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BSC 216 Metabolism and Nutrition Part 2

by: Vanessa Notetaker

BSC 216 Metabolism and Nutrition Part 2 BSC 216

Marketplace > University of Alabama - Tuscaloosa > Biology > BSC 216 > BSC 216 Metabolism and Nutrition Part 2
Vanessa Notetaker
GPA 3.71

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Second part of the chapter on Metabolism and Nutrition. This contains the lecture content from Tuesday. October 18. Lecture mostly included catabolism of fatty acids and amino acids as well as anab...
Anatomy & Physiology II
Austin Hicks
Class Notes
catabolism, anabolism, metabolism, glucose, amino acids, fatty acids, Anatomy & Physiology II
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This 8 page Class Notes was uploaded by Vanessa Notetaker on Tuesday October 18, 2016. The Class Notes belongs to BSC 216 at University of Alabama - Tuscaloosa taught by Austin Hicks in Fall 2016. Since its upload, it has received 3 views. For similar materials see Anatomy & Physiology II in Biology at University of Alabama - Tuscaloosa.


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Date Created: 10/18/16
BSC 216 Metabolism and Nutrition Part 2 10/18 Why do We Breathe  Oxygen is inhaled and carbon dioxide is exhaled o Oxygen is NOT converted to carbon dioxide o Oxygen is delivered to the cells through the blood and is the final electron acceptor in the Electron Transport Chain, producing WATER  Carbon dioxide begins to be produced in the intermediate step of glycolysis and the Citric Acid Cycle o When pyruvate is transformed to Acetyl CoA Carbon is driven off in the form of CO2  If oxygen levels are low pyruvate will not enter the citric acid cycle to preserve carbon dioxide production  High levels of oxygen allow for pyruvate to undergo the TCA cycle and create more carbon dioxide o Carbons removed during the Citric Acid Cycle are also lost as CO2 o It diffuses through the cytosol and enters the blood where it is delivered to lungs for exhalation ATP Synthesis: ETC and Oxidative Phosphorylation  ATP synthase: Large protein in inner mitochondrial membrane  Ion channel and turbine that catalyzes the synthesis of ATP o As hydrogen ions flow through ATP synthase the rotor spins and the enzyme releases ATP ATP Yield from Glucose Catabolism and ATP Synthesis  Energy released from the pumping of electrons from 1 NADH produce 3 ATP o Yield of FADH 2s 2 ATP  1 glucose full oxidized= 38 ATP Fatty Acid and Amino Acid Catabolism  Cells are capable of breaking down fatty and amino acids in addition to glucose o Glucose is the preferred fuel source by the body  All three nutrients (carbohydrates, fatty acids and amino acids) are converted into chemicals and can be oxidized and their electrons transferred to electron carriers o Sent to Electron Transport Chain for oxidative phosphorylation o Converge at different places on the catabolic pathway: can be as pyruvate, Acetyl CoA, glyceraldehyde-3-phosphate, etc. Fatty Acid Catabolism  Most fats in the body exist as triglycerides o 3 Fatty acid chains linked to a glycerol via an ester linkage  Lipolysis: Enzyme catalyzed process that liberates fatty acids and glycerol o Lipo means fat. lysis means breakdown of o Fatty acids and glycerol can be used for energy production o Most energy in triglycerides derived from fatty acid beta oxidation  Glycerol: converted to glyceraldehyde-3-phosphate o Enters glycolysis at energy producing step after cleavage  Fatty Acids: catabolized to acetyl CoA by beta oxidation o Ketone bodies produce by ketogenesis  Beta-oxidation: Fatty acids enter the mitochondrial matrix of cells that can oxidize them (skeletal and cardiac cells) o Each fatty acid is bound to CoA (Coenzyme A) and initiates a series of reactions called beta oxidation o Fatty acid chain is oxidized and has two carbons removed  Produces NADH, FADH , a2etyl CoA and a shorter fatty acid chain with 2 fewer carbons  As long as there are two carbons “to be cleaved” more acetyl CoA will be produced  NADH and FADH pr2ceed to Electron Transport Chain  Acetyl CoA enters the Citric Acid Cycle o Another CoA molecules binds the shortened fatty acid and beta oxidation continues until the entire fatty acid has been converted to acetyl CoA o Fatty acids can be converted into greater amounts of ATP as compared to glucose because more FADH , N2DH and acetyl CoA are produced Fatty Acid Catabolism  Skeletal and cardiac muscle cells can use ketone bodies readily while cells in the brain only use them for periods of starvation  Liver will begin to rapidly oxidize fatty acids for energy during o Extreme caloric restriction o Carbohydrate restriction o Full starvation  Ketosis: large quantity of ketone bodies in the blood o As a result of carbohydrate deprivation  Ketoacidosis: dangerous lowering of blood pH brought on by ketosis Amino Acid Catabolism  Proteins used for catabolism either come from the diet or are already in the cytosol  Dietary proteins are broken down in the digestive system and absorbed into the body as amino acids o Immediately delivered to the liver via the hepatic portal vein o Amino acids contain a carbon skeleton with an amino group  Nitrogen in the amino group cannot be used for energy  Removed via transamination  Remaining carbon skeleton can be oxidized for fuel  Events of protein catabolism occur in the following sequence o Transamination: amino group is removed and transferred to alpha ketoglutarate  Products are a carbon skeleton and the amino acid glutamate  Carbon skeleton can be converted to a variety of compounds which can then be oxidized o Oxidative deamination occurs in the mitochondria of hepatocytes (Liver cells)  Produces ammonia and alpha ketoglutarate  Some amino acids are removed