Fed State

What is the first organ that glucose passes through?

Liver

q1 p498 A patient with type 1 diabetes melitus takes an insulin inhjection before eating dinner but hten gets distacted and does not eat. 3 hours later the patient becomes shakey, sweaty, and confused. Why have these symptoms occurred?

Low blood glucose levels. ONce insulin is injected, glucose transport into peripoheral tissues is enhanced and the normal fasting level of glucose drops even further.

8e) Describe the different uses that adipocytes and muscle cells are likely to make of these fatty acids.

Muscle cell uses fatty acids to make ATP aerobically (CO2) Adipocytes store fatty acids as TAGs (triacylglycerols) Liver cells can use the glycerol from the chylomicrons to synthesize TAGs and also take the chylomicron remnants and recycle its components

q3 p517 If a insulin diabetic neglets to take insulin over a weekend what would be affected most? braqin, liver, muscle, rbc, or pancreas?

Muscle, because insulin is required to stimulate glucose transport into them.

7 cont) and describe the chemical structure of a typical fatty acid. (figure 1.6)

a carboxylic acid with a long hydrocarbon chain, which is either saturated or unsaturated

3-Lactose Intolerance - see pp. 501-02 and 508

condition of pain, nausea, and flatulence after the ingestion of foods with lactose. Caused by lack of lactase, which in most people begins declining from high levels 1 month after birth and reaches adult levels by 5 to 7 years of age. For most of the world, hypolactasia is the normal condition. Can also be caused by intestinal injury, called secondary lactase deficiency. Ex: kwashiorkor (protein malnutrion), clitis, gastoenteritis, tropical and nontropical sprue, and excessive alcohol consumption. Lactase is usu. the first enzyme affected and the last to recover.

3-What carbohydrates do not require digestion?

glucose and fructose

q4 p517 after digesting a piece of cake with flour, milk and sucrose as its main ingredients, the major carbohydrates are what?

glucose, galactose, and fructose

3-Location of description for digestion and absorption of dietary carbohydrates:

(part A on page 24; pages 493-506; figures 27.2, 27.12, 10.13, 27.13, 27.3, 27.4, and 27.5) pp. 494, Fig. 27.2 Overview of Carbohydrate digestion.

11) Recall the general structure of a protein (or polypeptide) chain. Define peptide bonds, and explain why they are classified as amide bonds. Draw the chemical structure of a generalized amino acid (figure 1.5) Figure 1.5 General structure of proteins and amino acids.

... ...

q4 p30 Elevated levels of chylomicrons were measured in the blood of a patient. WHat dietary therapy would be most helpfu in lowering chylomicron levels?

A decreased intake of fat

8c) Describe the reassembly and packaging of dietary triacylglycerols inside enterocytes.

Absorption - once fatty acids and 2-Monoacylglycerols (2-MG) are absorbed (taken into the enterocytes), they are reassembled. Fatty acids are placed back onto the glycerol backbone's top and bottom carbons to make a TAG again. Then the TAG is packaged to make lipoprotein molecules/chylomicrons (made by enterocytes). Similar to VLDLs. They also deliver fatty acids to particular tissues in the body.

5-Describe the chemical structure of insulin: Fig. 26.10, pp. 489 Cleavage of proinsulin to insulin

Active form is composed of two polypeptide chains (A and B chains) linked by two interchain disulfid bonds. THe A chain has an additional intrachain disulfide bond

12b) Define zymogens/proenzymes and proteolytic activation, and give examples from protein digestion. Name the cells that produce pepsinogen and stomach acid, describe the activation of pepsinogen to pepsin, and describe the role of pepsin as an endopeptidase. Fig. 37.2, p. 688 Activation of the gastric and pancreatic zymogens

All the enzymes are first secreted into the lumen of the digestive tract in inactive precursor forms: proenzymes/zymogens. They have to take on the right shape to become active; they need one piece of them snipped off. Activation of a proenzyme involves the breaking of at least one peptide bond: (partial) proteolysis. These proenzymes do that once they've reached their digestive destination. Pepsinogen is made by chief cells in the gastric pits of the wall of the stomach. Pepsinogen bites off its own tail when it gets into an acidic environment. The cells that make stomach acid (hydrochloric acid) are parietal cells. Pepsinogen is an endopeptidase - meaning it can cut a polypeptide somewhere within its chain, not at the ends.

q2 p29After digestion of a high carbohydrate meal, how is glucose most likely used?

