New User Special Price Expires in

Let's log you in.

Sign in with Facebook


Don't have a StudySoup account? Create one here!


Create a StudySoup account

Be part of our community, it's free to join!

Sign up with Facebook


Create your account
By creating an account you agree to StudySoup's terms and conditions and privacy policy

Already have a StudySoup account? Login here

BI 315 Notes for Chapters 15 and 16

by: JordanK

BI 315 Notes for Chapters 15 and 16 BI 315

Marketplace > Boston University > Biology > BI 315 > BI 315 Notes for Chapters 15 and 16
GPA 3.82

Preview These Notes for FREE

Get a free preview of these Notes, just enter your email below.

Unlock Preview
Unlock Preview

Preview these materials now for free

Why put in your email? Get access to more of this material and other relevant free materials for your school

View Preview

About this Document

Reading notes for required parts of chapters 15 and 16, will be on final exam.
Systems Physiology
Dr. Widmaier
Class Notes
Biology, Physiology
25 ?




Popular in Systems Physiology

Popular in Biology

This 16 page Class Notes was uploaded by JordanK on Sunday May 1, 2016. The Class Notes belongs to BI 315 at Boston University taught by Dr. Widmaier in Spring 2016. Since its upload, it has received 66 views. For similar materials see Systems Physiology in Biology at Boston University.


Reviews for BI 315 Notes for Chapters 15 and 16


Report this Material


What is Karma?


Karma is the currency of StudySoup.

You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!

