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Steps in the Process of Digestion In the oral cavity, saliva dissolves some organic nutrients, and mechanical processing with the teeth and tongue disrupts the physical structure of the material and provides access for digestive enzymes. Those enzymes begin the digestion of complex carbohydrates (polysaccharides) and lipids. In the stomach, the material is further broken down physically and chemically by stomach acid and by enzymes that can operate at an extremely low pH. In the duodenum, buffers from the pancreas and liver moderate the pH of the arriving chyme, and various digestive enzymes are secreted by the pancreas that catalyze the catabolism of carbohydrates, lipids, proteins, and nucleic acids. Nutrient absorption then occurs in the small intestine, primarily in the jejunum, and the nutrients enter the bloodstream. Indigestible materials and wastes enter the large intestine, where water is reabsorbed and bacterial action generates both organic nutrients and vitamins. These organic products are absorbed before the residue is ejected at the anus. Most of the nutrients absorbed by the digestive tract end up in a tributary of the hepatic portal vein that ends at the liver. The liver absorbs nutrients as needed to maintain normal levels in the systemic circuit. Within peripheral tissues, cells absorb the nutrients needed to maintain their nutrient pool and ongoing operations. Figure 22 Section 2 Digestion, Absorption, Transport Digestion Breakdown of food molecules for absorption into circulation Mechanical: Breaks large food particles to small Chemical: Breaking of covalent bonds by digestive enzymes Absorption and transport Molecules are moved out of digestive tract and into circulation for distribution throughout body Digestive System Regulation Nervous regulation Involves enteric nervous system Types of neurons: sensory, motor, interneurons Coordinates peristalsis and regulates local reflexes Chemical regulation Production of hormones Gastrin, secretin Production of paracrine chemicals Histamine Help local reflexes in ENS control digestive environments as pH levels Digestive System Anatomy Digestive tract Accessory organs Alimentary tract or canal GI tract Primarily glands Regions Mouth or oral cavity Pharynx Esophagus Stomach Small intestine Large intestine Anus Peritoneum and Mesenteries Peritoneum Visceral: Covers organs Parietal: Covers interior surface of body wall Retroperitoneal: Behind peritoneum as kidneys, pancreas, duodenum Mesenteries Routes which vessels and nerves pass from body wall to organs Greater omentum Lesser omentum Digestive Tract Histology Oral Cavity Mouth or oral cavity Lips (labia) and cheeks Palate: Oral cavity roof Vestibule: Space between lips or cheeks and alveolar processes Oral cavity proper Hard and soft Palatine tonsils Tongue: Involved in speech, taste, mastication, swallowing Teeth Two sets Primary, deciduous, or milk: Childhood Permanent or secondary: Adult (32) Types Incisors, canine, premolar and molars Tooth structure: Salivary Glands Produce saliva Prevents bacterial infection Lubrication Contains salivary amylase Breaks down starch Three pairs Parotid: Largest Submandibular Sublingual: Smallest Deglutition (Swallowing) Three phases Voluntary Bolus of food moved by tongue from oral cavity to pharynx Pharyngeal Reflex: Upper esophageal sphincter relaxes, elevated pharynx opens the esophagus, food pushed into esophagus Esophageal Reflex: Epiglottis is tipped posteriorly, larynx elevated to prevent food from passing into larynx Phases of Deglutition (Swallowing) The process of peristalsis Bolus of food arrives in digestive system. Food bolus Toward anus Longitudinal muscle Circular muscle Circular muscles contract behind bolus. Longitudinal muscles ahead of bolus contract. Contraction in circular muscle layer forces bolus forward. Stomach Anatomy: Openings Gastroesophageal: To esophagus Pyloric: To duodenum Regions Cardiac Fundus Body Pyloric Stomach Anatomy cont. Rugae: Folds in stomach when empty Gastric pits: Openings for gastric glands Contain cells Surface mucous: Mucus Mucous neck: Mucus Parietal: Hydrochloric acid and intrinsic factor Chief: Pepsinogen Endocrine: Regulatory hormones The structure of the wall of the stomach Layers of the Stomach Wall Mucosa Consists of a simple columnar epithelium that produces an alkaline carpet of mucus that covers the interior surfaces of the stomach and protects epithelial cells against the acid and enzymes in the gastric lumen Lamina propria Lymphatic vessel Muscularis mucosae Artery and vein Submucosa Muscularis Externa Oblique muscle Circular muscle Longitudinal muscle Serosa Myenteric plexus The structure of gastric pits and gastric glands Lamina propria Mucous epithelial cells Gastric pit Neck Cells of Gastric Glands Parietal cells (secrete HCl and intrinsic factor) G cells (produce a variety