Carbohydrate, Protein And Lipid Metabolism Notes
Part 1 – Metabolism Concepts and Measurement Carbohydrates, protein and fat are macronutrients. In the human body metabolism is the oxidization of carbohydrates, protein and fat to give CO2, H2O and energy. What is Metabolic Rate? Metabolic Rate is the amount of energy liberated per unit time. The Basal Metabolic Rate is the rate of energy expenditure at rest in a neutrally temperate environment, in the post-absorptive state (meaning that the digestive system is inactive, which requires about twelve hours of fasting in humans). The Basal Metabolic Rate is the largest component of total caloric expenditure in humans: 70% Physical activity contributes: 20% Thermogenesis & digestion contributes: 10% Units used for Metabolic Energy calorie (cal – note lowercase) is the standard unit of metabolic heat energy, being the amount of energy needed to raise 1g of water by 1 degree, from 15o to 16o C. Calorie (kilocalorie, kcal, big calorie, large calorie, kilogram calorie) is more commonly used, representing 1000 calorie. Joule is the SI unit for energy, such that 1 calorie = 4.2 joule. To convert from Calories (kilocalories) to kilojoules, multiply by 4.2. How do we measure Metabolic Energy and Metabolic Rate? Direct calorimetry A Bomb Calorimeter, or constant-volume calorimeter, is used to measure the energy released by food during complete oxidization. The food is placed in a sealed metal container surrounded by water in an insulated container. The food is ignited by an electrical spark and the temperature change of a known volume of water is used to calculate the energy released by the food. Standard caloric values for macronutrients are: Carbohydrates: 4.1 kcal/g Protein: 5.3 kcal/g (but in the body is only 4.1 kcal/g due to incomplete oxidation) Fat: 9.3 kcal/g Ethanol: Continue reading >>
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Crossfit | An Introduction To Metabolism
Living organisms can be thought of as heat machines and metabolism as the inner workings of the machine. The metabolism converts energy from the combustion of food into useful work (mostly chemical work that makes new material for the living cell) so efficiency (useful work rather than wasted heat) can be maintained. The human machine has two main metabolic fuels: carbohydrate and fat. Human metabolism also has two goals. First, we have to maintain significant energy production, the useful part of which is usually measured by the availability of biological intermediates that can drive life processes. Second, we must maintain more or less constant levels of blood glucose. Some tissues, particularly those that make up the brain and nervous system, require glucose as a fuel, so hypoglycemia (low blood sugar) represents a clear danger. High blood sugar (hyperglycemia) is also not good. Figure 1:The two major fuels for energy: carbohydrate and fat. A critical characteristic of human metabolism is that, with a few exceptions, it cannot make glucose from fat. To meet the goals of maintaining energy and keeping constant blood sugar, metabolism interconverts different compounds and fuels. This allows flexibility in what we eat and how we carry out other life processes. But theres one problem: What happens when theres no food? Our ancestors did not get three squares a day. We all store enough fat to live for weeks or even months, so the first goal of maintaining energy is easily met. The threat in starvation, however, is failing to meet the requirement for constant blood glucose. Unlike fat storage, which can be extensive, we store very little glucose. The bodys rather limited solution to the need for storage is to form a polymer of glucose called glycogen. Glycogen is similar i Continue reading >>
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Buy cheap Elimite online no RX - Trusted online Elimite Home Buy cheap Elimite online no RX - Trusted online Elimite DeSales University. M. Gonzales, MD: "Buy cheap Elimite online no RX - Trusted online Elimite". Most of these are converted by individual pathways to citric acid cycle intermediates cheap elimite online american express acne lesions, then to malate purchase elimite line acne pictures, following the same path from there to glucose purchase 30gm elimite otc acne 8 months postpartum. It is important to note that glucose produced by hepatic gluconeogenesis does not represent an energy source for the liver buy elimite 30 gm with visa skin care manufacturers. Therefore, hepatic gluconeogenesis is always dependent on ~-oxida- tion of fatty acids in the liver. During hypoglycemia, adipose tissue releases these fatty acids by breaking down triglyceride. Although the acetyl-CoA from fatty acids cannot be converted to glucose, it can be converted to ketone bodies as an alternative fuel for cells, including the brain. Chronic hypoglycemia is thus often accompanied physiologically by an increase in ketone bodies. Coordinate Regulation of Pyruvate Carboxylase and Pyruvate Dehydrogenase by Acetyl-CoA The two major mitochondrial enzymes that use pyruvate, pyruvate carboxylase and pyruvate dehydrogenase, are both regulated by acetyl-CoA. The alanine cycle is a slightly different version of the Cori cycle, in which muscle releases alanine, delivering both a gluconeogenic substrate (pyruvate) and an amino group for urea synthesis. In the presence of high glycero13-P, fatty acids are inap- propriately stored in the liver as triglyceride. He quickly consumed a 6-pack of ice-cold beer and shortly thereafter became very weak and light-headed and nearly fainted. Although the ef Continue reading >>