By liver and skeletal muscle as their major fuel

9) Describe the structure of a generalized lipoprotein complex, such as a VLDL particle or a chylomicron, distinguishing clearly between the molecules in the core and those in the monolayer on the surface. Compare the compositions of VLDLs and chylomicrons. (figures 32.8, 32.9, and 33.21)

Ch. 32, Fig. 32.8 Example of the structure of a blood lipoprotein. This picture works for a chylomicron as well as an VLDL, although with a few changes. The lipoprotein has a surface monolayer of amphipathic (polar and nonpolar parts) molecules (phospholipids - polar head, nonpolar tail). This forms a surface acceptable to water. Cholesterol molecules also have polar heads and nonpolar tails. Why is this monolayer instead of bilayer? Internal compartment is not aqueous, but hydrophobic in nature. The proteins are on the surface, not in the core of a lipoprotein particle. They have some important jobs: Apoprotein B-100 - that's a clue that this lipoprotein was made by liver cells, must be VLDL because only liver cells make Apoprotein B-100. Apoprotein B-48 is made by enterocytes. In the core, there are purely nonpolar, hydrophobic molecules - triacylglycerols & cholesterol esters. Instead of a polar head on cholesterol, there's a fatty acid attached.

q5 p30 A male patient exhibited a body mass index of 33 kg/m'2 and a waist circumference of 47 in. WHat dietary therapy would be most effective?

Decreased intake of total calories because all fuels can be converted to adipose tissue triacyglycerols.

3-Describe dietary fiber and its metabolism by bacterial gut flora: pp. 494, Fig. 27.2

Dietary fiber - carbohydrates/mostly polysaccharides that human enzymes cannot hydrolyze. But in the colon, they may be used by colonic bacteria and converted to gases (H2, CO2, CH4), short-chain fatty acids (SCFA), an important product, and lactate. Extra detail: Examples of SCFA- propionic acid (3C long), butyric acid (4C long), and acetic acid Those are then taken in from the lumen of the colon by coloncytes. The short-chain fatty acids are very beneficial, good fuel and may have other functions.

8b) Describe the reactions catalyzed by lipases in general. Describe the action of pancreatic lipase and the products that are absorbed by enterocytes.

Emulsification leads to an increase in surface area so that it's easier for the enzymes to do their work. Lipase catalyzes hydrolysis of some of the ester bonds in the digested triacylglycerol molecules. Pancreatic lipase comes from the pancreas and does its job in small intestine. Fatty acids are removed from the top and bottom carbons of glycerol. One fatty acid is left in the middle. The others are now free fatty acids. This is enough digestion to absorb the pieces - monoacylglycerols (one fatty acid attached) into enterocytes.

7) Recall the chemical structure of triacylglycerols, and explain why the hydrolyzable bonds in a triacylglycerol are classified as ester bonds.

Fats and oils are composed of triacylglycerols, the neutral fats. These are compounds prepared by the union of glycerol (1,2,3-trihydroxypropane) and 3 fatty acids to form a triester. It contains the functional group ester which will react with water. The enzyme pancreatic lipase acts at the ester bond, hydrolysing the bond and "releasing" the fatty acid. In triglyceride form, lipids cannot be absorbed by the duodenum. Fatty acids, monoglycerides (one glycerol, one fatty acid), and some diglycerides are absorbed by the duodenum, once the triglycerides have been broken down. In other lipids The functional group is usually an ester and the list of compounds includes neutral fats, waxes, phospholipids, and glycolipids. Nonhydrolyzable lipids lack such functional groups and include steroids and fat-soluble vitamins (e.g. A, D, E, and K).

13) Describe the changes in the blood levels of nitrogen, glucose, insulin, and glucagon after a high-protein meal. (figures 26.12, 31.12, and 31.13)

Fig. 26.12, p. 486 Release of insulin and glucagon in response to a high-protein meal Nitrogen level - UP Glucose level - STAYS ABOUT THE SAME Insulin level - GOES UP SOME (insulin causes amino acid absorption by cells) Glucagon - UP dramatically You need gluconeogenesis to be working well after this meal. If you didn't eat any carbohydrate and just ate protein, how do you keep your glucose level from falling? Gluconeogenesis - using amino acids from the meal to make glucose (done in liver).