of hormones) Gastric glands Chief cells (secrete pepsinogen) Figure 21.9 2 The secretory activities of parietal cells Hydrogen ions (H+) are generated inside a parietal cell as the enzyme carbonic anhydrase converts CO2 and H2O to carbonic acid (H2CO3), which then dissociates. Diffusion Carbonic anhydrase A countertransport mechanism ejects the bicarbonate ions into the interstitial fluid and imports chloride ions into the cell. Interstitial fluid To bloodstream KEY Parietal cell The chloride ions then diffuse across the cell and exit through open chloride channels into the lumen of the gastric gland. Carrier-mediated transport The hydrogen ions are actively transported into the lumen of the gastric gland. Active transport Countertransport Lumen of gastric gland Figure 21.9 3 Phases of Gastric Activity I Phases of Gastric Activity II Movements in Stomach Phases of Gastric Activity III Ingested food The pattern of hormone release and the effects of those hormones within the digestive system Hormone Action KEY Food in stomach inhibits Acid production by parietal cells stimulates Gastrin Stimulation of gastric motility; mixing waves increase in intensity GIP Chyme in duodenum Release of insulin from pancreas Release of pancreatic enzymes and buffers Secretin and CCK VIP Bile secretion and ejection of bile from gallbladder facilitates Dilation of intestinal capillaries facilitates Material arrives in jejunum Nutrient absorption NUTRIENT UTILIZATION BY ALL TISSUES The two central reflexes triggered by the stimulation of stretch receptors in the stomach wall Central Gastric Reflexes Gastroenteric reflex: stimulates motility and secretion along the entire small intestine Gastroileal reflex: triggers the opening of the ileocecal valve, allowing materials to pass from the small intestine into the large intestine Ileocecal valve Figure 21.13 2 Small Intestine Site of greatest amount of digestion and absorption Divisions Modifications Duodenum Jejunum Ileum: Peyer’s patches or lymph nodules Circular folds or plicae circulares, villi, lacteal, microvilli Cells of mucosa Absorptive, goblet, granular, endocrine The characteristic features of each of the three segments of the small intestine Jejunum Serosa Duodenum Muscularis externa Duodenal glands Plicae circulares Villi Submucosa Mucosa Muscularis mucosae Ileum Aggregated lymphoid nodules Figure 21.11 2 Small Intestine Secretions Mucus Digestive enzymes Protects against digestive enzymes and stomach acids Disaccharidases: Break down disaccharides to monosaccharides Peptidases: Hydrolyze peptide bonds Nucleases: Break down nucleic acids Duodenal glands Stimulated by vagus nerve, secretin, chemical or tactile irritation of duodenal mucosa Mixing: Segmental contraction that occurs in small intestine Involves contraction of circular muscles only Intestinal adaptations for absorbing nutrients A photomicrograph showing the brush border of an intestinal villus The structure of an intestinal villus Plica circulares Capillaries The complex internal structure of an intestinal villus Villi Mucous cells A plica circulares and villi in the small intestinal wall Lacteal Brush border Tip of villus A diagrammatic sectional view of the intestinal wall showing features common to all segments of Villi Submucosal Lacteal the small intestine artery and vein (lymphatic Columnar epithelial cell Mucous cell capillary) Lacteal Nerve Layers of the Small Intestine Intestinal gland Capillary network Mucosa Arteriole Muscularis mucosae Lymphatic vessel Lamina propria Venule Lymphoid nodule Submucosa Submucosal plexus Circular layer of smooth muscle Muscularis externa Myenteric plexus Serosa Longitudinal layer of smooth muscle Lymphatic vessel Muscles that move the villi back and forth to expose the epithelial surfaces to the intestinal contents Muscularis mucosae Figure 21.10 LM x 250 Intestinal adaptations for absorbing nutrients Plica circulares Villi A plica circulares and villi in the small intestinal wall A diagrammatic sectional view of the intestinal wall showing features common to all segments of Lacteal Submucosal Villi the small intestine (lymphatic artery and vein capillary) Layers of the Small Intestine Intestinal gland Mucosa Muscularis mucosae Lymphoid nodule Submucosa Submucosal plexus Circular layer of smooth muscle Muscularis externa Myenteric plexus Serosa Longitudinal layer of smooth muscle Lymphatic vessel Figure 21.10 1 – 3 Plica circulares Villi A plica circulares and villi in the small intestinal wall Figure 21.10 2 A diagrammatic sectional view of the intestinal wall showing features common to all segments of Lacteal Submucosal Villi (lymphatic the small intestine artery and vein capillary) Layers of the Small Intestine Intestinal gland Mucosa Muscularis mucosae Lymphoid nodule Submucosa Submucosal plexus Circular layer of smooth muscle Muscularis externa Myenteric plexus Serosa Longitudinal layer of