Date Created: 05/01/16
CHAPTER 15 NOT REQUIRED from chapter 15: Case Study, figure 15.31; p538 section on iron; p546-548 section on Gastric Motility; p552-553 section on Motility; p553-554 Large Intestine, the short sections on ulcers, gallstones, and lactose intolerance near the end of the chapter 15.1 – Overview of the Digestive System  Digestive system: gastrointestinal tract (alimentary canal) and accessory organs and tissues o Alimentary canal: mouth, pharynx, esophagus, stomach, small and large intestines  Appx. 30 feet long from mouth to anus  Lumen is continuous with external environment, so contents are technically outside the body o Accessories: salivary glands, liver, gallbladder, exocrine pancreas  Not part of alimentary canal but secrete substances into it veia connecting ducts  Purpose: to process ingested foods into molecular forms (digestion) to be transferred to the body’s internal environment o Food that enters as macromolecules can’t absorb through epithelium o Accomplished by HCl in stomach, bile from liver, and digestive enzymes released by the system’s exocrine glands (all released by secretion)  Under local neural control of enteric NS and also the CNS  Smooth muscle contraction in GI tract wall (motility) allows for luminal contents to mix with various secretions, and to move contents through tract from mouth to anus o Peristalsis: muscular movement in wavelike fashion in one direction  Will absorb as much of any particular substance that is ingested  no regulation on total amount of nutrients absorbed/concentrations in internal environment (that must be controlled by hormones and kidneys)  Elimination: excretion of small amounts of certain metabolic end products via GI tract (feces) 15.2 – Structure of the GI Tract Wall  Figure 15.3 – general structure o Mucosa  Apical surface is highly convoluted (increased surface area = increased absorption)  In stomach, this layer is covered by a single layer of epithelial cells linked by tight junctions  Invaginations of epithelium form exocrine glands to secrete acid, enzymes, water, ions, and mucus into lumen (also hormones)  Lamina propria: layer of loose connective tissue through which small blood vessels, nerve fibers, and lymphatic vessels pass  Separated from underlying tissues by muscularis mucosa (smooth muscle involved in movement of intestinal structures called villi) o Submucosa: submucosal plexus, network of neurons, blood and lymphatic vessels  Vessels branch into both overlying mucosa and underlying layers of smooth muscle (muscularis externa: thick inner layer of circular muscle and thinner outer layer of longitudinal muscle)  Muscle contractions here provide forces for moving and mixing GI contents  Myenteric plexus: second network of neurons between two muscle layers of muscularis externa; innervated by nerves from SNS and PSNS has hs neurons projecting into submucosal plexus o Serosa: surrounds outer surface of the tube; made of connective tissues; connected to abdominal wall by thin sheets of connective tissue  Microscopic structure of the small intestinal wall (Figure 15.4) o Circular folds: mucosa and submucosa, covered with villi (fingerlike projections)  Each villus is covered with epithelial cells whose surface membranes form small projections called microvilli (forms brush border) o Goblet cells secrete mucus to lubricate and protect inner surface of small intestine o Enteroendocrine cells: at base of villi, secrete hormones that help functions such as motility and exocrine pancreatic secretions o Lacteal: single, blind-ended lymphatic vessel at center of each intestinal villus, along with associating capillary network  How most of fat in small intestine is absorbed  Material absorbed by lacteals reaches general circulation by emptying from lymphatic system into large veins via the thoracic duct  Epithelial cells in GI tract are constantly being replaced o Ex: small intestine epithelial cells arise from base of villi and differentiate as they migrate to top of the villus, replacing older cells that die ( get discharged into intestinal lumen where they release their digestive enzymes) o 17 billion epithelial cells are replaced each day  entire small intestine epithelium replaced every 5 days  Makes intestinal tract lining very susceptible to damage by treatments that inhibit cell division (anticancer drugs, radiation therapy)  Absorbed nutrients (other than fat  lacteals) are absorbed and enter blood capillaries after passing through the hepatic portal vein to the liver (then going on to the heart) o Liver has a chance to process digested/absorbed materials and metabolize (detoxify) harmful compounds and prevent them from entering circulation  GI tract also has immune functions  can produce antibodies and fight infectious microorganisms not destroyed by stomach acid o Lymphatic nodules: regions of immune tissue in small intestine 15.3 – General Functions of the GI and Accessory Organs  Saliva: secreted by 3 pairs of exocrine salivary glands located in the head that drains into the mouth through a series of short ducts o Contains HCO and 3ucus to moisten/lubricate food particles to facilitate swallowing o Contains amylase which partially digests polysaccharides o Dissolves some food molecules (molecules must be in dissolved state to be recognized by chemoreceptors in mouth  taste) o Has antipathogenic properties  Pharynx and esophagus: do not contribute to digestion but provide pathway for ingested materials to reach stomach; muscles in walls control swallowing  Stomach: located between esophagus and small intestine; stores, dissolves, and partially digests macromolecules in food and regulates rate at which contents are emptied into small intestine o Acidic environment alters ionization of polar molecules, which allows denaturation of proteins (exposes more sites for digestive enzymes and disrupts connective-tissue protein networks that form tissues in food)  Polysaccharides and fat do not get broken down in acidic pH  Low pH also kills most bacteria (surviving bacteria