4-describe the changes in the blood levels of glucose, insulin, and glucagon after a high carbohydrate meal. (section II on page 24; italicized introduction to Chapter 26 on pages 477-478; sections II and III A on pages 480-483; figure 26.8)

Fig. 26.8 p 487 Blood glucose, insulin, and glucagon levels after a high-carbohydrate meal Glucose UP (skyrockets, but modulated by liver) Insulin UP (30-45 min after meal) Glucagon DOWN Extraq detail: Insulin is a protein, but not all hormones are proteins (ie steroid hormones, thyroid hormone). β-cells in the pancreas produce insulin. Insulin doesn't even enter the cells it sends messages to. The target cell is stimulated by a membrane (surface) receptor. Steroid hormones are famous for entering target cells. Glucagon released by α-cells of the pancreas - stimulates the breakdown of glycogen to raise blood sugar. Glucose is gone - gluca-gon. It tells the cells that glucose is gone and needs to get more into the blood. Insulin lowers the blood level of glucose (the glucose goes to adipocytes and muscle cells).

10) Describe the sources, function, and fates of VLDLs and chylomicrons. (Section IV on page 26; figures 2.2 and 33.24)

Fig. 32.13 p. 591 Fate of chylomicrons Chylomicrons come out of enterocytes (intestinal epithelial cells) and don't successfully enter the blood capillaries; rather they enter into the lymphatic capillaries - lacteals projecting into the villi of the gut wall. Chylomicrons spend some time in the lymph before they ever get to the bloodstream. All these lacteals converge so that the lymph flows into a major lymphatic vessel: the thoracic duct. Like an onramp onto the freeway the contents of the thoracic duct feed into the left subclavian vein. Chylomicrons, VLDLs, LDLs, and HDLs are all lipoproteins-- chylomicrons are the least dense lipoproteins of all of these (classifying them as lipoproteins makes sense when you examine their component molecules, and their job is a lipoprotein type of job-- the transport of lipid through the bloodstream)

8) Describe the digestion, absorption, and packaging for transport of dietary triacylglycerol: (part C on page 24; pages 583-591; figures 32.3, 32.13, 32.1, 32.4, 32.8, 32.9, and 32.10)

Fig. 32.3, p. 586 Digestion of triacylglycerols (in an ADULT) Breakdown of fats begins in the mouth with mechanical mastication. Digestion of some fats can begin in the mouth where lingual lipase breaks down some short chain lipids into diglycerides. The presence of fat in the small intestine produces hormones that stimulate the release of pancreatic lipase from the pancreas and bile from the liver for breakdown of fats into fatty acids. Complete digestion of one molecule of fat (a triglyceride) results in 3 fatty acid molecules and one glycerol molecule. No real digestion of fat in the stomach (in an infant there is a lipase in the stomach) The triacylglycerols of the diet are emulsified in the intestine by bile salts, which are syntheiszsed in the liver and stored in the gallbladder. The enzyme pancreatic lipase converts the tracylglycerols in the lumen of the intestine to fatty acids and 2-monoacylglycerols, which interact with bile salts to form tiny microdroplets called micelles. The fatty acids and 2-monoacylglycerols are absorbed from these micelles into the intestinal epithelial cells, where they are resynthesized into triacylglycerols. the triacylglycerols are packeaged with proteins, phosopholipids, cholesterol, and othe compounds into lipprotein complexes knwon as chylomicrons, which are secreted into the lymp and ultimately enter the bloodstream (fig 2.2, circle 4). FAts must be tansported in the blood bound to protein or in lipoprotein comlexes because they are insoluble in water. Thus, both triacylglycerols and cholesterol are found in lipoprotein complexes.