smooth muscle Lymphatic vessel Figure 21.10 3 A photomicrograph showing the brush border of an intestinal villus The structure of an intestinal villus Capillaries The complex internal structure of an intestinal villus Mucous cells Lacteal Brush border Tip of villus LM x 250 Columnar epithelial cell Mucous cell Lacteal Nerve Capillary network Arteriole Lymphatic vessel Lamina propria Venule Muscles that move the villi back and forth to expose the epithelial surfaces to the intestinal contents Muscularis mucosae Figure 21.10 4 – 5 Accessory Glands and Structures Liver Exocrine Pancreas Gall bladder Pancreatic duct Hepatic Portal System Duct System Pancreas Anatomy Endocrine Exocrine Pancreatic islets produce insulin and glucagon Acini produce digestive enzymes Regions: Head, body, tail Secretions Pancreatic juice (exocrine) Trypsin Chymotrypsin Carboxypeptidase Pancreatic amylase Pancreatic lipases Enzymes that reduce DNA and ribonucleic acid Duodenum and Pancreas Exocrine Pancreas – Enzymes Trypsinogen Chymotrysinogen Carboxypeptidases Pro-elastase Phospholipase pancreatic lipase Pancreatic amylase Enzymes that reduce DNA and ribonucleic acid Gallbladder Bile is stored and concentrated Stimulated by cholecystokinin and vegal stimulation Dumps into small intestine Production of gallstones possible Drastic dieting with rapid weight loss Liver Lobes Major: Left and right Minor: Caudate and quadrate Ducts Common hepatic Cystic From gallbladder Common bile Joins pancreatic duct at hepatopancreatic ampulla Functions of the Liver Bile production Storage Hepatocytes remove ammonia and convert to urea Phagocytosis Glycogen, fat, vitamins, copper and iron Nutrient interconversion Detoxification Salts emulsify fats, contain pigments as bilirubin Kupffer cells phagocytize worn-out and dying red and white blood cells, some bacteria Synthesis Albumins, fibrinogen, globulins, heparin, clotting factors Clicker Question: Which of the following enzymes is critical to the primary function of the gastric parietal cells? A) Pepsin B) Gastrin C) Carbonic Anhydrase D) Lipase E) None of the above Clicker Question: Where would you find a high frequency of Peyer’s patches? A) Stomach B) Duodenum C) Jejunum D) Ileum Clicker Question: The Plicae Circularis perform which of the following functions? A) They impart a spin to the chyme as it travels through the jejunum. B) They act like an accordion bellows, to allow the wall of the jejunum to stretch. C) They provide attachment sites for beneficial bacteria. D) They increase the surface area of the duodenum and jejunum. E) None of the above. Clicker Question: Activity in the myenteric plexus is inhibited by by: A) Gastrin B) CCK C) Secretin D) All of the above E) B and C above Blood and Bile Flow Start As it remains in the gallbladder, bile becomes more concentrated. The liver secretes bile continuously —roughly 1 liter per day. Liver The functional relationships involved in the storage and ejection of bile Duodenum CCK Bile salt emulsifying lipid droplet in the lumen of the digestive tract Lipid droplet The release of CCK by the duodenum triggers dilation of the hepatopancreatic sphincter and contraction of the gallbladder. This ejects bile into the duodenum through the duodenal ampulla. Figure 21.19 3 Bile …each day around 600 – 1000 ml of bile is produced… Bile acid Phospholipids Cholesterol Bilirubin Waste products Electrolytes Mucin Figure 24-26: A Summary of the Chemical Events in Digestion REGION AND HORMONAL CONTROLS CARBOHYDRATES ORAL CAVITY LIPIDS Salivary amylase PROTEINS Lingual lipase ESOPHAGUS STOMACH Pepsin Stimulus: Anticipation or arrival of food Hormone: Gastrin Source: G cells of stomach Disaccharides Trisaccharides Polypeptides Proenzyme released: Pepsinogen by chief cells, activated to pepsin by HCl SMALL INTESTINE Bile salts and pancreatic lipase Stimulus: Arrival of chyme in duodenum Pancreatic alpha-amylase Hormone: CCK Proenzymes released: Chymotrypsinogen, procarboxypeptidase, proelastase, trypsinogen. Enterokinase activates trypsin, which activates other enzymes Disaccharides Trisaccharides Monoglycerides, Fatty acids in micelles Trypsin Chymotrypsin Elastase Carboxypeptidase Short peptides, Amino acids Enzymes released: Pancreatic amylase, pancreatic lipase, nuclease, enterokinase INTESTINAL MUCOSA Brush border Cell body Maltase, Sucrase Lactase DIFFUSION Dipeptidases FACILITATED DIFFUSION AND COTRANSPORT Monoglycerides, Fatty acids FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Triglycerides Amino acids Chylomicrons FACILITATED DIFFUSION EXOCYTOSIS FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Chylomicrons Amino acids BLOODSTREAM Capillary (a) Lacteal (b) Capillary (c) Carbohydrates Carbohydrates are usually preferred substrates for catabolism and ATP production when resting Steps of carbohydrate digestion In mouth, salivary amylase digests complex carbohydrates into disaccharides