Alanine And Other Compounds Typical Fatty Acids Cannot Be Converted To Glucose | Course Hero
alanine and other compounds Typical fatty acids cannot be converted to glucose Alanine and other compounds typical fatty acids This preview shows page 30 - 41 out of 41 pages. alanine) and other compoundsTypical fatty acids cannot be converted to glucose, although glycerol canDisposal of Excess Amino GroupsConverted to ammonia; then urea cycleUrea excreted in the urine Alcohol Metabolism32ADH Pathway10-30% in stomach and the rest in liverAlcohol converted to acetaldehydeAcetaldehyde converted to acetyl-CoA, producing NADH + H+MEOS Moderate to excessive alcoholUses energy rather than producing energyCatalase Pathway Regulation of Energy Metabolism34LiverNutrient interconversions and storageATP Concentrations regulate metabolismHigh ATP promote anabolic reactionsHigh ADP stimulate catabolic reactionsEnzymes, Hormones, Vitamins and Minerals Fasting and Feasting38Fasting encourages:Glycogen breakdownBody fat and protein breakdownGluconeogenesisKetogenesisUrea synthesisFeasting encourages:Glycogen synthesisBody fat synthesis (lipogenesis)Protein synthesis Inborn Errors of Metabolism40Newborn screeningPhenylketonuria (PKU)Unable to metabolize phenylalanineGalactosemiaUnable to metabolize galactoseGlycogen Storage DiseaseInability to convert glycogen to glucose You've reached the end of your free preview. As a current student on this bumpy collegiate pathway, I stumbled upon Course Hero, where I can find study resources for nearly all my courses, get online help from tutors 24/7, and even share my old projects, papers, and lecture notes with other students. Kiran Temple University Fox School of Business 17, Course Hero Intern I cannot even describe how much Course Hero helped me this summer. Its truly become something I can always rely on and help me. In the end, I was not on Continue reading >>
What Are Ketone Bodies And Why Are They In The Body?
If you eat a calorie-restricted diet for several days, you will increase the breakdown of your fat stores. However, many of your tissues cannot convert these fatty acid products directly into ATP, or cellular energy. In addition, glucose is in limited supply and must be reserved for red blood cells -- which can only use glucose for energy -- and brain tissues, which prefer to use glucose. Therefore, your liver converts many of these fatty acids into ketone bodies, which circulate in the blood and provide a fuel source for your muscles, kidneys and brain. Video of the Day Low fuel levels in your body, such as during an overnight fast or while you are dieting, cause hormones to increase the breakdown of fatty acids from your stored fat tissue. These fatty acids travel to the liver, where enzymes break the fatty acids into ketone bodies. The ketone bodies are released into the bloodstream, where they travel to tissues that have the enzymes to metabolize ketone bodies, such as your muscle, brain, kidney and intestinal cells. The breakdown product of ketone bodies goes through a series of steps to form ATP. Conditions of Ketone Body Utilization Your liver will synthesize more ketone bodies for fuel whenever your blood fatty acid levels are elevated. This will happen in response to situations that promote low blood glucose, such as an overnight fast, prolonged calorie deficit, a high-fat and low-carbohydrate diet, or during prolonged low-intensity exercise. If you eat regular meals and do not typically engage in extremely long exercise sessions, the level of ketone bodies in your blood will be highest after an overnight fast. This level will drop when you eat breakfast and will remain low as long as you eat regular meals with moderate to high carbohydrate content. Ketone Bodi Continue reading >>
Stage Ii Of Lipid Catabolism