12a) Describe the digestion and absorption of dietary protein: Describe the completion of the digestion of dietary protein, sodium dependent uptake of amino acids from the intestinal lumen, and the travel of the amino acids to the liver. (part B on page 24; Sections I and II on pages 688-691; figures 37.1, 37.2, 37.3, and 37.4)

Fig. 37.1, p.688 Digestion of proteins Protein digestion begins in the stomach with hydrochloric acid and pepsin (a protein enzyme that digests other proteins). Pepsin is a protease. It catalyzes hydrolysis of peptide bonds in proteins. Proteases=peptidases Trypsin, chymotrypsin, elastase, carboxypeptidases A and B come from the pancreas and are pancreatic proteases. Even as a team they don't completely break every single peptide bond before the pieces are small enough to be absorbed. Di- and tri- peptides & amino acids can be absorbed by enterocytes. Digestion may be completed in enterocytes with di- and tri-peptidases. The amino acids are quite water soluble and go directly into the bloodstream. Aminopeptidases are located on brush border/luminal surface of enterocytes.

14) Describe the fates of amino acids in the fed state. (section V on pages 26-27; figures 38.2A and 2.2)

Fig. 38.2A, p. 698 Roles of various tissues in amino acid metabolism. This figure shows what the liver does with amino acids in the fed state. The liver builds protein for its own use and for export - albumin and blood clotting factors. The liver makes other nitrogen-containing compounds. To use the amino acids as fuel, nitrogen must be removed. Amino acids can be used to make fat (shipped out as VLDLs) or glucose (gluconeogenesis). Glucose could used for glycogen stores or exported to the blood. What happened to the nitrogen? Urea cycle.

1-What two things are the fuels glucose, amino acids, and fats all used for in the Fed State?

For energy and synthesis

What is the Fed State?

From the start of absorption to the end of absorption where fuels are oxidized for energy or transported to storage, which is determined by insulin and glucagon.

Chp 27 #1 p517: The facilitative tansporter that is most responsible for transporting fructose from the blood into cells is GLUT 1, 2, 3, 4, or 5?

GLUT 5:

Two main mechanisms that maintain blood sugar?

Gluconeogenesis and Glycogenolysis

4) Define hormone:

Hormones - chemical messengers secreted by some type of cell in the body that deliver their message throughout the body (as opposed to locally) by traveling through the bloodstream.

2-Draw Protein/amino acids fig 1.5

Identify this chemical structure:

2-Draw carbohydrate Lactose: fig 27.1

Identify this chemical structure:

2-Draw triacylglycerol: fig 1.6

Identify this chemical structure:

The major functions of enterocytes include[1]:

Ion uptake, water uptake, Sugar uptake, peptide and amino acid uptake, lipid uptake, Vit B12 uptake, Secretion of immunoglobulins Extra detail: Ion uptake, including sodium, calcium, magnesium, and iron. This typically occurs through active transport. Water uptake. This follows the osmotic gradient established by Na+/K+ ATPase on the basolateral surface. This can occur transcellularly or paracellularly. Sugar uptake. Polysaccharidases and disaccharidases in the glycocalyx break down large sugar molecules, which are then absorbed. Glucose crosses the apical membrane of the enterocyte using the sodium-glucose cotransporter. It moves through the cytosol (cytoplasm) and exits the enterocyte via the basolateral membrane (into the blood capillary) using GLUT2. Galactose uses the same transport system. Fructose, on the other hand, crosses the apical membrane of the enterocyte, using GLUT5. It is thought to cross into the blood capillary using one of the other GLUT transporters. Peptide and amino acid uptake. Peptidases in the glycocalyx cleave proteins to amino acids or small peptides. Enteropeptidase (also known as enterokinase) is responsible for activating pancreatic trypsinogen into trypsin, which activates other pancreatic zymogens. They are involved in the Krebs and the Cori Cycles and can be synthesized with lipase. Lipid uptake. Lipids are broken down by pancreatic lipase and bile, and then diffuse into the enterocytes. Smaller lipids are transported into intestinal capillaries, while larger lipids are processed by the Golgi and smooth endoplasmic reticulum into lipoprotein chylomicra and exocytozed into lacteals. Vitamin B12 uptake. Receptors bind to the vitamin B12-gastric intrinsic factor complex and are taken into the cell. Resorption of unconjugated bile salts. Bile that was released and not used in emulsification of lipids are reabsorbed in the ileum. Also known as the enterohepatic circulation. Secretion of immunoglobulins. IgA from plasma cells in the mucosa are absorbed through receptor mediated endocytosis on the basolateral surface and released as a receptor-IgA complex into the intestinal lumen. The receptor component confers additional stability to the molecule.