and trisaccharides Enzyme active only down to pH 4.5 and denatured in stomach At duodenum, pancreatic alpha-amylase continues carbohydrate digestion Carbohydrates Steps of carbohydrate digestion (continued) In jejunum, brush border enzymes finish carbohydrate digestion down to simple sugars (monosaccharides) Maltase (digests maltose: glucose + glucose) Sucrase (digests sucrose: glucose + fructose) Lactase (digests lactose: glucose + galactose) In large intestine, remaining indigestible carbohydrates (such as cellulose) are food source for colonic bacteria Produce intestinal gas (flatus) during metabolic activities Carbohydrates Carbohydrate absorption and transport Transported into small intestine epithelial cells Leave cells by facilitated diffusion through basolateral surface Enter cardiovascular capillaries to transport to liver in hepatic portal vein Processed by liver to maintain glucose levels (~90 mg/dL) Released as glucose or Stored as glycogen Carbohydrates Cellular use of digested carbohydrates Generally preferred for catabolism Proteins and lipids more important for structural components of cells and tissues In skeletal muscle, stored as glycogen In most tissues, transported into cell by carrier molecule (regulated by insulin) May be converted to ribose May be converted to 2 pyruvate molecules in glycolysis Produces 2 ATP Pyruvates used by mitochondria Uses 3 O2, generates 3 CO2, 6 H2O, 34 ATP The events in carbohydrate catabolism and ATP production from glucose GLUCOSE In most tissues, the transport of glucose into the cell is dependent on the presence of a carrier protein stimulated by insulin. (6-carbon) Insulin Other simple sugars ATP Inside the cell, the glucose may be converted to another simple sugar, such as ribose, used to build glycoproteins, other structural materials, or nucleic acids. They may also be converted to glycerol for the synthesis of glycerides. If needed to provide energy, the 6-carbon glucose molecule is broken down into two 3-carbon molecules of pyruvate. This anaerobic process, called glycolysis, yields a net gain of 2 ATP for every glucose molecule broken down. Pyruvate (3-carbon) Pyruvate (3-carbon) Carbohydrates (such as glucose) are generally preferred for catabolism because proteins and lipids are more important as structural components of cells and tissues. CO2 Coenzyme A Each pyruvate molecule can then be used by mitochondria, after conversion to acetyl-CoA. Acetyl-CoA (2-carbon) Citric acid cycle ATP Coenzymes Electron transport system O2 H2O CO2 For each molecule of pyruvate processed by mitochondria, the cell gains 17 ATP, consumes 3 molecules of O2, and generates 3 molecules of CO2 and 6 molecules of water. Thus for each pair of pyruvate molecules catabolized, the cell gains 34 ATP. Figure 24-26: A Summary of the Chemical Events in Digestion REGION AND HORMONAL CONTROLS CARBOHYDRATES ORAL CAVITY LIPIDS Salivary amylase PROTEINS Lingual lipase ESOPHAGUS STOMACH Pepsin Stimulus: Anticipation or arrival of food Hormone: Gastrin Source: G cells of stomach Disaccharides Trisaccharides Polypeptides Proenzyme released: Pepsinogen by chief cells, activated to pepsin by HCl SMALL INTESTINE Bile salts and pancreatic lipase Stimulus: Arrival of chyme in duodenum Pancreatic alpha-amylase Hormone: CCK Proenzymes released: Chymotrypsinogen, procarboxypeptidase, proelastase, trypsinogen. Enterokinase activates trypsin, which activates other enzymes Disaccharides Trisaccharides Monoglycerides, Fatty acids in micelles Trypsin Chymotrypsin Elastase Carboxypeptidase Short peptides, Amino acids Enzymes released: Pancreatic amylase, pancreatic lipase, nuclease, enterokinase INTESTINAL MUCOSA Brush border Cell body Maltase, Sucrase Lactase DIFFUSION Dipeptidases FACILITATED DIFFUSION AND COTRANSPORT Monoglycerides, Fatty acids FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Triglycerides Amino acids Chylomicrons FACILITATED DIFFUSION EXOCYTOSIS FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Chylomicrons Amino acids BLOODSTREAM Capillary (a) Lacteal (b) Capillary (c) Protein digestion and amino acid metabolism Steps of protein digestion In mouth, mechanical processing occurs In stomach: Mechanical processing due to churning Stomach acid denatures protein secondary and tertiary structures Pepsin (from parietal cells) attacks certain peptide bonds Digests proteins to polypeptide and peptide chains Protein digestion and amino acid metabolism Steps of protein digestion (continued) In duodenum: Enteropeptidase (from duodenal epithelium) converts trypsinogen (pancreatic proenzyme) to trypsin Trypsin activates other pancreatic proenzymes Chymotrypsin, carboxypeptidase, and elastase Activated pancreatic enzymes digest specific peptide bonds producing short peptides and amino acids Protein digestion and amino acid metabolism Digested protein absorption and transport Epithelial brush border enzymes (peptidases) finish protein digestion Amino acids absorbed through: Facilitated diffusion Cotransport Released from epithelial cell basal surface through same cell transport mechanisms Amino acids transported to liver through intestinal capillaries to hepatic portal vein Protein digestion and amino acid metabolism Amino acid processing in liver Control of plasma amino acid levels is less precise than glucose Normal range: 35–65 mg/dL Can increase after protein-rich meal Liver amino acid use Synthesize plasma proteins Create 3-carbon molecules for gluconeogenesis Protein digestion and amino acid metabolism Amino acid processing in liver (continued) Amino acid catabolism Deamination (removal of amino group) Ammonium ions released are toxic Liver enzymes convert to urea excreted into urine = Urea cycle The liver does not control circulating levels of amino acids as precisely as it does glucose concentrations. Plasma amino acid levels normally range between 35 and 65 mg/dL, but they may become elevated after a protein-rich meal. The liver itself uses many amino acids for synthesizing plasma proteins, and it has all of the enzymes needed to synthesize, convert, or catabolize amino acids. In addition, amino acids that can be broken down to 3-carbon molecules can be used for gluconeogenesis when other sources of glucose are unavailable. Amino Acid Synthesis Liver cells and other body cells can readily synthesize the carbon frameworks of roughly half of the amino acids needed to synthesize proteins. There are 10 essential amino acids that the body either cannot synthesize or that cannot be produced in amounts sufficient for growing children. In an amination reaction, an ammonium ion (NH4+) is used to form an amino group that is attached to a molecule, yielding an amino acid. NH4+ H2O H+ α–Ketoglutarate Glutamic acid In a transamination, the amino group of one amino acid gets transferred to another molecule, yielding a different amino acid. The remaining carbon chain can then be broken down or used in other ways. Transaminase Glutamic acid Organic acid 1 Organic acid 2 Tyrosine Figure 22.7 Figure 24-26: A Summary of the Chemical Events in Digestion REGION AND HORMONAL CONTROLS CARBOHYDRATES ORAL CAVITY LIPIDS Salivary amylase PROTEINS Lingual lipase ESOPHAGUS STOMACH Pepsin Stimulus: Anticipation or arrival of food Hormone: Gastrin Source: G cells of stomach Disaccharides Trisaccharides Polypeptides Proenzyme released: Pepsinogen by chief cells, activated to pepsin by HCl SMALL INTESTINE Bile salts and pancreatic lipase Stimulus: Arrival of chyme in duodenum Pancreatic alpha-amylase Hormone: CCK Proenzymes released: Chymotrypsinogen, procarboxypeptidase, proelastase, trypsinogen. Enterokinase activates trypsin, which activates other enzymes Disaccharides Trisaccharides Monoglycerides, Fatty acids in micelles Trypsin Chymotrypsin Elastase Carboxypeptidase Short peptides, Amino acids Enzymes released: Pancreatic amylase, pancreatic lipase, nuclease, enterokinase INTESTINAL MUCOSA Brush border Cell body Maltase, Sucrase Lactase DIFFUSION Dipeptidases FACILITATED DIFFUSION AND COTRANSPORT Monoglycerides, Fatty acids FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Triglycerides Amino acids Chylomicrons FACILITATED DIFFUSION EXOCYTOSIS FACILITATED DIFFUSION AND COTRANSPORT Monosaccharides Chylomicrons Amino acids BLOODSTREAM Capillary (a) Lacteal (b) Capillary (c) Lipids Steps of lipid digestion In mouth, mechanical processing and chemical digestion by lingual lipase In stomach, lingual lipase continues to function but can only access surface of lipid drops that have formed In duodenum Bile salts break up lipid drops into smaller droplets (= emulsification) Pancreatic lipase digests triglycerides into fatty acids, monoglycerides, and glycerol Forms micelles (lipid–bile salt complexes) Lipoproteins Types Chylomicrons VLDL LDL Enter lymph Transports cholesterol to cells HDL Transports cholesterol from cells to liver Lipids Absorption and transport of digested lipids Lipids diffuse from micelle into intestinal epithelial cell Intracellular anabolic reactions synthesize new triglycerides from digested lipids New triglycerides packaged in chylomicrons (chylos, milky lymph, mikros, small) and released via exocytosis Chylomicrons diffuse into intestinal lacteals due to their size Transported through lymphatic vessels (including thoracic duct) to bloodstream Enzyme in capillaries (lipoprotein lipase) breaks down chylomicron and releases digested lipids to tissues Lipids Digested lipid distribution and processing Tissues that use or process digested lipids Skeletal muscles Adipose tissue Use fatty acids to generate ATP for contraction and to convert glucose to glycogen Uses fatty acids and monoglycerides to synthesize triglycerides for storage Liver Absorbs intact chylomicrons and extracts triglycerides and cholesterol from chylomicron Lipids Cholesterol distribution