colonize and multiply in remainder of GI tract) o Chyme: product of stomach digestion; contains molecular fragments of proteins and polysaccharides, droplets of fat, salt, water, and other ingested small molecules (none of these molecules can cross epithelium except water  needs to be broken down further)  Small intestine: majority of absorption and digestion, between stomach and large intestine o Hydrolytic enzymes break down molecules of intact or partially digested carbs, fats, proteins, and nucleic acids into respective monomers (either on apical membranes of intestinal lining cells or secreted by pancreas) o Products of digestion and other molecules that didn’t have to get broken down (water, vitamins, etc.) are absorbed across epithelial cells and enter blood and/or lymph o Duodenum: initial short segment of SI, site of chyme digestion/absorption along with part of jejunum  Large reserve for absorption of most nutrients  removal of part of SI for disease treatment does not necessarily result in nutritional deficiencies o Jejunum: middle segment o Ileum: longest, final segment of SI  Pancreas: located behind stomach, has endocrine and exocrine functions (only exocrine involved in GI function) - o Exocrine part secretes digestive enzymes and a fluid rich in HCO (ne3ded to neutralize acidic chyme coming from stomach so small intestinal enzymes don’t inactive)  Liver: located in upper-right portion of abdomen; secretes bile  Bile: contains HCO , cholesterol, phospholipids, bile pigments, organic wastes, and bile 3 salts (needed to solubilize dietary fat that would otherwise be insoluble in water) o Secreted by liver into small ducts that join to form common hepatic duct o Stored in gallbladder in between meals, which concentrates organic molecules in bile by absorbing some ions and water  When a meal is consumed, gallbladder muscles are stimulated to contract and push bile into duodenum via the common bile duct  Specific transporter-mediated processes in plasma membrane of intestinal epithelial cells absorb monosaccharides and amino acids (fatty acids enter cells via diffusion, mineral ions absorbed actively by transporters, water moves by osmosis)  Motility of SI mixes luminal contents with various secretions, brings contents into contact with epithelial surface where absorption takes place, and slowly advances luminal material toward large intestine o Only small quantities of material move to large intestine (rest is absorbed)  Defecation occurs when contractions of rectum and relaxation of associated sphincter muscles allow expulsion of feces  Most fluid loss from body is via kidneys and respiratory system  CNS receives info from GI tract (afferent input) and has a vital influence on GI function (efferent output) 15.4 – Digestion and Absorption  Carbohydrates o Adults require about 250-300 g (50% daily intake of calories) o Few monosaccharides, dietary fiber (cellulose/plant polysaccharides that do not get broken down in small intestine), disaccharides (mainly sucrose and lactose) o Only small amount is digested by salivary amylase in mouth; most by pancreatic amylase in small intestine (~95%)  Products: disaccharide maltose and a mixture of short branched glucose chains  all get broken down into monosaccharides by enzymes on brush border o Monosaccharides are transported across intestinal epithelium into blood  Glucose undergoes secondary active transport coupled to Na +  Most carbs get digested/absorbed within 20% of small intestine  Proteins o Adults need a minimum of 40-50 g per day  supply essential amino acids and replace nitrogen contained in amino acids that have been metabolized to urea (usually consume 60-90 g; 1/6 daily caloric intake)  Proteins also get digested from enzymes and mucus that was secreted into the GI tract/enters it via death & disintegration of epithelial cells o Broken down into dipeptides, tripeptides, and amino acids  absorbed by SI  Pepsin: enzyme in stomach that breaks down proteins into peptide fragments (produced from inactive precursor pepsinogen)  Trypsin and chymotrypsin further break down peptide fragments in small intestine (secreted by pancreas)  Carboxypeptidases and aminopeptidases further digest small fragments into free amino acids by splitting off carboxyl or amino ends of fragments o Most protein digestion product is absorbed as short chains of 2-3 amino acids by + secondary active transport coupled to the H gradient  Free amino acids can enter epithelial cells via secondary active transport coupled to Na + o In cytosol of epithelial cells, di/tripeptides are hydrolyzed into free amino acids, then leave cell and enter interstitial fluid through facilitated-diffusion transporters in basolateral membranes  Some exo- and endocytosis of intact proteins across epithelium does occur (greater in infants than adults  ex: antibodies from mother’s milk is absorbed intact by infant)  Fat o Daily intake is 70-100 g per day (1/3 daily caloric intake) most as triglycerides o Triglyceride digestion occurs to a limited extent in mouth and stomach, but predominantly in small intestine via pancreatic lipase  Forms two free fatty acids and a monoglyceride o Emulsification: process in which large lipid droplets get divided into smaller droplets (an emulsion, 1 mm in diameter) to increase surface area and accessibility to lipase action (lipids are hydrophobic while lipase is water-soluble)  Mechanical disruption of large lipid droplets into smaller droplets provided by motility of GI tract when it grinds and mixes luminal content  Emulsifying agents come from phospholipids (amphipathic molecules) in foods/bile and bile salts (formed from cholesterol, also amphipathic) from bile  Colipase secreted by pancreas to bind lipase enzyme to surface of lipid droplets for digestion o Micelles (similar to emulsion droplets, but smaller and formed by bile salts/fatty acids/monoglycerides/phospholipids) form to speed up digestion/absorption  Are in equilibrium with small concentration of fat-digestion products that are free in solution and are