Describe the reactions needed to completely oxidize a fatty acid to carbon dioxide and water. Like glucose, the fatty acids released in the digestion of triglycerides and other lipids are broken down in a series of sequential reactions accompanied by the gradual release of usable energy. Some of these reactions are oxidative and require nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD). The enzymes that participate in fatty acid catabolism are located in the mitochondria, along with the enzymes of the citric acid cycle, the electron transport chain, and oxidative phosphorylation. This localization of enzymes in the mitochondria is of the utmost importance because it facilitates efficient utilization of energy stored in fatty acids and other molecules. Fatty acid oxidation is initiated on the outer mitochondrial membrane. There the fatty acids, which like carbohydrates are relatively inert, must first be activated by conversion to an energy-rich fatty acid derivative of coenzyme A called fatty acyl-coenzyme A (CoA). The activation is catalyzed by acyl-CoA synthetase. For each molecule of fatty acid activated, one molecule of coenzyme A and one molecule of adenosine triphosphate (ATP) are used, equaling a net utilization of the two high-energy bonds in one ATP molecule (which is therefore converted to adenosine monophosphate [AMP] rather than adenosine diphosphate [ADP]): The fatty acyl-CoA diffuses to the inner mitochondrial membrane, where it combines with a carrier molecule known as carnitine in a reaction catalyzed by carnitine acyltransferase. The acyl-carnitine derivative is transported into the mitochondrial matrix and converted back to the fatty acyl-CoA. Further oxidation of the fatty acyl-CoA occurs in the mitochondrial matrix via a Continue reading >>
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Volatile Fatty Acid - An Overview | Sciencedirect Topics
Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Propionate, a volatile fatty acid (VFA) produced from microbial carbohydrate digestion in ruminants and other herbivores (see Chapter 54), is a major hepatic gluconeogenic substrate. The percentage of glucose derived from propionate in the liver varies with diet (and species), from a maximum of about 70% under heavy grain feeding in ruminants, to very little during starvation. The importance of propionate as a gluconeogenic substrate is illustrated by the observation that the lactating udder of the goat may utilize 60-85% of glucose produced by the liver for milk production. In contrast to propionate, acetate and butyrate, the other two major VFAs produced through microbial carbohydrate digestion, do not contribute carbon atoms directly to the net synthesis of glucose. Certain glucogenic amino acids (namely isoleucine, valine, threonine, and methionine), the terminal 3 carbons of odd-chain fatty acids undergoing mitochondrial -oxidation, and the -aminoisobutyrate generated from thymine degradation, can also enter hepatic gluconeogenesis at the level of propionyl-CoA. While the former may be quantitatively significant to carnivores, and to all animals during starvation, the latter two are not since: Few odd-chain fatty acids exist in mammalian organisms (with the exception of ruminant animals; see Chapter 54), and Only small amounts of -aminoisobutyrate normally become available to the liver through pyrimidine degradation (see Chapter 17). Entry of propionate into gluconeogenesis (as well as amino acids that are converted to propionyl-CoA), requires pantothenate (a source of coenzyme A.SH), vitamin B12, and biotin (see Fig. 37-1). These vitamins are normally synthesized by micro Continue reading >>
Principles Of Biochemistry/gluconeogenesis And Glycogenesis
Gluconeogenesis (abbreviated GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids. It is one of the two main mechanisms humans and many other animals use 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). Gluconeogenesis is a ubiquitous process, present in plants, animals, fungi, bacteria, and other microorganisms. In animals, gluconeogenesis takes place mainly in the liver and, to a lesser extent, in the cortex of kidneys. This process occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise and is highly endergonic. For example, the pathway leading from phosphoenolpyruvate to glucose-6-phosphate requires 6 molecules of ATP. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type II diabetes, such as metformin, which inhibits glucose formation and stimulates glucose uptake by cells. Lactate is transported back to the liver where it is converted into pyruvate by the Cori cycle using the enzyme lactate dehydrogenase. Pyruvate, the first designated substrate of the gluconeogenic pathway, can then be used to generate glucose. All citric acid cycle intermediates, through conversion to oxaloacetate, amino acids other than lysine or leucine, and glycerol can also function as substrates for gluconeogenesis.Transamination or deamination of amino acids facilitates entering of their carbon skeleton into the cycle directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. Whether fatty acids can be converted into glucose in animals has been a longst Continue reading >>
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Why Can't Fat Produce Glucose?