Released from liver attached to low-density lipoproteins (LDL) for distribution to peripheral tissues LDLs absorbed and broken down by lysosomes in cells High-density lipoproteins (HDL) (plasma proteins from liver) absorb peripheral cholesterol and return to liver Cholesterol extracted and used Unused cholesterol released into bloodstream Cholesterol released again with LDLs or excreted in bile Ratio of LDL/HDL and total cholesterol used diagnostically for cardiovascular problems Thoracic duct The chylomicrons enter the bloodstream at the left subclavian vein, then pass through the pulmonary circuit before entering the systemic circuit. Resting skeletal muscles absorb fatty acids and break them down, using the ATP provided both to power the contractions that maintain muscle tone and to convert glucose to glycogen. Capillary walls contain the enzyme lipoprotein lipase, which breaks down the chylomicrons and releases fatty acids and monoglycerides that can diffuse into the interstitial fluid. Adipocytes absorb the monoglycerides and fatty acids, and use them to synthesize triglycerides for storage. Lipoproteins and Lipid Transport and Distribution The liver absorbs chylomicrons, removes the triglycerides, combines the cholesterol from the chylomicron with synthesized or recycled cholesterol, and alters the surface proteins. It then releases low-density lipoproteins (LDLs) into the circulation, which deliver cholesterol to peripheral tissues. Some of the cholesterol is used by the liver to synthesize bile salts; excess cholesterol is excreted in the bile. The HDLs return the cholesterol to the liver, where it is extracted and packaged in new LDLs or excreted with bile salts in bile. From the lacteals, the chylomicrons proceed along the lymphatic vessels and into the thoracic duct. Chylomicrons Triglycerides removed LDL The LDLs released by the liver leave the bloodstream through capillary pores or cross the endothelium by vesicular transport. Cholesterol extracted Excess cholesterol is excreted with HDL the bile salts HDL High cholesterol Once in peripheral tissues, the LDLs are absorbed. LDL Low cholesterol Lysosomal breakdown HDL Cholesterol release Used in synthesis of membranes, hormones, other material Figure 22.5 Clicker Question: The Respiratory Rhythmicity Centre (RRC) in the medulla contains: A) The apneustic centre B) The dorsal respiratory group C) The pneumotaxic centre D) The limbic system E) The cardioregulatory centre Clicker Question: The neurones of the dorsal regulatory group: A) Stimulate the muscles of expiration. B) Directly inhibit the muscles of expiration C) Stimulate the muscles of inspiration D) Inhibit activity in the apneustic centre Clicker Question: The anatomic dead space: A) Consists of all the conducting zone airways, including the upper tract B) Consists of the trachea, bronchi, and bronchiole down to, and including, the respiratory bronchiole C) The pharyngeal region D) None of the above Clicker Question: In order to do well on the final exam, Students need to: A) Party hard B) Study hard C) Bribe the lecturer D) Ask questions about processes they don’t understand E) B and D above Large Intestine: Extends from ileocecal junction to anus Consists of cecum, colon, rectum, anal canal Movements sluggish (18-24 hours) The wall of the large intestine Aggregated lymphoid nodule Simple columnar epithelium Intestinal gland Mucous cells Muscularis mucosae Submucosa Muscularis Externa Circular layer Longitudinal layer (taenia coli) Figure 21.15 1 Large intestine General characteristics of the large intestine Also known as large bowel Length is ~1.5 m (4.9 ft) and width is 7.5 cm (3 in.) Major functions during mass movement (peristalsis) 1. 2. 3. Reabsorption of water and compaction of contents into feces Absorption of important vitamins liberated by bacterial action Storage of feces prior to defecation Three segments: cecum, colon, rectum Large intestine Large intestine segments and structures Cecum (expanded pouch beginning colon) Begins compaction (compression into feces) Contains ileocecal valve Has attached appendix ~9 cm (3.6 in.) in length Contains numerous lymphoid nodules Appendicitis (inflammation) Large intestine Large intestine segments and structures (continued) Colon Ascending Transverse Across abdomen from right colic flexure to left colic flexure Descending Along right margin of peritoneal cavity from cecum to right colic flexure Along left margin of peritoneal cavity from left colic flexure to sigmoid flexure Sigmoid S-shaped last segment empties into rectum Large intestine Large intestine segments and structures (continued) Rectum Forms last 15 cm (6 in.) of digestive tract Expandable for temporary feces storage Fecal material within rectum triggers defecation urge The characteristic features of the rectum Rectum Anal canal Anal columns Internal anal sphincter External anal sphincter Rectum Anus