Describe the source and location of, and the reaction catalyzed by, lipoprotein lipase (LPL). (Section IV on page 26; figures 2.2 and 33.24)

LPL stands for an enzyme: lipoprotein lipase: it works on lipoprotein particles. If the meal had some carbohydrate in it as well as fat, there could be VLDLs there too. VLDLs from the liver also interact with lipoprotein lipase. This is how either one would deliver fatty acids from the cargo they carry. A lipase catalyzes the hydrolysis of lipids - it breaks the ester bonds in triacylglycerol molecules. That releases fatty acids from the glycerol backbones. The fatty acids go into muscle cells and adipocytes. The recipients are adipocytes and muscle cells because those are the two tissues that make lipoprotein lipase. LPL location is on the inner wall of a capillary that feeds either adipocytes or muscle tissue. It's produced by adipocytes and muscle cells and then presents on the inner walls of the capillaries. It's waiting there for the chylomicrons and VLDLs and when these lipoproteins dock at the LPLs, they release their contents.

3-Role of Pancreatic amylase in digestion and absorption of starch?

No digestion of carbohydrates occurs in the stomach. To help break down the starch further (after leaving the stomach) there is a second enzyme - pancreatic α-amylase. Produced by cells in the pancreas and secreted into the duodenum. But neither one of these enzymes breaks the 1,6 linkages.

1-Describe the major fate of glucose in the Fed State? (page 22; figures 2.1 and 2.2)

Oxidation, Storage, and synthesis. Oxidation: Dietary carbohydrates are mostly broken down to this major monosaccharide in the blood, then oxidized to CO2 for energy, Storage: excess stored as glycogen or TAG, which can later be converted to glucose. Note that fatty acids cannot be converted back to glucose. Synthesis: of many compounds as it is the major biosynthetic precursor for most bodily compunds

5-The messages delivered to target tissues by insulin: (parts B and C on pages 483-485; table 26.1 on page 488 and table 26.2 on page 491; figures 26.10 (p489), 26.11, 26.6, 15.13, 15.14, and 27.13)

Promotes fuel storage after a high-carbohydrate meal and promotes growth - insulin rises and causes increased absorption of glucose in some cells. Table 26.1, p. 482 Glucose storage as glycogen in muscle and the liver (glycogenesis - going from glucose to glycogen) is stimulated by insulin. Fatty acid synthesis (lipogenesis) and storage as TAG after a high-carbohydrate meal is stimulated by insulin signals - we find this in two places: liver cells and adipocytes. When TAG is made by liver cells, they don't store it, they ship it out, export it. These fat packages for export from the liver are VLDL particles - very low density lipoproteins. They go into the bloodstream and have the very important job of delivering fatty acids to a couple important tissues - can deliver VLDLs to adipose tissue and muscle tissue. They carry fatty acids attached to glycerol backbones - for end delivery, they must split apart glycerol and fatty acids via hydrolysis. Insulin signals stimulate growth, or the uptake of amino acids for protein synthesis. Tissues will take in amino acids after a meal that contains protein in a way that's stimulated by insulin. After a protein meal insulin stimulates the tissues to take in amino acids and conduct protein synthesis. Insulin is an anabolic hormone - promoting growth. Both protein synthesis AND amino acid uptake are stimulated by insulin. It helps by increasing the number of amino acid doorways. Extra detail: Uses of glucose: Brain - uses glucose to make ATP aerobically (production of CO2) under non-starvation conditions Red Blood Cell - uses glucose to make ATP anaerobically (production of lactate), goes through glycolysis (glucose → pyruvate) Adipose tissue - uptake of glucose stimulated by insulin - what doorways or mechanisms involved? Insulin increases the number of GLUT-4 doorways in the membrane. The adipocyte then uses glucose to make fat. Muscle tissue - uptake of glucose stimulated by insulin via GLUT-4 doorways. The muscle cell synthesizes glycogen for storage in the muscle cell. How does the brain get glucose from the blood? It's not GLUT-4 transporters that they use. They use a different GLUT transporter - one that does NOT depend on insulin. RBCs have a GLUT transporter, but not GLUT-4; they also don't require insulin to absorb glucose. ADIPOCYTES & MUSCLE CELLS DO USE INSULIN. What happens when amino acids reach the liver? After a pure-protein meal you need the liver to turn the amino acids into sugar. Table 26.2, p. 485 Regulators of Insulin Release β-cells of pancreas produce insulin. When blood sugar level rises the β-cells are stimulated to release insulin. Amino acids also produce insulin release. Neural (brain) input causes insulin release, epinephrine decreases insulin release - epinephrine wants stored fuel mobilized and used.

