate small intestine).
Fig , p.653

Small intestine: fat absorption
*monoglycerides and free fatty acids passively diffuse from the micelles through the lipid component of the epithelial cell membranes (the luminal side) -> micelles are then free to pick up more products *bile salts are reabsorbed in the terminal ileum by special active transport *once inside the cells, triglycerides are formed -> these droplets are coated with a layer of lipoprotein (so water soluble *chylomicrons extruded by exocytosis, secreted into central lacteals

Figure 14–24 Fat digestion and absorption (vertebrate small intestine).
Fig , p.654

Fig a, p.654

Fig b, p.654

Small intestine: vitamin absorption
*water-soluble: passive absorption with water *fat-soluble: carried in micelles and absorbed passively with fat digestion products *vitamin B12: combined with gastric intrinsic factor for absorption by special transport in terminal ileum

Absorbed nutrients pass thru liver
*venules that leave GI tract empty into portal vein (liver) -> pass thru liver before entering general circulation *after metabolic processing and detoxification in liver, venous blood return to heart through vena cava *fat (chylomicrons) is absorbed in the central lacteal -> lymphatic system -> thoracic duct, which empties into venous system in the chest

Absorbed nutrients pass thru liver
*liver does not act on fat until it is diluted in the circulatory system and uptake by adipose cells *liver plays an important role in lipid transport synthesizing three types of plasma lipoproteins: a. high-density lipoprotein b. low-density lipoprotein c. very-low-density lipoprotein (a+b: transport cholesterol for cell membrane production c: triglycerides for energy storage in adipose tissue)

The only secretory product that escapes form the body: bilirubin
Table 14-7, p.655

Biochemical balance among middle GI
*the acid-base balance of the body: secretion = absorption *stomach -> pancreas -> small intestine between digestive tract lumen and blood

Figure 14–25 Biochemical balance among the stomach, pancreas, and small intestine in a vertebrate. When digestion and absorption proceed normally, no net loss or gain of acid or base or other chemicals from the body fluids occurs as a consequence of digestive secretions. The parietal cells of the stomach extract Cl-, CO2, and H2O from and add HCO3 - to the blood during HCl secretion. The pancreatic duct cells extract the HCO3 - as well as Na+ from the blood during NaHCO3 secretion. Within the smallintestine lumen, pancreatic NaHCO3 neutralizes gastric HCl to form NaCl and H2CO3, which decomposes into the blood, thereby replacing the constituents that were extracted from the blood during gastric and pancreatic secretion. Fig , p.656

Diarrhea *highly fluid fecal matter, increased frequency of defection
*beneficial but also damaging -> dehydration, loss of nutrient and secretions, metabolic acidosis (due to loss of HCO3) *most common cause: excessive intestinal motility *bacterial or viral infection, or emotional stress *no sufficient time for intestinal absorption

Large intestine Transverse colon Haustra Taeniae coli Descending colon
Ascending colon Ileocecal valve Figure 14–26 Anatomy of the large intestine (mammal, shown for a human). Appendix Sigmoid colon Cecum Rectum External anal sphincter (skeletal muscle) Internal anal sphincter (smooth muscle) Anal canal Fig , p.657

Large intestine: haustra contractions
*outer longitudinal smooth-muscle layer consists of 3 separate, longitudinal bands of muscle: taeniae coli *the longer, underlying circular smooth-muscle (than the outer longitudinal layer) are gathered into pouches or sacs called haustra *movements of large intestine are slow -> appropriate for its absorptive and storage functions *primary method of motility for colon is haustral contractions

Large intestine: haustra contractions
*initiated by autonomous rhythmicity of smooth muscle cells, similar to small intestinal segmentation, but 30 mins between contractions (controlled by intrinsic plexuses) *slowly mix to expose colonic contents to absorptive mucosa, and allow more time for microbial digestion *contents delivered to colon consist of indigested food, unabsorbed biliary components, and remaining fluid *after H2O and salt extraction, extreta or feces remain -> primary function of large intestine is to store them

Large intestine: mass movements
*general after meals, a marked increase in motility takes place -> large segments of colon contract simultaneously *mass movements: drive colonic contents into the distal portion of the large intestine -> storage until defecation *when food enters stomach, mass movements occur by gastrocolic reflex -> mediated by gastrin and extrinsic autonomic nerves -> colonic contents into rectum *gastroileal reflex also moves the remaining small-intestine contents into the large intestine -> so a general GI tract response when new food enters

Large intestine: defecation
*mass movements move fecal materials into rectum -> distension of rectum -> stimulate stretch receptors in rectal wall -> defecation reflex -> *internal anal sphincter (smooth muscle): relax *rectum and sigmoid colon: contract *external anal sphincter (skeletal muscle): voluntary *defecation is assisted by increase in intra-abdominal pressure: contraction of abdominal muscles and forcible expiration

Large intestine: secretion and absorption
*large intestine does not secrete any digestive enzymes, colonic buffers consists of alkaline mucus solution *large intestine lacks the adequate luminal surface area, and specialized transport mechanisms (for glucose or amino acids) *Na is actively absorbed in large intestine, Cl follows passively (electrical gradient), then H2O follows osmotically *fecal materials (100g H2O and 50g solids) include undigested/unabsorbed food, bacteria, bilirubin

Digestive systems perform four basic digestive processes

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Digestive systems perform four basic digestive processes

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