constantly breaking down and reforming  As free lipid concentration decreases as they diffuse into epithelial cells, more lipids are released from micelles into free phase  New micelles form from newly digested lipids; provides a means of keeping most of the insoluble fat-digestion products in small, soluble aggregates while replenishing small amount of products in solution to freely diffuse o Fatty acids and monoglycerides are resynthesized in triglycerides in epithelial cells in the smooth ER ( decreases free fatty acids/monoglycerides in cytosol to maintain concentration gradient) – Figure 15.13  Fat droplets follow same pathway as a secreted protein to exit cell via vesicles (droplets are called chylomicrons once extracellular)  Chylomicrons pass into lacteals via large pores  pass into lymph  eventually empties into veins  Vitamins o Fat-soluble vitamins (A, D, E, K) follow pathway for fat absorption  solubilized in micelles  Malabsorption: pathological condition in which fat-soluble vitamin absorption decreases due to interference in bile secretion/action of bile salts; leads to deficiency in these vitamins  Nontropical space (celiac disease): due to autoimmune-mediated loss of intestinal brush border surface area due to wheat protein (gluten) sensitivity  often associated with vitamin D malabsorption ( decrease in Ca absorption  disrupts homeostasis) o Water-soluble vitamins are absorbed by diffusion or mediated transport  B 12 only exception  very large and charged, must bind to intrinsic factor secreted by acid-secreting cells in stomach, which can bind to specific sites on epithelium and allow B12o be absorbed via endocytosis  Pernicious anemia: anemia caused by deficiency in RBC formation due to B deficiency; occurs when stomach has been all/partly removed or 12 fails to secrete intrinsic factor or when ileum has been removed/dysfunctions (site of B a12orption); treat with B in12ctions  Water and minerals o Water is most abundant substance in chyme; 80% of fluid is reabsorbed into body via the small intestine  Epithelial membranes of small intestine are very permeable to water; net water diffusion occurs whenever a concentration gradient exists o Na accounts for much of the actively transported solute  uses Na /K -ATPase pumps - - +  Cl and HCO ar3 absorbed with Na o Other minerals (potassium, magnesium, phosphate, calcium ions) and trace elements (zinc, iron, iodine) are also present 15.5 – How Are GI Processes Regulated?  GI reflexes are stimulated by a relatively small number of luminal stimuli: distension of wall by volume of luminal contents, chyme osmolarity, chyme acidity, chyme concentrations of specific digestion products o All act on mechanoreceptors, osmoreceptors, and chemoreceptors  Neural regulation by the enteric NS (specific to GI tract) o Form the myenteric plexus (influences smooth muscle) and the submucosal plexus (influences secretory activity)  both either synapse with other neurons in a given plexus or near smooth muscles/glands/epithelial cells  Allows neural reflexes that are independent of CNS o Neural activity in one plexus influences the activity in the other; impulses can be conducted longitudinally up and down the tract o Contains adrenergic and cholinergic neurons and other neurons that release neurotransmitters (NO, neuropeptides, ATP) o Short reflexes: receptors to nerve plexuses to effecter cells all in GI tract o Long reflexes: receptors to CNS via afferent neurons to nerve plexuses to effector cells via autonomic nerve fibers o Hunger, the sight/smell of food, and emotional states can have significant effects on GI tract (not always signal that initiates with tract)  Hormonal regulation o Hormones involved are mainly secreted by enteroendocrine cells in epithelium of stomach/small intestine  Various chemical substances in chyme stimulate cells to secrete their hormones from the opposite side of the cell into the blood o Best understood GI hormones: secretin, cholecystokinin (CCK), gastrin, and glucose-dependent insulinotropic peptide (GIP) – Table 15.4  Most hormones participate in a feedback control system that regulates some aspect of the GI luminal environment  Most GI hormones affect more than one type of target cell o CCK secretion is stimulated by fatty acids and amino acids in small intestine  CCK stimulates pancreas to increase secretion of digestive enzymes and causes the sphincter of Oddi to relax and the pyloric sphincter to close  CCK causes gallbladder to contract  bile salts go to intestines for micelle formation o Potentiation: cell contains a variety of receptors  variety of inputs exist that can affect the cell’s response  Ex) CCK amplifies secretin’s response: two enzymes together can cause more release of HCO th3n individually or expected together  Consequences: small changes in the plasma concentration of one GI hormone can have large effects on the actions of other GI hormones o GI hormones have growth-promoting (trophic) effects on various tissues (gastric and intestinal mucosa, exocrine portions of pancreas) o Additional GI hormones are involved in control of blood glucose by serving as a feedforward signal from the GI tract to endocrine pancreas or regulate appetite  Phases of gastrointestinal control o Cephalic phase: initiated when sensory receptors in the head are stimulated by sight/smell/taste/chewing or by emotional states  Efferent pathways for reflexes are mediated by parasympathetic fibers which affect secretory and contractile activity o Gastric phase: initiated by distension, acidity, amino acids, and peptides formed during partial digestion of ingested protein  Responses mediated by short and long neural reflexes and by release of gastrin o Intestinal phase: initiated by stimuli in small intestine (distension, acidity, osmolarity, various digestive products)  Responses mediated by short and long neural reflexes and by secretin, CCK, and GIP o Phases do not occur in temporal sequence except at beginning of a meal; otherwise all three phases can occur simultaneously during