1-Describe the major fate of fats in the Fed State? (page 22; figures 2.1 and 2.2)

Storage, oxidation, and synthesis. Storage: as TAG Oxidation: for energy (mainly carbons) Synthesis: source of building blocks for membrane lipids like phospholipids

3-Can you name the enzymes that catalyze the hydrolysis of sucrose? Lactose? Isomaltose?

Sucrase. Lactase. Isomaltase.

1-Describe the major fate of amino acids in the Fed State? (page 22; figures 2.1 and 2.2)

Synthesis, Oxidation, and Gluconeogenesis. Protein Synthesis: various Syntheisis of N-containing compounds: in cells, like neurotransmitters, heme Oxidation: proteins may be used for energy for aerobic use or converted to glucose Gluconeogenesis: in liver cells - to maintain blood sugar levels.

6) Describe the fates of glucose in various tissues after a high carbohydrate meal. (section III on pages 25-26; figures 2.2, 33.24, 31.15, 22.2, and 33.23)

Table 31.15, pp. 571 Glucose metabolism in various tissues Adter a meal, the fuels we eatr are oxidized to meet our immediate enrgy needs. Glucose is themajor fule for most tissues. Excess glucose and other fuels are stored as glycogen mainly in muscles, conversion to Glycogen, tracylglycerols, CO2 and biosynthetic reacitons in liver, and as triacylglycerols in in adipose tissue. Amino acids from dietary proteins are converted to body proteins or oxidized as fuels. Extra detail: In liver cells - Glucose is used to make VLDLs and glycogen. VLDL particles allow fat to travel through the bloodstream. Some is oxidized in ATP to meet immediate energy needs of liver cells. Oxidation to CO2: glucose--pyruvate (glycolysis)--A CoA---A CoA enters TCA--where completely oxidized to CO2 In adipocytes - Fat is synthesized from glucose. Glucose goes through glycolysis (i.e. glucose to pyruvate). One of the main reasons adipocytes are doing glycolysis (same for liver cell) is to make building blocks that can be used to build fat. All of the carbon for fat molecules can come from glucose. Can be used to make glycerol and fatty acids. The use of glucose as building blocks or energy requires glycolysis. Detail in adipocyte is applicable to liver cell. It's a building project converting glucose to fat. Before you can attach fatty acids to a glycerol, you need a phosphate group attached to the third carbon of glycerol. Looks like a phosphoester. However, first you need to convert DHAP (dihydroxy acetone) to the Glycerol-3-P backbone. See Image They only differ at the middle carbon - ketone/alcohol relationship. DHAP becomes Glycerol-3-P via reduction of the ketone to an alcohol. DHAP is an intermediate between glucose and pyruvate, an intermediate of glycolysis (10 steps total). Some of DHAP is used as fuel, some used to make fat molecules. REDUCTION OF A KETONE PRODUCES AN ALCOHOL. The use of glucose to make fatty acids requires the entire process of glycolysis (review: an intermediate in between pyruvate and fatty acids is acetyl CoA.) In muscle cells - glucose is converted into glycogen for storage and the muscle cells can receive VLDLs (made from glucose) from the liver

3-Enzymes that complete the digestion of starch and catalyze the hydrolysis of disaccharides (lactose and sucrose)?

The enzymes pasted to the wall of the small intestine (on the luminal/brush border) finish digesting the starch and disaccharide molecules. Brush border enzymes are produced by intestinal cells, not the pancreas. The enzymes are tethered to the enterocytes in the microvilli. AKA: Gut mucosal cells/intestinal mucosal cells/gut epithelial cells/intestinal epithelial cells/absorptive cells/enterocytes. After being broken down into monosaccharides, these sugars leave the small intestine and enter the enterocyte.

3-Role of Salivary amylase in digestion /absorption of starch?

