Part 1: Metabolic Pathways Part 2: GI Physiology Part 3: GI Disorders

Part 1: Metabolic Pathways Part 2: GI Physiology Part 3: GI Disorders

Simple and Complex Carbohydrates
There are three main simple sugars (AKA monosaccharides or simple carbohydrates) Glucose Fructose Galactose If you join a glucose to any of these, you get a disaccharide Glucose + Glucose = Maltose Glucose + Galactose = Lactose Glucose + Fructose = Sucrose

Simple and Complex Carbohydrates
If you join many monosaccharides and/or disaccharides together, it is called a polysaccharide (AKA complex carbohydrate). These are stored in the liver as glycogen. They can be broken down later into glucose as needed. The storage form of glucose in plants is called starch. When we eat starch, we convert it to glycogen and store it, or break it down to glucose to use it.

Glucagon and Insulin Glucagon, a hormone secreted by the pancreas, raises blood glucose levels. Its effect is opposite that of insulin, which lowers blood glucose levels. The pancreas releases glucagon when blood sugar (glucose) levels fall too low. Glucagon causes the liver to beak down the stored glycogen into glucose, which is released into the bloodstream. Since glycogen is being broken down, this process is called glycogenolysis. Don’t confuse this with glycolysis (break down of glucose to ATP)! High blood glucose levels stimulate the release of insulin. Insulin allows glucose to be taken up and used by insulin-dependent tissues. Thus, glucagon and insulin are part of a feedback system that keeps blood glucose levels at a stable level.

GI Kit Line up the white label organs
Place each colored substance under the proper organ

Pancreas, Islets of Langerhans Alpha cells Stomach
Pancreas, acinar cells Liver Salivary Glands Pancreas, Islets of Langerhans Alpha cells Stomach Duodenum Pancreas, Islets of Langerhans Beta cells Pancreas, Islets of Langerhans Delta cells Stomach, Parietal Cells Stomach, Chief Cells KEY Yellow = fat enzyme Green = protein enzyme Red = sugar enzyme Blue = hormones Orange = substances Stomach, G-Cells Duodenum, K-Cells

Bicarbonate Carboxypeptidase Trypsin Pepsin Chymotrypsin Sucrase
Maltase Lactase Amylase Amylase Lipase Lipase Lipase Lipase Gastrin Somatostatin Motilin GIP Insulin Glucagon CCK Secretin Bicarbonate Mucus Prostaglandins Intrinsic factor Bile HCl

Bicarbonate Pancreas, acinar cells Amylase Trypsin
Pancreas, Islets of Langerhans Alpha cells Chymotrypsin Glucagon Carboxypeptidase Lipase Pancreas, Islets of Langerhans Beta cells Bicarbonate Insulin KEY Fat enzyme Protein enzyme Sugar enzyme Hormone Substances Pancreas, Islets of Langerhans Delta cells Somatostatin

Stomach, Parietal Cells
Liver Salivary Glands Lipase Lipase Amylase Prostaglandins Bile Lipase Mucus Stomach, Chief Cells Pepsin Stomach, Parietal Cells KEY Fat enzyme Protein enzyme Sugar enzyme Hormone Substances Intrinsic factor HCl Stomach, G-Cells Gastrin

Duodenum Duodenum, K-Cells Sucrase GIP Maltase Lactase Secretin CCK Motilin KEY Fat enzyme Protein enzyme Sugar enzyme Hormone Substances

Organ Region of the Organ Substances Function
Pancreas Acinar cells Amylase (enzyme) Breaks down starch and carbohydrates into glucose Lipase (enzyme) Breaks down fat into fatty acids Protease enzymes (trypsin, chymotrypsin, carboxypeptidase) Breaks down proteins into amino acids and also kills intestinal parasites and bacteria Bicarbonate (not an enzyme) Raises pH in duodenum Islet of Langerhans; Alpha cells glucagon (hormone) Causes glycogenolysis, the process which breaks down glycogen into glucose to raise blood glucose. Also causes gluconeogenesis to make new glucose molecules Beta cells insulin (hormone) Removes glucose in bloodstream and brings it into cells. Lowers blood glucose levels. Delta cells Somatostatin (hormone) Inhibits gastrin, insulin, and glucagon (inhibits digestive system) Liver Bile (a detergent) Emulsifies fat Lipase Breaks down fat Salivary glands Breaks down starch and carbohydrates into glucose Breaks down fat Stomach Mucous (not an enzyme) Protect the stomach lining Prostaglandins (not an enzyme) Lipase Parietal cells HCl (not an enzyme) Allows Pepsinogen to be converted to pepsin, and it also kills bacteria Intrinsic factor (not an enzyme) Allows Vit B12 to be absorbed, which is needed to make RBCs. Without it, you get megaloblastic (pernicous) anemia. Chief cells Pepsinogen --> pepsin (enzyme) Breaks proteins into amino acids G cells Gastrin (hormone) Tells parietal cells to secrete HCl Duodenum Secretin (hormone) Tells pancreas to secrete bicarbonate CCK (hormone) Tells pancreas to secrete proteases and lipase, and tells gallbladder to release stored bile (stimulates fat and protein digestion) Motilin (hormone) Initiates peristalsis and tells Chief cells to secrete pepsinogen Maltase, Lactase, Sucrase (enzymes) Break down complex carbohydrates into glucose K cells GIP (hormone) Tells pancreas to release insulin and also causes fat to be broken down into fatty acids

Glycolysis Glycolysis is the process where cells take in glucose and break it down into pyruvate, and ATP is released. This is how we get ATP from glucose. Fructose and galactose can also be broken down into pyruvate and ATP. During glycolysis, NAD (an energy molecule) is reduced to NADH. If you run out of NAD, glycolysis will stop. Therefore, we need to oxidize NADH to convert it back into NAD. This can be done by aerobic or anaerobic respiration, or fermentation.

Glycolysis There is a net gain of 2 ATP molecules.
Notice that 2 ATP molecules are used during glycolysis, but 4 are made (2 pyruvate molecules are made, each of which generates 2 ATP). There is a net gain of 2 ATP molecules.

After Glycolysis Immediately upon finishing glycolysis, the cell must continue respiration in either an aerobic or anaerobic direction; this choice is made based on the circumstances of the particular cell. A cell that can perform aerobic respiration and which finds itself in the presence of oxygen will continue on to the aerobic citric acid cycle in the mitochondria. If a cell able to perform aerobic respiration is in a situation where there is no oxygen (such as muscles under extreme exertion), it will move into anaerobic respiration. Some cells such as yeast are unable to carry out aerobic respiration and will automatically move into a type of anaerobic respiration called alcoholic fermentation.