ingestion/absorptive period  Chewing: controlled by somatic nerves to skeletal muscles of the mouth and jaw (voluntary) o Rhythmic chewing motions are reflexively activated by pressure of food against gums, hard palate at the roof the mouth, and tongue (activation of mechanoreceptors causes reflexive inhibition of muscles that keep jaw closed) o Prolongs subjective pleasure of taste o Breaks up food particles  creates a bolus that is easier to swallow/digest (prevents choking)  Saliva: o Released by parotid, sublingual, and submandibular glands; controlled by sympathetic and parasympathetic neurons (stimulated by both, para is faster) o No hormonal regulation; secretion increases in response to smell or sight of food o Secretion is accomplished by large increase in blood flow to salivary glands, mediated by increase in parasympathetic neural activity o Sjogren’s syndrome: immune disorder in which many exocrine glands are rendered nonfunctional by infiltration of WBCs and immune complexes  Includes loss of salivary gland function that leads to dry mouth, impaired sense of taste, difficulty chewing, ulcers; treat with frequent sips of water and oral fluoride treatment to prevent tooth decay  Swallowing: initiated when pressure receptors in walls of pharynx are stimulated by food/drink forced into rear of mouth by the tongue o Send impulses to the swallowing center in the medulla oblongata of brainstem  elicits swallowing via efferent fibers to the muscles in the pharynx and esophagus as well as the respiratory muscles  Inhibit respiration, raise larynx, close glottis (around vocal cords) to keep food from entering trachea  Soft palate elevates and lodges against back wall of pharynx to prevent food from entering nasal cavity when swallowing  Epiglottis raises to protect glottis and prevent aspiration of food o Skeletal muscles in upper third of esophagus and smooth muscle in lower 2/3s move food down esophagus  Esophagus ends are closed by sphincters: upper esophageal sphincter and the lower esophageal sphincter  Relaxation of upper ES  food enters, sphincter closes ( glottis opens, breathing resumes)  progressive wave of muscle contractions moves food to end of esophagus (allows people to swallow even upside down)  opening of lower ES  food enters stomach  lower ES closes o Neural and muscular reflex coordinated by swallowing center; afferent fibers from receptors can alter efferent activity (ex: initiating secondary peristalsis if first one didn’t move all the food to the stomach) o Location of last portion of esophagus beneath diaphragm prevents pressure gradient between stomach and esophagus that could force stomach contents into esophagus  Growth of fetus during pregnancy  push terminal segment through diaphragm into thoracic cavity; causing gastroesophageal reflux (acid reflux; gastric contents are forced up into esophagus)  heartburn caused by HCl irritating cell walls  Stomach o Glands formed by invagination of mucosa by the epithelium of stomach (canaliculus) secrete mucus, HCl, and pepsinogen; increases surface area of parietal cells  Cells at opening of glands secrete protective coating of mucus and HCO 3-  Parietal cells line walls of glands, secrete HCl and intrinsic factor  Chief cells secrete pepsinogen  Enterochromaffin-like (ECL) cells release histamine (paracrine substance)  G cells release gastrin  D cells secrete somatostatin o Fundus: upper part of the stomach; functionally part of the rest of the body o Antrum: lower portion, much thicker layer of smooth muscle and is responsible for mixing and grinding stomach contents  Pyloric sphincter: at junction of antrum and small intestine  HCl production and secretion o 2 L secreted by stomach per day; concentration in stomach is up to 1-3 million times greater than in blood o Generated from CO from2parietal cell  carbonic anhydrase catalyzes reaction between CO and water to produce H CO  H and HCO + - + 2+ 2 3 3  H /K -ATPase pumps hydrogen ions into lumen of the stomach (# of pumps increases with increasing H ) +  Removal of end products enhances rate of reaction  production and secretion of H are coupled + + o Gastrin, ACh, and histamine stimulate insertion of H /K -ATPase pumps into plasma membrane  All potentiate each other’s effect  Cephalic phase stimulates all three (prepare for incoming food) o Somatostatin inhibits acid secretion o Distension from volume of ingested material also stimulates acid secretion; presence of protein/polypeptides causes further secretion  Stimuli can use some of the same neural pathwyas used during cephalic phase ( increased parasympathetic neural input to increase release of ACh, gastrin, and histamine) o H inhibits gastrin secretion and stimulates release of somatostatin from D cells  Somatostatin acts on parietal cells to inhibit acid secretion and inhibits release of gastrin and histamine o Polypeptides from proteins act on gastrin to stimulate acid secretion and acts as a buffer so stomach doesn’t get too excited (causes more acid secretion too) o High acidity in duodenum triggers reflexes that inhibit gastric acid secretion  Beneficial as enzymes/bile salts in SI do not function in acidic pH o Acid/distension/hypertonic solutions/amino acids in solution/and fatty acids in SI all inhibit gastric acid secretion; effect depends on amount  Net result must maintain balance of secretory activity of the stomach with digestive and absorptive capacities of the small intestine  In intestinal phase  mediated by short and long neural reflexes and hormones o Enterogastrones: hormones released by the intestinal tract that reflexively inhbit gastric activity  Includes secreting and CCK  Pepsin secretion o Secreted by chief cells; pepsinogen  pepsin (low pH in lumen of the stomach activates a very rapid, autocatalytic process that produces pepsin) o Zymogens: proteolytic enzymes in GI tract that are synthesized and stored intracellularly in inactive forms (do not act on cells that produce them) o Active only in high H concentration  inactivates in small intestine (HCO 3- neutralizes