The first enzyme that works on the starch molecules (disaccharides are not digested until the small intestine - lactose, sucrose) - is salivary α-amylase. Extra detail: The only linkages that this enzyme can catalyze hydrolysis of are the 1,4 linkages. This would lead to the production of α-dextrins, four-to-nine glucose rings big - still have some 1,6 linkages. The size of those dextrins might be described as oligosaccharide-sized. Much smaller than a polysaccharide but bigger than a disaccharide.

q1 p29 During the digestion of a mixed meal, what most likely happens to blood glucose levels?

The levels increase in the blood.

3-Describe the absorption of monosaccharides from a carbohydrate containing meal, and their transport to the liver: pp.505, Fig. 27.12

The monosaccharides have to be taken into enterocytes on the mucosal side and secreted from the serosal side to reach the capillaries and get to tissues of the body, which occurs thru protein mediated Na+ dep. active transport and facilitaitive diffusion. Then are transported from intestinal epithelial cells into blood where they circulate to liver and perifpheral tissues. Extra detail: Glucose and galactose go through the same doorway - the Na+-glucose cotransporter (specific to enterocytes). It's Na+-dependent absorption. These Na+-dependent doorways allow the active transport of glucose and galactose across the luminal (mucosal) membrane. That costs the cell some energy because glucose is going against its concentration gradient. The Na+-gradient provides the energy for this active transport (that's the reason why it's a Na+-dependent process). The concentration of sodium in the lumen of the small intestine is always higher than in the enterocyte. Gradient - situation of inequality in concentration of a substance across a membrane. Letting the sodium through works as a power source. But in order for this to work, the [Na+] in the enterocyte needs to stay low, hence we have the Na+-K+ pump. A pump implies you are going against a concentration gradient. The Na+ - K+ pump keeps the intracellular [Na+] low. (THIS OCCURS ON THE BASOLATERAL MEMBRANE) So we pump sodium out against its concentration gradient and bring potassium in against its concentration gradient. So we have secondary active transport of the glucose because you spend a sodium gradient to bring glucose in, not ATP directly. You spend ATP later to pump the sodium out.

Glycogenolysis

The other means of maintaining blood glucose levels is through the degradation of glycogen

Name the cells that produce trypsinogen, describe the activation of trypsinogen to trypsin, and describe the role of trypsin as an endopeptidase. Name the cells that produce chymotrypsinogen, proelastase, and procarboxypeptidases A and B, describe the activation of each one, and describe the roles of the resulting proteases as either endopeptidases or exopeptidases. Fig. 37.3, p. 689 Action of the digestive proteases

The pancreatic proteases: trypsin, chymotrypsin, elastase, and the carboxypeptidases Pancreatic zymogen activation - trypsinogens are activated by enteropeptidases. Enteropeptidases are on the brush border. It turns the first trypsinogens into trypsins, but after that, the activated trypsins can help other trypsinogens become trypsins. They can also proteolitically activate chymotrypsinogen, proelastase, and procarboxypeptidase. As a team, pepsin, trypsin, chymotrypsin, and elastase can only break peptide bonds that are within the chain of the polypeptide (as opposed to the end). Endo- vs. exo-peptidases. Only an endopeptidase can make a break within the chain (e.g. make two equal size pieces). An exopeptidase can only work at the very end, the terminal amino acids. Aminopeptidases work at the N-terminus and carboxypeptidases are exopeptidases working at the C-terminus.

q3 p30 Amino acids derived from digestion of dietary protein can be used for what?

To provide nitrogen for synthesis of nonessential amino acids in the liver.

8a) Mention the production of, storage of, components of, and roles of bile. Mention the formation of micelles in the small intestine, and how this facilitates the digestion of dietary fat.

To successfully digest the triacylglycerol, it must be in pieces small enough to be absorbed by enterocytes. Thus, we need to emulsify the lipid that was swallowed. Emulsification - break up of lipids into small droplets. Detergent-kind of action. Emulsifiers are largely introduced into the small intestine by the liver that makes bile. The emulsifiers in bile are the bile salts. BILE DOES NOT MEAN BILE SALTS. Bile is a complex mixture of things and bile salts are just one component of the mixture. (e.g. Bilirubin is in bile - the bile is helping to remove waste from the body. Bile has several functions.) There other emulsifiers in bile - phospholipids molecules. The bile is produced in the liver and may spend some time stored in the gallbladder. The gallbladder contains more concentrated bile because water is reabsorbed over time. Upon eating, the gallbladder wall is hormonally stimulated to contract and release its contents into the duodenum.