The Activities of Major Digestive Tract Hormones
Let’s do the hormones again, this time with the big picture involved. Once food enters the stomach, the G-cells within the gastric glands of the antrum release Gastrin. Gastrin stimulates the parietal cells to release more acid and also promotes more motility of the stomach. This means the contents of the stomach are churned and mixed to form chyme. Next, the chyme travels through the pylorus and enters the duodenum. The presence of chyme now triggers the release of the other 3 major digestive tract hormones: cholecystokinin, secretin, and gastric inhibitory peptide. Secretin stimulates the pancreas to release bicarbonate rich buffer. Gastric inhibitory peptide primarily slows down stomach motility and slows the rate at which the stomach empties chyme into the duodenum. Cholecystokinin stimulates the liver, gallbladder and pancreas. The liver and gallbladder are stimulated to secrete and release, respectively, bile into the duodenum through the hepatopancreatic ampulla. CCK stimulates the pancreas to release its digestive enzymes that include enzymes for carbohydrate digestion, lipase, nucleases, and peptidases. All four hormones stimulate the pancreas to release insulin in a sort of “anticipatory” effect for food. The insulin then stimulates insulin dependent cells of the body to start inserting glucose transport proteins into the cell membranes. These glucose transporters bind to glucose and facilitate its movement from the plasma to the cytoplasm. OF the four hormones, Gastric inhibitory peptide seems to have the strongest influence on insulin release. Figure 24.22

Aerobic vs. Anaerobic Respiration
(in the mitochondria)will result in 6 ATP’s. Anaerobic respiration (in our cytoplasm) will result in only 2 ATP’s. More importantly, we get our NAD back, so glycolysis can continue.

Making ATP by Aerobic Respiration
Takes place in the mitochondria Requires oxygen Breaks down glucose to pyruvate and produces ATP Waste products are CO2 and H2O (we exhale them) The good thing about making ATP from our mitochondria is that we can make a LOT of it. The bad things are that it takes longer to make it, and it requires oxygen, and a muscle cell may have used up all the oxygen during a sprinting run.

Making ATP by Anaerobic Respiration
Takes place in the cytoplasm Does not require oxygen Breaks down glucose to pyruvate and produces ATP Waste product is lactic acid The good thing about making ATP this way is that we can make it FAST. The bad thing is that it does not make much ATP, and we deplete the reserves quickly.

Lactic Acid Build-up During strenuous workouts where oxygen becomes deficient, the pyruvate product of glycolysis does not have enough oxygen to use for aerobic respiration, so it has to undergo anaerobic respiration. The enzyme lactate dehydrogenase (LDH) is used to transfer hydrogen from the NADH molecule to the pyruvate molecule. Pyruvate with the extra hydrogen is called lactate. Lactic acid is formed from lactate. This causes muscle aches and fatigue. Lactic acid is deactivated by the addition of oxygen to it. Therefore, breathing heavily adds the oxygen to our system to deactivate lactic acid, and the muscle pains go away. Warm water or ultrasound will also increase oxygenated blood to the muscles, easing muscle cramps from lactic acid. When you add oxygen to lactic acid, it either goes back to being pyruvate, which is used to fuel the Krebs cycle (aerobic respiration), or it is converted to glucose in the liver.

ATP and Creatine Phosphate
What do we do when we run out of ATP? Muscle fibers cannot stockpile ATP in preparation for future periods of activity. However, they can store another high energy molecule called creatine phosphate. Creatine phosphate is made from the excess ATP that we accumulate when we are resting. During short periods of intense exercise, the small reserves of ATP existing in a cell are used first. Then creatine phosphate is broken down to produce ATP.

Aerobic vs. Anaerobic Respiration
When do we use aerobic respiration? Resting (can breathe easily) Running marathons (can breathe easily on long runs) Marathon runners want to make sure there will be enough readily available energy for the muscles, so they eat a lot of carbohydrates over a two-day period before the marathon. That’s why they load up on pasta (carbo-loading)before a marathon. When do we use anaerobic respiration? Sprint running (can’t talk while sprinting!)

Gluconeogenesis Gluconeogenesis is a metabolic pathway that results in the generation of new glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and amino acids. Therefore, if we do not have enough glucose in our body, we will break down proteins (muscles) to make glucose. It is one of the two main mechanisms to keep blood glucose levels from dropping too low (hypoglycemia). The other means of maintaining blood glucose levels is through the degradation of glycogen (glycogenolysis).

Part 2 GI Physiology Well come to your articulate file for the Digestive system –or alimentary tract. The alimentary tract begins with the oral cavity, continues into the oropharynx and laryngopharynx to the esophagus, to the stomach, to the small intestine with its three parts (duodenum, jejunum, and ileum—I remember this as “Down Jones Industrial” finally the ingested contents travel through the one-way ileocecal valve and enter the large intestine leading to the rectum and anus. Many accessory digestive organs are passed along the way: such as the pancreas, liver, and gallbladder. The alimentary tract provides the body with continual supply of water, electrolytes, and nutrients. This requires (1) movement of food through the alimentary tract; (2) secretion of digestive juices and digestion of food; (3) absorption of digestive products, water, and various electrolytes; (4) circulation of blood to carry away absorbed substances; and (5) nervous and hormonal control of all these functions. I will be discussing the basic principles and function of the entire alimentary tract during this lecture Figure 62-1; Guyton & Hall

Digestion Problems Incomplete digestion may be a contributing factor in the development of many ailments including flatulence, bloating, belching, food allergies, nausea, bad breath, bowel problems and stomach disorders. Digestive enzymes are primarily responsible for the chemical breakdown of food and constitute a large portion of digestive secretions. The human body makes approximately 22 different enzymes that are involved in digestion.

Digestive Enzymes Saliva is secreted in large amounts (1-1.5 liters/day) Salivary glands contain the enzyme salivary amylase. This enzymes breaks starch into smaller sugars and is stimulated by chewing. It is important to chew food thoroughly as this is the first stage of the digestive process.

Saliva The saliva serves to clean the oral cavity and moisten the food. It also contains digestive enzymes such as salivary amylase, which aids in the chemical breakdown of polysaccharides such as starch into disaccharides such as maltose. It also contains mucus, a glycoprotein which helps soften the food and form it into a bolus.

Swallowing The mechanism for swallowing is coordinated by the swallowing center in the medulla oblongata and pons (in the brain stem). The reflex is initiated by touch receptors in the pharynx (back of the throat)as the bolus of food is pushed to the back of the mouth.