Rectum, sectioned Figure 21.15 2 Large intestine Other large intestine structures Taeniae coli Three longitudinal muscle bands along outer colon surface Haustra Corresponds to muscularis externa Pouches along colon wall Allow for expansion and elongation of colon Fatty appendices Teardrop-shaped fat sacs attached to serosa Movement in Large Intestine Mass movements Local reflexes in enteric plexus Gastrocolic: Initiated by stomach Duodenocolic: Initiated by duodenum Defecation reflex Common after meals Distension of the rectal wall by feces Defecation Usually accompanied by voluntary movements to expel feces through abdominal cavity pressure caused by inspiration Transport and Secretion by Large Intestine Mucus provides protection Parasympathetic stimulation increases rate of goblet cell secretion Ion Pumps Exchange of bicarbonate ions for chloride ions Exchange of sodium ions for hydrogen ions Bacterial actions produce gases called flatus Production and elimination of feces Large intestine characteristics associated with fecal production Diameter is larger and wall is thinner than small intestine Lack of villi Abundance of mucous cells Many intestinal glands dominated by mucous glands Mucus provides lubrication for drier and more compact fecal material No digestive enzymes produced Production and elimination of feces Rectum and anal structure Anal canal (distal portion of rectum) Contains longitudinal folds (= anal columns) Epithelium transitions from columnar to stratified squamous epithelium Large network of veins contained within wall Enlarged veins = hemorrhoids Internal anal sphincter (inner circular smooth muscle layer) External anal sphincter (outer skeletal muscle layer) Anus (exit of anal canal) Stratified epithelium becomes keratinized Production and elimination of feces Defecation reflex Begins with distension of rectum wall after arrival of feces Involves two positive feedback loops 1. Long reflex 2. Coordinated by sacral parasympathetic system Stimulates mass movements in feces toward rectum from descending and sigmoid colon Short reflex Stimulation of myenteric plexus to move feces in sigmoid colon and rectum Water and Ions: Water Can move in either direction across wall of small intestine depending on osmotic gradients Ions Sodium, potassium, calcium, magnesium, phosphate are actively transported The events in the defecation reflex, which includes two positive feedback loops Stimulation of somatic motor neurons stimulates Stimulation of parasympathetic motor neurons in sacral spinal cord Stimulation of myenteric plexus in sigmoid colon and rectum Long Reflex Short Reflex The first loop is a short reflex that triggers a series of peristaltic contractions in the rectum that move feces toward the anus. Increased peristalsis throughout large intestine Stimulation of stretch receptors Start Increased local peristalsis inhibits The long reflex is coordinated by the sacral parasympathetic system. This reflex stimulates mass movements that push feces toward the rectum from the descending colon and sigmoid colon. DISTENSION OF RECTUM Relaxation of internal anal sphincter; feces move into anal canal Voluntary relaxation of the external sphincter can override the contraction directed by somatic motor neurons (L2a). Involuntary contraction of external anal sphincter If external sphincter is voluntarily relaxed, DEFECATION OCCURS Figure 21.15 4 Appetite regulation Appetite is controlled by two areas of hypothalamus 1. 2. Feeding center Satiety center Causes inhibition of feeding center Regulation of appetite can occur on two levels 1. 2. Short-term regulation Long-term regulation Appetite regulation Short-term regulation of appetite Stimulation of satiety center Elevation of blood glucose levels Hormones of digestive tract (like CCK) Digestive tract wall stretching Stimulation of feeding center Neurotransmitters Example: neuropeptide Y or NPY from hypothalamus Ghrelin Hormone secreted by gastric mucosa when stomach is empty Appetite regulation Long-term regulation of appetite Leptin Peptide hormone secreted by adipocytes Stimulates satiety center and suppresses appetite Effects are gradual Short-Term Regulation of Appetite Stimulation of Satiety Center Hypothalamus Satiety center Elevated blood glucose levels depress appetite, and low blood glucose stimulates appetite. The likely mechanism is glucose entry stimulating the neurons of the satiety center. Several hormones of the digestive tract, including CCK, suppress appetite during the absorptive state. Feeding center Stimulation of stretch receptors along the digestive tract, especially in the stomach, causes a sense of satiation and suppresses appetite. Long-Term Regulation of Appetite Stimulation of Feeding Center Several neurotransmitters have been linked to appetite regulation. Neuropeptide Y (NPY), for example, is a hypothalamic neurotransmitter that (among other effects) stimulates