8d) Describe the route taken by chylomicrons to reach the bloodstream, and how chylomicrons can then deliver fatty acids from dietary triacylglycerols to adipocytes and muscle cells. Name the enzyme that facilitates this process, and give its location.

Transport of TAGs - These chylomicrons contain TAG that came from your dietary TAG, packaged together with some things that make them more acceptable for travel through the bloodstream. The TAGs are very nonpolar, hydrophobic by themselves. Thus, packaging is required to travel through the bloodstream. Phospholipids (polar heads acceptable to water) are added to the TAG, and proteins like apoB make the fat water-soluble. Apo = protein. Chylomicrons and VLDLs are both lipoproteins and they look very much alike. VLDLs come from liver cells and they contain fat made from sugar - thus, these lipoproteins are endogenous (made within you) Chylomicrons are made by enterocytes carrying fat from your meal - dietary fat, exogenous But both have the same job - deliver and transport of fatty acids.

TAG

Triacylglycerol

q5 p517 a patient that has a genetic defect that causes lower levels of disaccharidases will exhibit higher levels of what after eating a bowl of milk and oatmeal with table sugar?

maltose, sucrose, and lactose in stool.

Gluconeogenesis

metabolic pathway that results in the generation of glucose from non-carbohydrates such as lactate, glycerol, and glucogenic amino acids (to prevent low blood glucose, yhpoglycemia). This process occurs during periods of fasting, starvation, or intense exercise and is highly endergonic.

q4 p589 what is most likely to occur with glucagon and insulin after a high carb meal?

only insulin levels increase

5) the synthesis and secretion of insulin, and the messages delivered to target tissues by insulin. (parts B and C on pages 483-485; table 26.1 on page 482 and table 26.2 on page 485; figures 26.10 (p489), 26.11, 26.6, 15.13, 15.14, and 27.13)

p489-91 Synthesis of insulin: Proinsulin is made in the β-cells of the pancreas or more specifically, on a ribosome. The ribosome has to attach itself to the endoplasmic reticulum (ie rough endoplasmic reticulum). Then, on the rough ER, the polypeptide proceeds through the Golgi apparatus, producing a secretory vesicle for exocytosis. Extra detail: For a hormone, we definitely want to secrete something outside the cell. The building blocks for this hormone are amino acids - it's a polypeptide chain held together by peptide bonds. The convention for listing the sequence of amino acids is to start with the amino (N-terminus) end and finish with the acid (C-terminus) end. May happen in the secretory vesicle. This happens by breaking four peptide bonds. Two on each side of the C-peptide. The proteolytic processing leaves us with two polypeptide chains. To number the amino acids from 1-30, you start at the N-terminus.

q4 p714 which enzyme is activated thru an autocatalytic process: enteropeptidase, trypsinogen, pepsinogen, aminopeptidase, proelastase

pepsinogen under acidic conditions autocatalyzes its own conversion to pepsin in the stomach

q2 p517 A patient with pancreatitis has discomfort after eating a high carb meal. He most likely had a reduced ability to digest what?

starch

6- Define Glycogenesis

the conversion of excess simple sugar (glucose) into a complex form of sugar (starch) for storage in the liver for later use as needed Glucose → Glucose - 6P (Hexokinase [liver] Glucokinase [muscle]) Glucose - 6P → Glucose - 1P (Phosphoglucomutase) Glucose - 1P + UTP → UDPG(active glucose) + Pi-Pi (UDPG pyrophosphorylase) Primer + UDPG → Primer + 1 glucose + UDP (glycogen synthase) alpha(1-4) Glucose(n) → transfers 7 glucoses and forms α1-6 - branch (branching enzyme) Rinse and repeat

define enterocytes

the predominant cells in the small intestinal mucosa (also found in colon). They are tall columnar cells and responsible for the final digestion and absorption of nutrients, electrolytes and water.

q1 p604 the most abundant component of chylomicrons is apoB-48, triglycerirde, phospholipid, cholesterol or cholesterol ester?

triglyceride

q1 p714 an individual with a deficiency in conversion of trypsinogen to trypsin would experience a detrimental effect on protein digestion as a result of what?

trypsin activates the other zygomens that are secreted by the pancreas.