Tousief Irshad Ahmed Sirwal Author has 77 answers and 106.2k answer views Acetyl CoA is NOT a substrate for gluconeogenesis in animals 1. Pyruvate dehydrogenase reaction is irreversible. So, acetyl CoA cannot be converted back to pyruvate. 2. 2C Acetyl CoA enters the TCA cycle by condensing with 4C oxaloacetate. 2 molecules of CO2 are released & the oxaloacetate is regenerated. There is no NET production of oxaloacetate. Animals cannot convert fat into glucose with minimal exceptions 1. Propionyl CoA derived from odd chain fatty acids are converted to Succinyl CoA Glucogenic 2. Glycerol derived from triglycerides are glucogenic. Answered Mar 26, 2017 Author has 942 answers and 259.1k answer views Yijia Xiong pointed out that the glycerol portion of triglycerides (fats) can indeed be converted to glucose. It is not so energy-inefficient that it is avoided by our bodies. If nutritionally, we are in a gluconeogenesis mode (building up glucose stores rather than consuming them), glycerol would be a perfectly acceptable precursor. However, I think the original question had more to do with the vast bulk of the triglycerides that are not glycerol, but are fatty acids. And it is true that we cant produce glucose from fatty acids. The reason is that the catabolic reactions of fatty acids break off two carbon atoms at a time as Acetyl-CoA. But our metabolic suite of pathways has no way to convert a two-carbon fragment to glucose. The end product of glycolysis is pyruvate, a three-carbon compound. Pyruvate can be back-synthesized into glucose. But the committing reaction for the Krebs cycle is the pyruvate dehydrogenase step, forming acetyl-CoA. That reaction is not reversible. Once pyruvate loses a carbon atom, it cant go back. The three main macronutrients are carbohydrates, pr Continue reading >>
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*Glycogen has a high energy yield per liter of O2 uptake (~5.1 kcal/L O2) *Glycogen can be metabolized both aerobically and anaerobically *Rapid activation of the metabolic pathways for glycogen metabolism *Glycogen concentration can be greatly increased by training and diet *Glycogen can be the sole source of energy during heavy exercise *Glycogen is stored with large amount of H20, thus reducing the caloric value of the storage form (1.1 kcal/g glycogen) *The total amount of glycogen that can be stored is relatively small *Anaerobic use of glycogen results in the accumulation of lactate (and thus pH), which may interfere with a number of cellular processes *Muscle cells are dependent upon their internal glycogen stores; when these stores are depleted, moderately heavy exercise cannot continue Process by which glycogen is broken into glucose-1-phosphate to be used by muscles *Requires 10-12 (depending on where the reaction stops) enzymatic reactions to breakdown glucose and glycogen into ATP *Glycolysis that occurs in glycolytic system is anaerobic *Glucose is a 6 carbon structure (C6H12O6) *Glucose is broken down into two 3-carbon structures called pyruvic acid *The pyruvic acid is then converted to Lactic acid *The breakdown of carbohydrates are the only nutrient whose stored energy can be used to generate ATP anaerobically *The Electron Transport Chain (ETS) is coupled to the Krebs Cycle *The hydrogen ions that are produced from glycolysis and the krebs cycle combine with NAD and FAD, forming NADH and FADH2 What does the forming of NADH and FADH2 in the Electron Transport Chain accomplish? 1) It prevents the build up of H+, thereby limiting acidification of the msucle and blood 2) Carries the H+ ion to the ETS where the H+ is passed through a series of reactions fo Continue reading >>
C2006/f2402 '11 Outline Of Lecture #16
Handouts: 15A -- Lining of the GI Tract & Typical Circuit 15B -- Homeostasis -- Seesaw view for Glucose and Temperature Regulation; 16 -- Absorptive vs Postabsorptive state I. Homeostasis, cont. See handouts 15A & B & notes of last time, topic VI. A. Regulation of Blood Glucose Levels -- Seesaw View #1 (Handout 15B) B. Regulation of Human Body Temperature -- Seesaw #2 (Handout 15B) C. The Circuit View (Handout 15A) II. Matching circuits and signaling -- an example: How the glucose circuit works at molecular/signaling level Re-consider the circuit or seesaw diagram for homeostatic control of blood glucose levels -- what happens in the boxes on 15A? It may help to refer to the table below. A. How do Effectors Take Up Glucose? 1. Major Effectors: Liver, skeletal muscle, adipose tissue 2. Overall: In response to insulin, effectors increase both uptake & utilization of glucose. Insulin triggers one or more of the following in the effectors: a. Causes direct increase of glucose uptake by membrane transporters b. Increases breakdown of glucose to provide energy c. Increases conversion of glucose to 'stores' (1). Glucose is converted to storage forms (fat, glycogen), AND (2). Breakdown of storage fuel molecules (stores) is inhibited. d. Causes indirect increase of glucose uptake by increasing phosphorylation of glucose to G-P, trapping it inside cells 3. How does Insulin Work? a. Receptor: (1). Insulin works through a special type of cell surface receptor, a tyrosine kinase linked receptor; See Sadava fig. 7.7 (15.6). Insulin has many affects on cells and the mechanism of signal transduction is complex (activating multiple pathways). (2). In many ways, insulin acts more like a typical growth factor than like a typical endocrine. (Insulin has GF-like effects on other cells; is i Continue reading >>