Stomach The stomach is responsible for the digestion of protein.
Mucous cells (in the stomach) secrete mucous. The pancreas secretes bicarbonate. Mucous, bicarbonate, and prostaglandins protect the stomach lining from being digested. The parietal cells of the stomach secrete hydrochloric acid (gastric acid) and intrinsic factor. Hydrochloric acid (HCl), along with pepsin (from the chief cells), breaks down proteins to their individual amino acids.

Stomach Protection and Damage
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Stimuli for Stomach Secretions
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Stomach Acid The acid itself does not break down food molecules.
It provides an optimum pH for the activation of pepsin, and kills many microorganisms that are ingested with the food. It can also denature proteins. The parietal cells of the stomach also secrete a glycoprotein called intrinsic factor, which enables the absorption of vitamin B-12.

Stomach Acid Diseases Hypochlorhydria Hyperchlorhydria
Diseases associated with low gastric acidity: Asthma, coeliac disease, eczema, osteoporosis and pernicious anemia. Hyperchlorhydria Diseases associated with high gastric acidity: Heartburn, gas and ulcers

Hypochlorhydria Deficient hydrochloric acid secretion
Causes malabsorption and may result in a number of signs and symptoms. These include bloating, belching, flatulence, nausea, a sense of fullness immediately after meals, indigestion, diarrhea, constipation, food allergies, anemia (Folic acid, vitamin B12 and iron will not be absorbed if there is too little acid), undigested food in stool, chronic intestinal parasites, abnormal flora and weak, peeling and cracked fingernails.

Small Intestine Duodenum Absorption of minerals
Receives pancreatic digestive enzymes Secretes hormones when acidic chyme enters duodenum Secretin Tells pancreas to secrete bicarbonate Tells liver to make bile Cholecystokinin (CCK) Tells pancreas to release protein-digesting enzymes Tells the gallbladder to release stored bile. Therefore, it stimulates digestion of fat and protein. GIP stimulates insulin secretion Motilin Initiates peristalsis (increases GI motility) Tells the Chief cells to secrete pepsinogen Secretes enzymes to break down polysaccharides Maltase: breaks maltose down into glucose Lactase: breaks lactose down to galactose plus glucose Sucrase: breaks sucrose down into fructose plus glucose

Maltose Maltose (malt sugar) is made of two glucose molecules joined together. Maltose is the disaccharide produced when amylase breaks down starch. Starch  Maltose  Glucose Maltose is found in germinating seeds such as barley as they break down their starch stores to use for food. It is also produced when glucose is caramelized (browning of sugar during cooking). Foods containing maltose include malted milk shakes, malt liquor and beer. People who lack the maltase enzyme get diarrhea and gas if they ingest malt sugars. Amylase Maltase

Lactose Lactose is needed for milk production.
It is made in the body by combining glucose with galactose. When milk products are consumed, lactose is broken down by the enzyme lactase. Many Asian and Hispanic people lack the enzyme lactase, so they are called lactose intolerant. If they consume milk products, they cannot break down lactose, so the E. coli in the colon get the sugar. E. coli metabolism then causes gas. The person may have diarrhea as well.

Sucrose and Fructose Sucrose is table sugar Fructose is fruit sugar
All polysaccharide sugars and starches are broken down into glucose, which is needed by the body for metabolism.

Small Intestine Duodenum
When there is no more chyme entering the duodenum, it secretes glucose-dependent insulinotropic peptide (GIP). GIP is synthesized by K cells, which are found in the duodenum and jejunum. GIP stimulates insulin secretion. Insulin is in the blood stream. It takes the absorbed sugars and pulls them into cells that need it. GIP also causes fat to be broken down into fatty acids.

Lipid digestion and absorption
Lipid digestion utilizes lingual and pancreatic lipases, to release fatty acids and monoglycerides. Bile salts improve chemical digestion by emulsifying lipid drops Lipid-bile salt complexes called micelles are formed I’d like to start the discussion of this slide with addressing the role of bile salts. Simply put, bile salts form micelles, which are small spherical cylindrical globules– shown here as the small structures at the bottom of the picture. These develop because each bile salt molecule has a fat-loving sterol group (i.e., it is hydrophobic) and a water loving group (hydrophilic) The fat loving portion surrounds a portion of the ingested fat globule and the water-loving portions will project outward to cover the surface of the micelle. Because these polar groups are negatively charged, they allow the entire micelle globule to dissolve in the water of the digestive fluids in the small intestine and remain in solution until the fat is digested and the fatty acids absorbed in the blood. The micelles are important for ferrying the resulting fatty acids and monoglycerides to the brush border, and once the fats are absorbed by the blood then the bile salts can be reused to ferry more digested fats to the brush border. So, once the bile salts form micelles of fat droplets, the cholesterol esters and phospholipids we consumed in our diet are broken down by cholesterol esterase and phospholipase, respectively. These enzymes release free cholesterol and fatty acids. I will leave this slide with a stern caution: bile salts from the liver and gallbladder do NOT DIGEST INGESTED FATS! Rather, they only emulsify the fats—packaging into smaller portions to increase the surface area so that the lipases have an easier time digesting the fats.

Fatty Acid Absorption INTESTINAL LUMEN:
Bile salts form micelles (small droplets of lipids) Lipase breaks down the lipids into fatty acids and monoglycerides. INTESTINAL CELLS: Fatty acids and monoglycerides enter intestinal cells via diffusion; bile salts are then reused to ferry more lipids to the intestinal cell. Fatty acids are used to make triglycerides for storage. The rest of the fatty acids and monoglycerides are combined with proteins within the intestinal cells to make chylomicrons. Chylomicrons enter lacteals and are transported to the blood circulation via lymph As I said in the previous slide, the bile salt micelles transport monoglycerides and fatty acids to the brush border. The digested fats diffuse into the epithelial cells. The fatty acids are used to form triglycerides and combine with proteins to form chylomicrons. Chylomicrons then transport the phospholipids to the underlying lacteal vessel which then transports the chylomicrons back to the circulating venous blood. The half life of a chylomicron is about 1 hour and most of the chylomicrons are removed from the circulating blood as they pass through the capillaries of adipose tissue or the liver. Adipose tissue and liver both contain large quantities of the enzyme lipoprotein lipase. Once the free fatty acids cross the cell membrane, they are resynthesized into triglycerides so they can be stored in the cells. If free fatty acids need to be released from storage cells like adipocytes, then the triglycerides are hydrolyzed into free fatty acids and glycerol (we will discuss hydrolysis during your metabolism lecture). And free fatty acids are transported by albumin for the body’s energy needs. In the post-absorptive state, the lipids are then transported in plasma in the form of lipoprotein. You’ve heard of “good cholesterol” and bad cholesterol. These terms are really referring to lipoproteins. HDL stands for high density lipoprotein and it is high density because there is mostly protein in this molecule and fewer fats. LDL stands for low density lipoprotein and this molecule has many more fats transported within it—hence the term “bad cholesterol.” The LDL transport triglycerides synthesized by the liver mainly to adipose tissue, whereas the HDL are important for the different stages of phospholipid and cholesterol transport from the liver to the peripheral tissues or from the peripheral tissues back to the liver. I always remember that HDL is the “good cholesterol” for two reasons: It contains more protein than fat and the fats being transported are either going to be used by the cells of the body for energy or removed from the body by the liver and expelled into the GI tract. LDL is “bad cholesterol” because it contains mostly fats and is merely transporting them to adipocytes for storage. Thus, we want a greater HDL to LDL ratio. Having a high HDL to LDL ratio also prevents atherosclerosis. Atherosclerosis is a disease of the large and intermediate-sized arteries in which fatty lesions or plaques, develop on the inside surfaces of the arterial walls. So how can you help your body excrete more fats? Eat more fiber. Remember the fiber is going to keep the fats soluble in the GI tract and makes it easier to defecate. IF you have pure fats being excreted from the GI tract this is called steatorrhea, an unpleasant fatty diarrhea.