to aid in the synthesis of new amino acids  Remaining ammonia ions are removed in the form of urea  Urea: formed when two ammonia molecules are combined with carbon dioxide and eliminated via the urinary system  High levels of ammonia are toxic so it must be excreted Intro to Anabolic Pathways  Anabolism: synthesis of large molecules o Requires energy (Usually endergonic) o Good for nutrient storage and synthesis, structural element synthesis (making things l+ke DNA and RNA) and synthesis of special molecules like FAD and NAD  Nutrients need to be stored for two reasons o Dietary intake exceeds energy immediately required o Body needs a ready supply of nutrients to maintain homeostasis between meals o Glycogen and adipose are the two main storage forms Glucose Anabolism  Gluconeogenesis: Storage of excess glucose obtained from diet o Glyco=glycogen neo=new genesis=creation of o Synthesis of glycogen via a series of enzyme catalyzed reactions o Occurs mostly in the muscle cells and hepatocytes o Glycogen made my combining glucose units  Glycogen=large branched molecule composed of thousands of glucose units  Glycogenolysis: catabolic process that cleaves glucose units off of glycogen to maintain blood glucose homeostasis  Gluconeogenesis: Mechanism by which glucose is synthesized from non- carbohydrate sources o Once glycogen runs out cells need to be fueled in alternate manner o Hepatocytes and some kidney cells can produce 3 and 4 carbon compounds into glucose  These compounds include glycerol, pyruvate, lactate, intermediates of the citric acid cycle, specific glucogenic amino acids  Not all amino acids can be converted into glucose only the glucogenic subset  Fatty acid cannot be converted into new glucose molecules but, it can produce energy Fatty Acid Anabolism  Synthesis of fatty acids resemble beta oxidation but backwards! o The difference is the pathway (completely different pathway), different enzymes and different manufacturing location  Lipogenesis: Process used to synthesize fatty acids o Takes place in cytosol o Occurs because of the enzyme fatty acid synthase which catalyzes a reaction that progressively lengthens fatty acid chains  Lengthens them 2 carbons at a time  Most fatty acids are attached to glycerol and assembled into triglycerides in the Endoplasmic reticulum and stored in adipocytes o Most energy storage of triglycerides occurs in the adipose tissue  Glycerol and fatty acids are derived from amino acids and glucose, not just dietary sources o Excess glucose that isn’t stored as glycogen is converted to Acetyl-CoA and then to fatty acids  Similarly excess amino acids can also be converted to fatty acids o Glycerol can be synthesized from other products of glycolysis Amino Acid Anabolism  Amino acids have no specific storage system like carbs do to glycogen and fats to adipose tissue o The body is capable of synthesizing 11-20 amino acids  The other 9 must be obtained from the diet (essential amino acids) o Synthesis involves reactions that add an amino group to a carbon skeleton molecule  Some products of synthesis are alpha-ketoglutarate, pyruvate and oxaloacetate  However, the cell only synthesizes a certain amount of amino acids and then the rest need to be converted to other molecules for storage o Glucogenic amino acids are converted to glucose by gluconeogenesis and stored as glycogen  Not all amino acids are glucogenic o Other amino acids are converted to fatty acids and stored in adipose tissue Metabolic States  Absorptive state: occurs immediately after feeding o Can last up to 4 hours o As nutrients are absorbed from the small intestine into the body the following occurs  Nutrient molecules are oxidized to fuel cells (ATP production)  Glyconeogenesis  Lipogenesis  Protein synthesis o Triggered by insulin  Postabsorptive state: begins once nutrient absorption is complete o After the 4 hour window is over  Late morning, late afternoon and most of the night o Anabolic processes decline o Processes that occur are mostly catabolic and include  Breakdown of proteins into amino acids  Ketogenesis  Gluconeogenesis  Lipolysis  Oxidation of molecules to provide fuel  Glucose sparing: phenomenon where non-nervous cells breakdown just synthesized fatty acids preferentially o Normally glucose is the preferred source of fuel but, to conserve glucose for the nervous system glucose is spared o Non-nervous system cells can use ketone bodies or amino acids for energy  Glucagon: released from pancreas when blood drops o Triggers Glycogenolysis and gluconeogenesis Regulation of Feeding  Feeding is controlled by hormonal and neural signals that either stimulate or inhibit feeding nuclei in the hypothalamus of the brain o Satiety center creates the feeling of fullness and blocks the desire to eat o Hunger center creates the feelings of hunger and increases the desire to eat  Long term regulated: Hormones o Leptin: produced by adipocytes that stimulate the satiety center and inhibit the hunger center  Drop in leptin levels allows hunger center to be activated  Tells you you’re full o Ghrelin: hormone produced by stomach mucosal cells that stimulate neurons in hunger center  Tells you you’re hungry  Short term signals o Insulin: Released in response to feeding and has similar effect as leptin, decreasing eating/food intake o Feeding stretches the stomach wall  Produces cholecystokinin (CCK) which inhibits hunger but, also functions in secretion of bile  Stimulates vagus nerve to indirectly suppress hunger center and decrease release of hunger related neurons o Levels of certain molecules in the blood can stimulate or inhibit the hypothalamic centers  Low blood sugar stimulates hunger and the release of orexin


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