environment) o Parallels acid secretion; most of the factors that stimulate acid secretion also stimulate pepsin secretion o Not essential for protein digestion because small intestine can do it; just favorable for accelerated digestion (and needed for breakdown of collagen from meat)  Pancreatic secretions - o Exocrine portion secretes HCO and d3gestive enzymes into ducts  converge to pancreatic duct  common bile duct  duodenum  HCO se3reted via apical membrane Cl /HCO exchanger3 + +  H exchanged for extracellular Na on basolateral side  Energy provided by Na/K-ATPase pumps on basolateral membrane o Cystic fibrosis transmembrane conductance regulator (CFTR) recycle Cl to - prevent accumulation; provides paracellular route that Na and water move into ducts (due to electrochemical gradient established) -  Cystic fibrosis: mutations in CFTR, results in decreased pancreatic HCO 3 secretion  thickening of pancreatic secretions, clogging of pancreatic ducts and pancreatic damage o Enzymes secreted by pancreas digest fat, polysaccharides, proteins, nucleic acids to respective monomers (Table 15.6)  Activation of zymogens is mediated by enterokinase (from apical plasma membrane of intestinal epithelium)  ex: trypsinogen  trypsin after enterokinase splits off peptide(s)  Non-proteolytic enzymes are secreted fully functional and active o Increases during a meal due to stimulation by secretin ( HCO ) and CC3 ( enzyme secretion)  Secretin stimulated by increased acidity in duodenum  CCK stimulated by fatty acids and amino acids in duodenum o Mostly stimulated by intestinal stage, but small influence of cephalic and gastric stimuli too (i.e. taste of food  more pancreatic secretion)  Bile formation and secretion o Functional unit of liver: hepatic lobule; each contains branches of the bile duct, hepatic and portal veins, and hapatic artery  Substances absorbed through the small intestine pass through liver before reaching vena cava or are taken up by hepatocytes (liver cells; for modification) o Hepatocytes rid the body of substances by secretion into the bile canaliculi (converges to form common hepatic bile duct) - o Bile: bile salts, lecithin (phospholipid, made in liver), HCO and3other ions, cholesterol, bil pigments, other small metabolic end products, trace metals  First three have purposes (previously described), last three were just removed from body -  Bile salts/cholesterol/lecithin/pigments – secreted by hepatocytes; HCO 3 secreted by epithelial cells of bile ducts  Most important: bile salts – can be recycled via the portal vein to the liver + (driven by secondary active transport coupled to Na ) in enterohepatic circulation (can occur numerous times to digest even one meal)  5% of bile is lost through feces; cholesterol is used in liver to make more o Cholesterol is removed from body and extracted via bile – maintains cholesterol homeostasis  Certain drugs and dietary fiber lower cholesterol in this way (removal of cholesterol = liver must remove it from blood or synthesis it to have more for bile salts) o Bile pigments: substances formed from heme portion of hemoglobin when old/damaged RBCs are broken down in spleen and liver  Bilirubin is most predominant; gives urine yellow color and feces brown color (after being modified by bacterial enzymes) o Sphincter of Oddi: when closed, bile secreted from liver enters gallbladder to become more concentrated (cannot enter small intestine)  After fatty meal: sphincter relaxes  gallbladder contracts/discharges concentrated bile into duodenum (signal: CCK; figure 15.33)  Small intestine secretion o Appx. 1500 mL secreted from blood into lumen every day o Water majorly secretes (moves) to balance mineral ion charges at billi; water follows ions by osmosis  Allows lubrication of surfaces of intestinal tract and protection of epithelium from excessive damage by digestive enzymes o Water also moves into lumen when chyme enters small intestine from stomach  Hypertonic solution causes water to move from isotonic plasma into lumen  Small intestine absorption o All fluid is reabsorbed back into the blood (including salivary, gastric, hepatic, and pancreatic secretions)  Net absorption of water from small intestine o Absorption is achieved mainly through Na and nutrient cotransport; water follows by osmosis CHAPTER 16 – PART A ONLY Section A of Chapter 16 except Cholesterol Balance (parts of pages 566-568) including Figure 16-2. The Case Study for chapter 16 WILL be required. 16.1 – Events of the Absorptive and Postabsorptive States  Absorptive state: ingested nutrients enter the blood from the GI tract o Some nutrients can provide immediate energy requirements of the body; rest is stored o Figure 16.1 shows all events of absorptive state o Recap: carbs/proteins absorbed through their monomers into blood from GI tract; lipids are absorbed in lymph as chylomicrons (lymph then drains to blood)  Absorbed carbs (mostly glucose – body’s main source of energy) o Glucose  CO + H 2 + A2P o Major consumer: skeletal muscle  Converts excess glucose into glycogen for storage o Adipose tissue cells use glucose for energy; but as precursor for triglycerides o Net uptake of glucose by liver; stored as glycogen or transformed into triglycerides  Lipoproteins: fat synthesized from glucose in liver; packaged with specific proteins into molecular aggregates  Very-low-density lipoproteins (VLDLs): lipoproteins in blood; contain more fat than protein (less dense)  Lipoprotein lipase: hydrolyzes VLDLs into monoglycerides and fatty acids; found on capillaries of endothelium o Adipose tissue will absorb fatty acids generated by lipoprotein lipase and use them to create new triglycerides in cytosol and stored o Glucose fates: used as energy source, glycogen storage in liver/skeletal muscle, storage as fat in adipose tissue  Absorbed lipids o Triglycerides in chylomicrons follow similar path to VLDLs  Fatty acids from chylomicrons released by lipoprotein lipase  absorbed into adipocytes  reform triglycerides with glucose metabolites  Glucose