Protein and Fat Digestion
During digestion, lipids are broken down into fatty acids plus glycerol by the enzyme lipase. Proteins are degraded by various proteolytic enzymes, and they break down into amino acids. Hydrolysis (water is added to break a bond) of proteins occurs in the stomach by pepsin, and this process requires the presence of hydrochloric acid in the stomach, but the rest of the proteins are broken down in the intestine. Both fat and protein digestion requires ATP.

Small Intestine Jejunum
Absorbs water-soluble vitamins, protein and carbohydrates. The proteins began to be broken down into amino acids in the stomach by pepsin and acid. Proteins are further broken down into amino acids in the duodenum by trypsin and chymotrypsin (made by the pancreas and secreted into the duodenum). The carbohydrates are broken down in the duodenum by enzymes from the pancreas and duodenum into sugars.

Small Intestine Ileum Absorbs fat-soluble vitamins, fat, cholesterol, and bile salts. Fats are broken down into fatty acids in the duodenum. First, bile emulsifies the fat (breaks it down into droplets). Then, lipase (made in the pancreas) breaks the fat into fatty acids, which are small enough to be absorbed.

Pancreas Enzymes The pancreas secretes about one and a half liters of pancreatic juice a day! Pancreatic juice secretion is regulated by the hormones secretin and cholecystokinin (CCK), which is produced by the walls of the duodenum upon detection of acid food, proteins and fats. The enzymes produced by the pancreas include Lipases Amylases Proteases

Pancreas Enzymes Lipases Amylases Proteases
Digestion of fats, oils, and fat-soluble vitamins Amylases Break down starch molecules into smaller sugars. Break down carbohydrates into maltose Proteases Break down protein into smaller amino acids Proteases include trypsin, chymotrypsin and carboxypeptidase. Proteases are also responsible for keeping the small intestine free from parasites (intestinal worms, yeast overgrowth and bacteria). A lack of proteases can cause incomplete digestion that can lead to allergies and the formation of toxins.

Regulation of Pancreatic Secretion
Secretin and CCK are released when fatty or acidic chyme enters the duodenum CCK and secretin enter the bloodstream Upon reaching the pancreas: CCK induces the secretion of enzyme-rich pancreatic juice Secretin causes secretion of bicarbonate-rich pancreatic juice Vagal stimulation also causes release of pancreatic juice I want to go over again the control over the exocrine function of the pancreas. When fatty or acidic chyme from the stomach arrives in the duodenum, hormones released from the intestinal gland will signal the pancreas to release its secretions. Secretin stimulates the pancreas to release the bicarbonate rich pancreatic juice to neutralize the stomach acids. Cholecystokinin will stimulate the pancreas to release its digestive enzymes that can digest lipids, nucleic acids, carbohydrates and proteins. In addition to this hormonal control over the pancreas, stimulation of the parasympathetic system can also cause the pancreas to release its secretions. This parasympathetic stimulus would be conveyed through the Vagus nerve (or Cranial nerve number 10) and its interesting how the stimulus arrives. The vagus nerve actually carries impulses to the digestive tract starting with the moment you see or even think about food. For example, 30% of the response to a meal is initiated by the anticipation of eating and the odor and taste of food. The vagus carries impulses to the stomach and GI tract and stimulates them—the stomach starts to secrete HCl. The gastric phase accounts for 60% of the acid response to a meal. It is initiated by distention of the stomach which leads to nervous stimulation of gastric secretion. During these first two phases, the vagus nerve is also transmitting stimuli to the pancreas and the pancreas is starting to secrete bicarbonate juices and enzymatic secretions in anticipation of chyme arriving soon. Then, the intestinal phase accounts for the last 10% and is initiated again by nervous stimuli associated with distention of the small intestine.

The Pancreas Exocrine function (98%) Endocrine function –
Acinar cells make, store, and secrete pancreatic enzymes Endocrine function – ( cells) release somatostatin (inhibitory to gastrin, insulin, and glucagon) β-cells –release insulin α-cells-Release glucagon Although the stomach has an enzyme to start protein digestion, and the small intestine has multiple enzymes within its brush border for carbohydrate digestion, protein digestion, and lipid digestion, the organ that releases the most substantial digestive enzymes is the pancreas. 98% of its physiology is dedicated to an exocrine function in the synthesis and release of digestive enzymes by the Pancreatic Acini (that’s the cell type in the pancreas that makes these enzymes—and I will cover all of these in the next few slides. The remainder of the pancreas is dedicated to an endocrine function with the production and secretion of hormones into the blood stream. These hormones include insulin (which stimulates insulin dependent cells of the body to express glucose transporters and then glucose can be imported within the cell’s cytoplasm. As glucose leaves the blood plasma and enters insulin dependent cells, the blood plasma glucose levels declines. Insulin is synthesized and released by the Beta-cells of the Islets of Langerhans. In contrast, when blood glucose levels decline too much, the alpha-cells of the islets of Langerhans release glucagon which stimulates the liver to cleave glycogen (a polymerized form of glucose) into single monomers of glucose. There are other endocrine cells within the Islets of Langerhans (delta cells for example) that release hormones like somatostatin which is a hormone that shuts down all hormonal functions of the kidney and stops gastrin.