the feeding center and increases appetite. The hormone ghrelin (GREL-in), secreted by the gastric mucosa, stimulates appetite. Ghrelin levels are high when the stomach is empty, and decline as the stomach fills. When appetite outpaces energy usage, excess calories are stored as fat in adipose tissue. Leptin is a peptide hormone released by adipose tissues as they synthesize triglycerides. In the CNS it stimulates the satiety center and suppresses appetite. The effects are gradual, and it is probably involved in long-term regulation of food intake. Mechanisms in the control of appetite Figure 22.12 Effects of Aging Decrease in mucus layer, connective tissue, muscles and secretions Increased susceptibility to infections and toxic agents Ulcerations and cancers Atherosclerosis is an Inflammatory Disease Vessel Lumen Monocyte Endothelium Cytokines Growth Factors Metalloproteinases Cell Proliferation Matrix Degradation Foam Cell Ross R. N Engl J Med 1999;340:115-126. Macrophage Intima Lipoprotein Classes and Inflammation Chylomicrons, VLDL, and their catabolic remnants > 30 nm LDL 20–22 nm Potentially proinflammatory HDL 9–15 nm Potentially antiinflammatory Doi H et al. Circulation 2000;102:670-676; Colome C et al. Atherosclerosis 2000; 149:295-302; Cockerill GW et al. Arterioscler Thromb Vasc Biol 1995;15:1987-1994. LDL is composed of a core of 1500 molecules of cholesterol enclosed in layers of phospholipid and unesterified cholesterol molecules. A large protein called apoprotein B-100 is embedded in this hydrophilic layer. LDL is generated by the bodies fat-transport system via two mechanisms; the exogenous and the endogenous pathways. Structure of LDL Surface Monolayer of Phospholipids and Free Cholesterol apoB Hydrophobic Core of Triglyceride and Cholesteryl Esters Murphy HC et al. Biochemistry 2000;39:9763-970. The exogenous pathway begins in the intestine, and commences as the dietary fats become packaged into lipoprotein particles called chylomicrons. Chylomicrons contain phospholipid, cholesterol, apolipoproteins (apo), for example apo B48, apo A-1, apo 11, C –11 and apo-E. Chylomicrons contain phospholipid, cholesterol, apolipoproteins (apo), for example apo B48, apo A-1, apo 11, C –11 and apo-E. Role of LDL in Inflammation LDL Readily Enter the Artery Wall Where They May be Modified Vessel Lumen LDL Endothelium Oxidation of Lipids and ApoB Aggregation LDL Hydrolysis of Phosphatidylcholine to Lysophosphatidylcholine Other Chemical Modifications Modified LDL Modified LDL are Proinflammatory Steinberg D et al. N Engl J Med 1989;320:915-924. Intima Modified LDL Stimulate Expression of MCP-1 in Endothelial Cells Vessel Lumen Monocyte LDL MCP-1 LDL Endothelium Modified LDL Monocyte chemotactic protein-1 Navab M et al. J Clin Invest 1991;88:2039-2046. Intima Differentiation of Monocytes into Macrophages Vessel Lumen Monocyte LDL MCP-1 Endothelium LDL Intima Modified LDL Macrophage Steinberg D et al. N Engl J Med 1989;320:915-924. Modified LDL Promote Differentiation of Monocytes into Macrophages Modified LDL Induces Macrophages to Release Cytokines That Stimulate Adhesion Molecule Expression in Endothelial Cells Vessel Lumen Monocyte LDL Adhesion Molecules MCP-1 Cytokines Endothelium LDL Modified LDL Macrophage Nathan CF. J Clin Invest 1987;79:319-326. Intima Macrophages Express Receptors That Take up Modified LDL Vessel Lumen Monocyte LDL Adhesion Molecules MCP-1 Endothelium LDL Modified LDL Taken up by Macrophage Foam Cell Macrophage Steinberg D et al. N Engl J Med 1989;320:915-924. Intima Macrophages and Foam Cells Express Growth Factors and Proteinases Vessel Lumen Monocyte LDL Adhesion Molecules Cytokines Macrophage MCP-1 LDL Modified LDL Foam Cell Ross R. N Engl J Med 1999;340:115-126. Endothelium Intima Growth Factors Metalloproteinases Cell Proliferation Matrix Degradation Structure of HDL apoA-I apoA-II Rye KA et al. Atherosclerosis 1999;145:227-238. Surface Monolayer of Phospholipids and Free Cholesterol Hydrophobic Core of Triglyceride and Cholesteryl Esters HDL Prevent Formation of Foam Cells Vessel Lumen Monocyte LDL Adhesion Molecules MCP-1 Endothelium LDL Modified LDL Cytokines Macrophage Foam Cell HDL Promote Cholesterol Efflux Miyazaki A et al. Biochim Biophys Acta 1992;1126:73-80. Intima HDL Inhibit the Oxidative Modification of LDL Vessel Lumen Monocyte LDL Adhesion Molecules MCP-1 Endothelium LDL Modified LDL Cytokines Macrophage Foam Cell HDL Promote Cholesterol Efflux Mackness MI et al. Biochem J 1993;294:829-834. HDL Inhibit Oxidation of LDL Intima Inhibition of Adhesion Molecules HDL Inhibit Adhesion Molecule Expression Monocyte LDL Vessel Lumen Adhesion Molecules MCP-1 Endothelium LDL Modified LDL Cytokines Macrophage HDL Inhibit Oxidation of LDL Foam Cell HDL Promote Cholesterol Efflux Intima Cockerill GW et al. Arterioscler Thromb Vasc Biol 1995;15:1987-1994. Macrophage Functions in Atherogenesis Activation