metabolites needed to provide necessary glycerol 3-phosphate o Major sources of fatty acids in adipose: glucose that enters and is broken down; glucose that is used in liver to form VLDL triglycerides and get absorbed; ingested triglycerides transported through body in chylomicrons  Emphasizes storage of ingested fat  Absorbed amino acids o Some get absorbed into liver cells to synthesize proteins (enzymes, plasma proteins) o Others are converted into α-keto acids by removal of amino group (deamination)  Amino groups used to synthesize urea in liver to be excreted by kidneys  α-keto acids can enter Krebs cycle to be catabolized for energy in liver cells or be used to synthesize fatty acids (fat synthesis in liver) o Most are taken up by other cells (not liver cells) to synthesize proteins  Net synthesis of protein during absorptive state, but this is just replacing proteins that were catabolized in postabsorptive state  Excess amino acids are not stored  once stable protein turnover rate is met, rest are converted into carbs and triglycerides (cannot eat extra protein for muscle gain unless weight-bearing exercise is included)  Postabsorptive state: DI tract is empty of nutrients and body’s own stores supply energy o Enough stored that the average person could fast for many weeks (with water) o Net synthesis of glycogen, triglycerides, and protein ceases  net catabolism of these substances begins  No glucose is being absorbed from GI tract, but homeostasis of it must be maintained (needed for CNS especially) or face detrimental side effects (mental function impairment, seizures, coma, death)  Sources of blood glucose o Glycogenolysis: hydrolysis of glycogen stores to glucose 6-phosphate (occurs in liver)  enzymatically converted to glucose  enters blood  Needs stimulus such as SNS activation; first line of defense in maintaining glucose homeostasis  Can only provide enough glucose for a few hours before being depleted  Can also occur in skeletal muscle; but glucose 6-phosphate directly undergoes glycolysis for ATP, pyruvate, and lactate (ATP and pyruvate used for energy; lactate circulates to liver to synthesize glucose) o Lipolysis: catabolism of triglycerides in adipose tissue  glycerol enters blood and goes to liver and can be used to synthesize glucose o Proteins catabolism can also be used (α-keto acids used in glucose synthesis in liver)  However, continual protein loss contributes to disruption of cell function, sickness, and death o Gluconeogenesis: creation of new glucose from precursors such as amino acids and glycerol (liver and kidneys)  In 24 hour fast, 180 g of glucose can by synthesized  Glucose sparing (fat utilization by organs so nervous system can have glucose) o Gluconeogenesis cannot provide all of energy requirements (720 kcals for 1500- 3000 kcal/day needs)  organs can switch from catabolizing glucose and increase fat utilization o Lipolysis of adipose-tissue triglycerides liberates glycerol and fatty acids into blood  Liberated fatty acids circulate (bound with plasma protein albumin) and get taken up and metabolized by all tissues (except nervous system)  undergo beta oxidation to yield hydrogen atoms (for oxidative phosphorylation) and acetyl CoA  acetyl CoA enters Krebs cycle and is catabolized (CO 2nd water)  Acetyl CoA in liver is processed into ketones  released into blood as important energy source for all tissues (including NS) o Nervous system can only utilize glucose for energy – receives all of the limited amount present in body (and ketones)  Ketone use  less glucose use  less protein breakdown in gluconeogenesis  prevents serious tissue damage 16.2 – Endocrine and Neural Control of the Absorptive and Postabsorptive States  Important controls in transition from feasting to fasting: insulin and glucagon (pancreatic hormones); epinephrine and cortisol (adrenal gland hormones); growth hormone (anterior pituitary gland); sympathetic nerves to liver and adipose tissue o Islets of Langerhans (pancreatic islets): clusters of endocrine cells that secrete insulin (beta cells) and glucagon (alpha cells)  Insulin: most important controller of organic metabolism; increased secretion during absorptive state (decreased in postabsorptive state) o Figure 16.5 – most important responses of target cells (muscle, adipocytes, hepatocytes)  Induces effects by binding to specific receptor son plasma membranes of target cells  Example effect: insulin causes increase in number of GLUTs on cell membrane for glucose uptake o Brain cells express a different subtype of GLUT (high affinity, not insulin- dependent) – ensures brain will always get glucose even during fasting (little insulin present) o Figure 16.7 – biochemical events that occur due to insulin  Major principle: insulin brings about its ultimate responses by multiple actions (ex: skeletal muscle – increased glucose transport, simulation of glycogen synthesis enzyme glycogen synthase, inhibition of glycogen phosphorylase to stop glycogen catabolism) o Insulin favors glucose transformation to and storage as glycogen in skeletal muscle o Insulin aids protein synthesis too by increasing number of active membrane transporters for amino acids, stimulates ribosomal enzymes for protein synthesis, and inhibits enzymes for protein catabolism  Control of insulin secretion o Major control factor: plasma glucose concentration (acts on beta cells of islets to stimulate insulin secretion; Figure 16.8)  homeostatic process regulated by negative feedback  Insulin stimulates entry of glucose into muscle/adipose tissue, net uptake of glucose by liver  Insulin secretion decreases as blood glucose levels return to normal after meal o Increased amino acid concentrations stimulate insulin secretion (negative feedback control) o Incretins: family of hormones secreted by enteroendocrine cells in GI tract in response to eating  amplify insulin response to glucose to prevent large spikes in glucose blood concentration after meals (prevents kidney reabsorption capcity from being exceeded)  Glucagon-like peptide I (GLP-1) and glucose-dependent insulinotropic peptide (GIP)  Feedforward component to glucose regulation during meal digestion  GLP-1 analog used as treatment for type II diabetes mellitus o Autonomic neurons in islets of Langerhans  Parasympathetic neurons (activated during meal digestion): stimulates secretion of insulin (feedforward regulation)  Sympathetic neurons or epinephrine increase: inhibits insulin secretion (associated with hypoglycemia, stress, exercise  want glucose in blood)  Glucose-counterregulatory controls: hormonal and neural factors that oppose action of insulin in some way o Glucagon: produced by alpha cells of islets; stimulates glycogenolysis, gluconeogenesis, and ketone synthesis  Wants to increase plasma concentrations of glucose and ketones (needed for postabsorptive state and to prevent hypoglycemia)  Stimulated by decrease in circulating glucose conc.  restores normal glucose levels (opposite effect for increase in glucose levels)  Ketones used in brain  Controlled by amino acids (increase = stimulation) and neural/hormonal inputs too (sympathetic = stimulation; part of fight-or-flight response) o Epinephrine and sympathetic nerves to liver and adipose tissue stimulate glucagon  Epinephrine: stimulates glycogenolysis in liver/skeletal muscle, gluconeogenesis in liver, lipolysis in adipocytes  Hormone-sensitive lipase (HSL): catalyzes breakdown of triglycerides to free fatty acids and glycerol (energy sources/gluconeogenic precursor); stimulated by epinephrine, inhibited by insulin  low blood glucose leads to increase in epinephrine/sympathetic nerve activity  increased glucagon o Cortisol: permissive functions in adjustment to fasting; maintains concentrations of key liver and adipose-tissue enzymes required for gluconeogenesis and lipolysis (ex: HSL)  Does not need to increase much during fasting  Cortisol deficient individuals can develop hypoglycemia during fasting  Effects increase during stress  can elicit many metabolic events associated with fasting  Decreases sensitivity of muscle/adipose cells to insulin to maintain blood glucose conc. During fasting/allow brain to have glucose o Growth hormone: stimulates growth and protein synthesis  Deficiency/excess of GH will not produce significant abnormalities in lipid/carb metabolism  Increase responsiveness of adipocytes to lipolytic stimuli, stimulates gluconeogenesis by liver, reduces ability of insulin to stimulate glucose uptake by muscle/adipose tissue (anti-insulin effects)  can be observed in those with acromegaly (excess GH)  Hypoglycemia: abnormally low plasma glucose concentration o Fasting hypoglycemia: caused by excess of insulin due to insulin-producing tumors, drugs that stimulate insulin secretion, or taking too much insulin, or by a defect in one or more glucose-counterregulatory controls (inadequate glycogenolysis due to liver disease/cortisol deficiency) o Symptoms: increased HR, trembling, nervousness, sweating, anxiety  activation of sympathetic NS; headache, confusion, dizziness, loss of coordination, slurred speech  too little glucose reaching brain 16.3 – Energy Homeostasis in Exercise and Stress  Large quantities of fuel are necessary during exercise for skeletal and cardiac muscle contraction o Plasma glucose, fatty acids, muscle glycogen o Liver also provides glucose via breakdown of glycogen stores and gluconeogenesis o HSL activation  increase in adipose-tissue lipolysis  glycerol and fatty acids for additional energy  In prolonged exercise (>90 min), plasma glucose concentration decrease less than 25% o Glucose output by liver increases in proportion to increased glucose utilization  Increase in hepatic glucose production, triglyceride breakdown, fatty acid utilization  similar to fasting (same endocrine controls) o Exercise is characterized by decrease in insulin secretion and increase in glucagon secretion (use of glucose by muscles  decrease plasma glucose levels) o Sympathetic NS, cortisol, GH, and epinephrine stimulated  Sympathetic NS contributes directly to energy mobilization: acts on liver/adipose tissue; indirectly: inhibits secretion of insulin and stimulates glucagon  Difference between exercise and fasting = glucose uptake is increased by skeletal and cardiac muscle in exercise (decreased utilization during fasting) o Muscle contraction somehow causes a migration of an intracellular store of glucose transporters to membrane (can use glucose despite lack of insulin)  Physical and emotional stresses can induce same conditions as exercise  prepares body for fight-or-flight response o Amino acids liberated by catabolism of protein stores (due to decreased insulin/increased cortisol) are ready for tissue repair if necessary and provide energy via gluconeogenesis o Chronic intense stress is bad for the body  nonessential functions are repressed for nutrients can go to CNS/muscle (ex: reproductive functions), delayed puberty  Exercise-induced amenorrhea: temporary infertility due to intense chronic exercise (mainly in women; ex: professional ballerinas) CASE STUDY FOR CHAPTER 16 REQUIRED FOR EXAM (not included in study guide)


Buy Material

Are you sure you want to buy this material for

25 Karma

Buy Material

BOOM! Enjoy Your Free Notes!

We've added these Notes to your profile, click here to view them now.


You're already Subscribed!

Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'

Why people love StudySoup

Steve Martinelli UC Los Angeles

"There's no way I would have passed my Organic Chemistry class this semester without the notes and study guides I got from StudySoup."

Amaris Trozzo George Washington University

"I made $350 in just two days after posting my first study guide."

Bentley McCaw University of Florida

"I was shooting for a perfect 4.0 GPA this semester. Having StudySoup as a study aid was critical to helping me achieve my goal...and I nailed it!"

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

Become an Elite Notetaker and start selling your notes online!

Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.