The Pancreas as an Endocrine Gland
Insulin Beta cells Skeletal muscle and adipose tissue need functional glucose receptors Promotes glucose uptake Prevents fat and glycogen breakdown and inhibits gluconeogenesis Increases protein synthesis Promotes fat storage Epi/Norepi inhibit insulin! Help maintain glucose levels during times of stress and increase lipase activity in order to conserve glucose levels Insulin is the only hormone known to have a direct effect in lowering blood glucose levels. It is synthesized and released into the blood stream by the beta cells of the islets of Langerhans. Most tissues of the body, like skeletal muscle and adipose tissue are insulin dependent in order to move glucose into the body tissues. The main exception is the brain. Because most cell membranes are impermeable to glucose, they require a special carrier, called a glucose transporter, to move glucose from the blood into the cell. Within seconds of binding insulin, the membranes of about 80% of body tissues increase their uptake of glucose by means of special glucose transporters. This is particularly true of skeletal muscle and adipose tissue. In addition to promoting glucose uptake, insulin prevents fat and glycogen breakdown and inhibits gluconeogenesis, and increases protein synthesis. Gluconeogenesis means the synthesis of new glucose molecules by converting amino acids or glycerol into new glucose molecules. Insulin also promotes fat storage by increasing the rate of movement of glucose into fat cells which is then converted into fat. Insulin also inhibits protein breakdown and increases protein synthesis. As a side note: catecholamines (like epi/norepi) help to maintain blood glucose levels during periods of stress. Epinephrine inhibits insulin release and promotes glycogenolysis by stimulating the conversion of muscle and liver glycogen to glucose. Muscle glycogen cannot be released into the blood; nevertheless, the mobilization of these stores for muscle use conserves blood glucose for use by other tissues such as the brain and the nervous system. During periods of exercise and other types of stress or fear, epinephrine inhibits insulin release from the beta cells and thereby decreases the movement of glucose into muscle cells. The catecholamines also increase lipase activity and thereby increase mobilization of fatty acids, a process that conserves glucose. The blood glucose-elevating effect of epinephrine is an important homeostatic mechanism during periods of hypoglycemia in insulin-treated patients with diabetes. I will talk about Diabetes Mellitus type 1 and type II in the next two slides. Picture from:

The Pancreas as an Endocrine Gland
Glucagon Increases blood glucose levels Maintains blood glucose between meals and during periods of fasting by breaking down glycogen (stored in liver) into glucose. Initiates glycogenolysis in liver (within minutes). Stimulates gluconeogenesis. This process involves breaking down amino acids (proteins) into glucose. Stimulates amino acid transport to liver to stimulate gluconeogenesis Nervous tissue (brain) is heavily dependent on glucose levels! Glucagon is a polypeptide molecule produced by the alpha cells of the islets of Langerhans and maintains blood glucose levels between meals and during periods of fasting. The most dramatic effect of glucagon is its ability to initiate glycogenolysis or the breakdown of liver glycogen as a means of raising blood glucose, usually within a matter of minutes. Glycogenolysis means that the liver hydrolyzes glycogen to release free glucose molecules into the blood stream. Although many tissues and organ systems are able to use other forms of fuel, such as fatty acids and ketones, the brain and nervous system rely almost exclusively on glucose as a fuel source. Because the brain can neither synthesize nor store more than a few minutes’ supply of glucose, normal cerebral function requires a continuous supply from the circulation. Severe and prolonged hypoglycemia can cause brain death and even moderate hypoglycemia can result in brain dysfunction. Glucagon also increases the transport of amino acids into the liver and stimulates their conversion into glucose. Image from:

Liver and Gallbladder The liver produces bile that is either stored by the gallbladder or secreted into the small intestine. Bile emulsifies fats and fat-soluble vitamins. It also helps keep the small intestine free from parasites. The liver does not make the digestive enzymes for carbohydrates, amino acids and proteins (the pancreas and small intestine do that), but the liver does metabolize proteins, carbohydrates and cholesterol. It also is responsible for the detoxification of toxins, drugs and hormones.

Large Intestine The large intestine absorbs water, electrolytes and some of the final products of digestion. It allows fermentation due to the action of gut bacteria, which break down the substances which remain after processing in the small intestine; some of the breakdown products are absorbed. In humans, these include most complex saccharides (at most three disaccharides are digestible in humans) Food products that cannot go through the villi, such as cellulose (dietary fiber), are mixed with other waste products from the body and become hard and concentrated feces.

Physiology of the large intestine
Reabsorption of water and electrolytes Coliform bacteria make: Vitamins – K, biotin, and B5 Organic wastes are left in the lumen – urobilinogens and sterobilinogens Bile salts Toxins Mass movements of material through colon and rectum Defecation reflex triggered by distention of rectal walls By the time our chyme passes through the ileocecal valve, the volume has diminished from 9L down to 1200ml. In the large intestine, the proximal half of the colon is important for absorption of electrolytes and water. The mucosa of the large intestine has a high capability for active absorption of sodium, and the electrical potential created by absorption of sodium causes chloride absorption as well. The tight junctions of the large intestine are tighter than those of the small intestine, which decreases back diffusion of ions through these junctions. This allows the large intestinal mucosa to absorb sodium ions against a higher concentration and prevents back leak of ions into the lumen. Thus the absorption of sodium and chloride ions creates an osmotic gradient across the large intestinal mucosa, which in turn causes absorption of water. The large intestine can reabsorb about 5-7 liters of fluid and electrolytes a day. If the total quantity of chyme entering the large intestine is greater than this, then the excess appears in the feces as diarrhea. What is in feces? It is about 30% dead bacteria, percent fat, percent inorganic matter, 2-3 percent protein, and 30% undigested roughage of food and bile and sloughed epithelial cells. The brown color is from the stercobilin and urobilin, which are derivatives of bilirubin. This concludes our discussion on the physiology of the digestive tract.

Coliforms Coliforms is the term used for the bacteria that normally inhabit our colon (large intestine). E. coli is just one species of coliform. A ratio of 80-85% beneficial to 15-20% potentially harmful bacteria generally is considered normal within the intestines. Harmful microorganisms also are kept at a minimum by an extensive immune system comprising the gut-associated lymphoid tissue (GALT).

Phases of gastric secretion
Cephalic phase Gastric phase Intestinal phase

Cephalic phase This phase occurs before food enters the stomach and involves preparation of the body for eating and digestion. Sight and thought stimulate the cerebral cortex. Taste and smell stimulus is sent to the hypothalamus and medulla oblongata. After this it is routed through the vagus nerve and release of acetylcholine. Gastric secretion at this phase rises to 40% of maximum rate. Acidity in the stomach is not buffered by food at this point and thus acts to stimulate Delta cells to secrete somatostatin. That causes the G cells to stop secreting gastrin. That caused the parietal cells to stop secreting HCl.

G cell secretion of gastrin D cell secretion of somatostatin

G cells and Gastrin G cells are found deep within the gastric glands of the stomach. When food arrives in the stomach, the parasympathetic nervous system is activated. This causes the vagus nerve to release a neurotransmitter called Gastrin-releasing peptide onto the G cells in the stomach. Gastrin-releasing peptide, as well as the presence of proteins in the stomach, stimulates the release of gastrin from the G cells. Gastrin tells parietal cells to increase HCl secretion, and it also stimulates other special cells to release histamine. Gastrin also tells the chief cells to produce pepsinogen. Gastrin is inhibited by low pH (acid) in the stomach. When enough acid is present, it turns off.

Gastrin Gastrin is released in response to Stomach distension
Vagus nerve stimulation The presence of proteins or amino acids Gastrin release is inhibited by The presence of enough HCl in the stomach (negative feedback) Somatostatin also inhibits the release of gastrin

D cells D cells can be found in the stomach, intestine and the Islets of Langerhans in the pancreas. When gastrin is present, D cells increase somatostatin output. When D cells are stimulated by Ach, they decrease somatostatin output.

D cells Ach that comes from the Vegas nerve branch that lands on D cells will decrease somatostatin output so that digestion can occur. Ach that comes from the Vegas nerve branch that lands on G cells will cause gastrin to be released, and when gastrin is present but there is no food left, that excess gastrin will stimulate the D cells to increase somatostatin to try to turn off the system.

Somatostatin Somatostatin is also known as growth hormone-inhibiting hormone. It suppresses the release of gastrointestinal hormones Gastrin Cholecystokinin (CCK) Secretin GIP It suppresses the release of pancreatic hormones. It slows down the digestive process. It inhibits insulin release. It inhibits the release of glucagon.

Gastric phase This phase takes 3 to 4 hours. It is stimulated by distension of the stomach, presence of food in stomach and decrease in pH. Distention activates the vagus nerve. This activates the release of acetylcholine which stimulates the release of more gastric juices. As protein enters the stomach, it binds to hydrogen ions, which raises the pH of the stomach. Inhibition of gastrin and gastric acid secretion is lifted. This triggers G cells to release gastrin, which in turn stimulates parietal cells to secrete gastric acid. Gastric acid is about 0.5% hydrochloric acid (HCl), which lowers the pH to the desired pH of 1-3. Acid release is also triggered by acetylcholine and histamine.

Intestinal phase This phase has 2 opposing actions: the excitatory and the inhibitory. Partially digested food fills the duodenum. This triggers gastrin to be released. It also triggers the enterogastric reflex, which inhibits the Vagus nerve. This activates the sympathetic nervouse system, which causes the pyloric sphincter to tighten to prevent more food from entering the duodenum.

Digestive Enzymes (fats in yellow, proteins in green, and sugars in red) Salivary glands -amylase Lipase Stomach pepsin Liver Duodenum sucrase maltase lactase Pancreas amylase trypsin chymotrypsin carboxypeptidase Lipase

Digestive Hormones and Substances
Stomach gastrin Intrinsic factor HCl Prostaglandins Mucous Duodenum Secretin CCK GIP Motilin Liver Bile Pancreas Glucagon Insulin Somatostatin Bicarbonate

The Activities of Major Digestive Tract Hormones
Let’s do the hormones again, this time with the big picture involved. Once food enters the stomach, the G-cells within the gastric glands of the antrum release Gastrin. Gastrin stimulates the parietal cells to release more acid and also promotes more motility of the stomach. This means the contents of the stomach are churned and mixed to form chyme. Next, the chyme travels through the pylorus and enters the duodenum. The presence of chyme now triggers the release of the other 3 major digestive tract hormones: cholecystokinin, secretin, and gastric inhibitory peptide. Secretin stimulates the pancreas to release bicarbonate rich buffer. Gastric inhibitory peptide primarily slows down stomach motility and slows the rate at which the stomach empties chyme into the duodenum. Cholecystokinin stimulates the liver, gallbladder and pancreas. The liver and gallbladder are stimulated to secrete and release, respectively, bile into the duodenum through the hepatopancreatic ampulla. CCK stimulates the pancreas to release its digestive enzymes that include enzymes for carbohydrate digestion, lipase, nucleases, and peptidases. All four hormones stimulate the pancreas to release insulin in a sort of “anticipatory” effect for food. The insulin then stimulates insulin dependent cells of the body to start inserting glucose transport proteins into the cell membranes. These glucose transporters bind to glucose and facilitate its movement from the plasma to the cytoplasm. OF the four hormones, Gastric inhibitory peptide seems to have the strongest influence on insulin release. Figure 24.22

Organ Region of the Organ Substances Function
Pancreas Acinar cells Amylase (enzyme) Breaks down starch and carbohydrates into glucose Lipase (enzyme) Breaks down fat into fatty acids Protease enzymes (trypsin, chymotrypsin, carboxypeptidase) Breaks down proteins into amino acids and also kills intestinal parasites and bacteria Bicarbonate (not an enzyme) Raises pH in duodenum Islet of Langerhans; Alpha cells glucagon (hormone) Causes glycogenolysis, the process which breaks down glycogen into glucose to raise blood glucose. Also causes gluconeogenesis to make new glucose molecules Beta cells insulin (hormone) Removes glucose in bloodstream and brings it into cells. Lowers blood glucose levels. Delta cells Somatostatin (hormone) Inhibits gastrin, insulin, and glucagon (inhibits digestive system) Liver Bile (a detergent) Emulsifies fat Lipase Breaks down fat Salivary glands Breaks down starch and carbohydrates into glucose Breaks down fat Stomach Mucous (not an enzyme) Protect the stomach lining Prostaglandins (not an enzyme) Lipase Parietal cells HCl (not an enzyme) Allows Pepsinogen to be converted to pepsin, and it also kills bacteria Intrinsic factor (not an enzyme) Allows Vit B12 to be absorbed, which is needed to make RBCs. Without it, you get megaloblastic (pernicous) anemia. Chief cells Pepsinogen --> pepsin (enzyme) Breaks proteins into amino acids G cells Gastrin (hormone) Tells parietal cells to secrete HCl Duodenum Secretin (hormone) Tells pancreas to secrete bicarbonate CCK (hormone) Tells pancreas to secrete proteases and lipase, and tells gallbladder to release stored bile (stimulates fat and protein digestion) Motilin (hormone) Initiates peristalsis and tells Chief cells to secrete pepsinogen Maltase, Lactase, Sucrase (enzymes) Break down complex carbohydrates into glucose K cells GIP (hormone) Tells pancreas to release insulin and also causes fat to be broken down into fatty acids

Where do the molecules go when you lose weight?
Think of fat as essentially a long-chain hydrocarbon CH3-(CH2)n-CH3. When your body uses that fat as fuel (either because you need fuel to exercise, or because you're not eating enough new fuel to support what you're doing), it burns that fat to extract the energy from it. That "burn" isn't a metaphor. The chemistry that your body does is exactly equivalent to literally burning it, just under more controlled conditions.

So, that hydrocarbon undergoes a controlled combustion with oxygen (O2) to produce a lot of energy, water (H2O), and carbon dioxide (CO2). Or, in chemical form: CH3-(CH2)n-CH3 + (3/2n+7/2)O2 ----> (n+2) CO2 + (n+3) H2O + Energy

So the carbon in the hydrocarbon goes to carbon dioxide and the hydrogen goes to water. But most of the mass of the hydrocarbon is carbon, so most of the mass gets converted to carbon dioxide, which is a gas and gets breathed out. Now this is incomplete, because lipids and fat really aren't just hydrocarbons. They have phosphates and nitrogen and other things too, and those parts don't get converted to gases for excretion. Excess nitrogen gets converted to urea, for example, which gets excreted in the urine. And protein produces a lot more impurities when it gets broken down (though generally the body prefers to recycle proteins rather than burn them for energy). But really, the way you lose most of your weight is just by breathing it off.

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Part 3 GI Disorders Figure 62-1; Guyton & Hall

GI Disorders Peptic ulcers Pancreatitis Celiac Disease
Inflammatory bowel disease (Crohn's disease and ulcerative colitis) Irritable bowel syndrome Appendicitis Diverticulitis Cancer Gastroenteritis ("stomach flu“); an inflammation of the stomach and intestines Cholera (bacteria in sewage-contaminated food or water) Giardiasis (protozoa in contaminated drinking water) Yellow Fever (virus transmitted by tropical mosquito)

Peptic Ulcers Classification By Region/Location
Duodenum (called duodenal ulcer) Esophagus (called esophageal ulcer) Stomach (called gastric ulcer) Classification by Type Type I: Ulcer along the body of the stomach, most often along the lesser curve. Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion. Type III: In the pyloric region. Associated with acid oversecretion. Type IV: Proximal gastroesophageal ulcer Type V: Can occur throughout the stomach. Associated with chronic NSAID use (such as aspirin).

Gastric and Duodenal ulcers
Strengthens mucus, HCO3- secretion, gastrin, PGs, epidermal growth factor Weakens H. pylori, aspirin, ethanol, NSAIDs, bile salts Peptic ulcers occur when damaging effects of acid and pepsin overcome ability of mucosa to protect itself Gastric ulcers - main problem is decreased ability of mucosa to protect itself Duodenal ulcers - main problem is exposure to increased amounts of acid and pepsin

Two major causes of Peptic Ulcers:
1) 60% of gastric and up to 90% of duodenal ulcers are due to a bacterium called Helicobacter pylori. The body responds by increasing gastrin secretion, which erodes the stomach lining. 2) NSAIDs (non-steroidal anti-inflammatory drugs, such as aspirin) block prostaglandin synthesis. Prostaglandins promote the inflammatory reaction. They also are found in the stomach, protecting it from erosion.

Does stress cause ulcers?
There is debate as to whether psychological stress can influence the development of peptic ulcers. Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid.

Diagnosis of Helicobacter pylori
Urea breath test (noninvasive) Patient drinks a tasteless liquid which contains a radioactive carbon atom as part of the substance that the bacteria breaks down. After an hour, the patient will be asked to blow into a bag that is sealed. If the patient is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. Biopsy Direct culture from a biopsy Histological examination and staining Direct detection of urease activity in a biopsy specimen by rapid urease test Measurement of antibody levels in blood Stool antigen test

Differential Diagnosis (DDx)
A differential diagnosis is a list of possible things that may be causing a patient’s symptoms. DDx for H. pylori infection Peptic ulcer Gastritis Stomach cancer Gastroesophageal reflux disease Pancreatitis Hepatic congestion Cholecystitis Biliary colic Inferior myocardial infarction Referred pain (pleurisy, pericarditis) Superior mesenteric artery syndrome

Risk and Transmission The lifetime risk for developing a peptic ulcer is approximately 10%. In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc.). Prevalence is higher in third world countries. Transmission is by food, contaminated groundwater, and through human saliva (such as from kissing or sharing toothbrushes or food utensils)

Treatment Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists (blocks the acid secretion of parietal cells). Patients who are taking NSAIDs may also be prescribed a prostaglandin analogue (Misoprostol) to help prevent peptic ulcers. When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI), sometimes together with a bismuth compound. An example of a PPI is Omeparazole (Prilosec).

Treatment Ranitidine (Zantac) and Cimetidine (Tagamet) provide relief of peptic ulcers, heartburn, indigestion and excess stomach acid and prevention of these symptoms associated with excessive consumption of food and drink. They decrease the amount of acid the stomach produces allowing healing of ulcers. Sucralfate, (Carafate) and strawberries have also been used in successful treatment of peptic ulcers.

Pancreas Disorders Gestational Diabetes Type I diabetes
Type II diabetes Pancreatitis Cancer Chronic pancreatitis alcohol cystic fibrosis Acute pancreatitis Gallstones

Disorders of the Pancreas: Diabetes Mellitus
Gestational Diabetes Type I diabetes – develops suddenly, usually before age 15 Destruction of the beta cells Skeletal tissue and adipose cells must use alternative fuel and this leads to ketoacidosis Hyperglycemia results in diabetic coma Diabetes Mellitus is a chronic health problem affecting more than 18 million people in the United States. There are 800,000 new cases of diabetes per year; almost all of these are type 2 diabetes. Diabetes is a significant risk factor in coronary heart disease and stroke, and it is the leading cause of blindness and end-stage renal disease, as well as a major contributor to lower extremity amputations. Type I diabetes develops when the beta cells have been destroyed, say from an autoimmune response, or an environmental triggering event (like an infection). These patients, therefore, lack the ability to make sufficient insulin. Because of this, the insulin dependent cells of the body (skeletal muscle and adipose tissue) can not insert their glucose transporters into their cell membranes. Even though the patient has ingested sufficient glucose, the skeletal muscle and adipose cells can not internalize the glucose and then resort to using fatty acids and proteins as fuel sources. These cells are literally starving in the face of plenty. Because these cells use alternative fuel sources that feed into metabolic pathways used by glucose, they generate many ketone bodies (this process will be discussed during your metabolism lecture). Because ketones are organic acids, they cause ketoacidosis when they are present in excessive amounts. These events can lead to diabetic coma due to the inability of the glucose to enter the insulin dependent cells of the body. The patient will need to take insulin for the remainder of their lifetime and need to regulate its use carefully—an overdose of insulin would result in hypoglycemia and now insulin independent cells (like the brain tissue) would not have any fuel and this would also result in diabetic coma.

Disorders of the Pancreas: Diabetes Mellitus
Type II diabetes– adult onset Usually occurs after age 40 Cells have lowered sensitivity to insulin Controlled by dietary changes and regular exercise As I said earlier, the majority of the new cases of diabetes mellitus constitute the type II variety- this is usually associated with adult onset, although more and more of our obese children are presenting with type II. Type 2 diabetes describes a condition of hyperglycemia despite the availability of insulin. Among the acquired risk factors I mention in slide 25, obesity and physical activity are of paramount importance. Obese people have increased resistance to the action of insulin and impaired suppression of glucose production by the liver, resulting in both hyperglycemia and hyperinsulinemia. Central obesity (or abdominal fat) is more closely linked with insulin resistance than is peripheral obesity (gluteal/subcutaneous). The metabolic abnormalities that lead to type 2 diabetes include: peripheral insulin resistance, deranged secretion of insulin by the pancreatic beta cells, and increased glucose production by the liver. I’d like to talk further about insulin resistance and the metabolic syndrome: there is increasing evidence to suggest that when people with type 2 diabetes present predominantly with insulin resistance, the diabetes may represent only one aspect of a syndrome of metabolic abnormalities. Hyperglycemia in these people is frequently associated with obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins (HDL), hypertension, systemic inflammation, abnormal fibrinolysis, abnormal function of the vascular endothelium, coronary artery disease, cerebrovascular disease, and peripheral arterial disease. This constellation of abnormalities often is referred to as the insulin resistance syndrome, syndrome X, or the preferred term, metabolic syndrome. The best treatment for these people is to lose weight and mange their diet-studies have shown with these changes that insulin sensitivity can return.

Pancreatic Failure Digestion is abnormal when pancreas fails to secrete normal amounts of enzymes. Pancreatitis Removal of pancreatic head - malignancy Without pancreatic enzymes - 60% fat not absorbed (steatorrhea) 30-40% protein and carbohydrates not absorbed

Pancreatitis Chronic pancreatitis -
Pancreatitis means inflammation of pancreas. Autodigestion theory can explain condition. Chronic pancreatitis - alcohol - most common cause in adults cystic fibrosis - most common cause in children CF patients lack chloride transporter at apical membrane. Watery ductal secretion decreases which concentrates acinar secretions in ducts. Destroys pancreas gland by autodigestion. Acute pancreatitis - Gallstones - most common cause

Celiac disease (Sprue; gluten intolerance)
Genetic autoimmune disorder of the small intestine, causing chronic diarrhea. The person is allergic to gluten. Causes destruction of microvilli and villi. It is characterized by having pale, loose and greasy stools (steatorrhea) which are voluminous and malodorous. It often presents with abdominal pain and cramping, abdominal distension, and sometimes mouth ulcers. Without adjusting the diet, coeliac disease leads to an increased risk of adenocarcinoma (small intestine cancer).

They may develop ulcerative jejunitis and stricturing (narrowing as a result of scarring with obstruction of the bowel). The changes in the bowel make it less able to absorb carbohydrates, fats, minerals (calcium and iron), and the fat-soluble vitamins A, D, E, and K. Anemia may develop in several ways: iron malabsorption may cause iron deficiency anemia, and folic acid and vitamin B12 malabsorption may give rise to megaloblastic anemia. Calcium and vitamin D malabsorption may cause osteopenia (decreased mineral content of the bone) or osteoporosis (bone weakening and risk of fragility fractures). A small proportion have abnormal coagulation due to vitamin K deficiency and are slightly at risk for abnormal bleeding. Coeliac disease is also associated with bacterial overgrowth of the small intestine, which can worsen malabsorption or cause malabsorption despite adherence to treatment.

Celiac disease is caused by an allergy to gluten. Gluten is present in Wheat subspecies (such as spelt, semolina and durum) and related species such as barley, rye, triticale and Kamut. A small minority of coeliac patients also react to oats. It is most probable that oats produce symptoms due to cross contamination with other grains in the fields or in the distribution channels. Generally, oats are therefore not recommended. Other cereals such as maize (corn), millet, rice, and wild rice are safe for patients to consume, as well as non cereals such as amaranth, quinoa or buckwheat. Non-cereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.

Gluten-free diet Several grains and starch sources are considered acceptable for a gluten-free diet. The most frequently used are corn, potatoes, rice, and tapioca. Various types of bean, soybean, and nut flours are sometimes used in gluten-free products to add protein and dietary fiber. Almond flour is a low-carbohydrate alternative to flour, with a low glycemic index. In spite of its name, buckwheat is not related to wheat; pure buckwheat is considered acceptable for a gluten-free diet, although many commercial buckwheat products are actually mixtures of wheat and buckwheat flours, and thus not acceptable. Gram flour, derived from chickpeas, is also gluten-free (this is not the same as Graham flour made from wheat).

Gluten-free diet Gluten is used in foods in some unexpected ways, for example as a stabilizing agent or thickener in products like ice-cream and ketchup. People wishing to follow a completely gluten free diet must also take into consideration the ingredients of any over-the-counter or prescription medications and vitamins. Also, cosmetics such as lipstick, lip balms, and lip gloss may contain gluten and need to be investigated before use. Glues used on envelopes may also contain gluten. Most products manufactured for Passover are gluten free. Exceptions are foods that list matzah as an ingredient, usually in the form of cake meal. A blood test for IgA antiendomysial antibodies can detect celiac disease.

Uses of animal gut by humans
The stomachs of calves have commonly been used as a source of rennet for making cheese. The use of animal gut strings by musicians can be traced back to the third dynasty of Egypt. In the recent past, strings were made out of lamb gut. With the advent of the modern era, musicians have tended to use strings made of silk, or synthetic materials such as nylon or steel. Some instrumentalists, however, still use gut strings in order to evoke the older tone quality. Although such strings were commonly referred to as "catgut" strings, cats were never used as a source for gut strings. Sheep gut was the original source for natural gut string used in racquets, such as for tennis. Today, synthetic strings are much more common, but the best gut strings are now made out of cow gut. Gut cord has also been used to produce strings for the snares which provide the snare drum's characteristic buzzing timbre. "Natural" sausage hulls (or casings) are made of animal gut, especially hog, beef, and lamb. Similarly, Haggis is traditionally boiled in, and served in, a sheep stomach. Chitterlings, a kind of food, consist of thoroughly washed pig's gut. The oldest known condoms, from 1640 AD, were made from animal intestine.

Part 1: Metabolic Pathways Part 2: GI Physiology Part 3: GI Disorders

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Part 1: Metabolic Pathways Part 2: GI Physiology Part 3: GI Disorders

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