Typical Fatty Acids Cannot Be Converted To Glucose Because
Typical fatty acids cannot be converted to glucose because Typical fatty acids cannot be converted to glucose because mariculture refers to the cultivation of marine organisms in seawater, usually in sheltered coastal or offshore waters. the farming of marine fish is an example of mariculture, and also is the farming of marine crustaceans (such as shrimp), molluscs (such as oysters), and seaweed. seawater ponds (prawns; fish; eels; crayfish) in seawater ponds, marine species are grown in ponds which get water from the sea. this has the benefit that plankton present in the seawater can be used as a food source. tank farming (prawn brood stock tanks; prawn culture tanks; barramundi) some species grow well in tanks which are aerated and have a continuous exchange of water to keep the dissolved oxygen levels high and remove wastes. algaculture is the type of aquaculture that cultivates algae. most algae harvested is either microalgae (phytoplankton, microphytes or planktonic algae) or macroalgae (seaweed) which can be hard to grow. microalgae are easier to harvest on a large scale. sea cage farming (salmon; tuna; snapper; mulloway; barramundi) at the age of one young salmon are transferred to cages in the sea. the salmon are fed an artificial diet, specially prepared to maximise growth. adults are harvested after two years wwighing approximately 3 to 4 kg. long line farming (pearl oysters, mussels) this method is used for offshore culture. it uses a series of styrofoam floats arranged in a row. the long-line is secured at each end with two anchors. one long-line is 100 m long and consists of about 51 floats connected by a polyurethane rope 15 mm in diameter. raceway farming (abalone; oysters; algae; barramundi) raceways are usually large concrete tanks, generally 30 m long Continue reading >>
Ann L. Albright and Judith S. Stern Department of Nutrition and Internal Medicine University of California at Davis Davis, CA USA Morphology and Development of Adipose TissueAdipose-Tissue MetabolismAdipose Tissue DistributionDefinition and Causes of ObesityFurther Reading Albright, A.L. and Stern, J.S. (1998). Adipose tissue. In: Encyclopedia of Sports Medicine and Science, T.D.Fahey (Editor). Internet Society for Sport Science: 30 May 1998. Adipose tissue is specialized connective tissue that functions as the major storage site for fat in the form of triglycerides. Adipose tissue is found in mammals in two different forms: white adipose tissue and brown adipose tissue. The presence, amount, and distribution of each varies depending upon the species. Most adipose tissue is white, the focus of this review. White adipose tissue serves three functions: heat insulation, mechanical cushion, and most importantly, a source of energy. Subcutaneous adipose tissue, found directly below the skin, is an especially important heat insulator in the body, because it conducts heat only one third as readily as other tissues. The degree of insulation is dependent upon the thickness of this fat layer. For example, a person with a 2-mm layer of subcutaneous fat will feel as comfortable at 15°C as a person with a 1-mm layer at 16°C. Adipose tissue also surrounds internal organs and provides some protection for these organs from jarring. As the major form of energy storage, fat provides a buffer for energy imbalances when energy intake is not equal to energy output. It is an efficient way to store excess energy, because it is stored with very little water. Consequently, more energy can be derived per gram of fat (9 kcal.gm-1) than per gram of carbohydrate (4 kcal.gm-1) or protein (4 kcal.g Continue reading >>
In Silico Evidence For Gluconeogenesis From Fatty Acids In Humans
In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans Affiliation Department of Bioinformatics, School of Biology and Pharmaceutics, Friedrich Schiller University of Jena, Jena, Germany Affiliation Department of Bioinformatics, School of Biology and Pharmaceutics, Friedrich Schiller University of Jena, Jena, Germany Affiliation Department of Bioinformatics, School of Biology and Pharmaceutics, Friedrich Schiller University of Jena, Jena, Germany Affiliation Systems Biology/Bioinformatics Group, Leibniz Institute for Natural Product Research and Infection Biology Hans Knll Institute, Jena, Germany Affiliations Department of Human Nutrition, Institute of Nutrition, University of Jena, Jena, Germany, Department of Clinical Nutrition, German Institute of Human Nutrition, Potsdam-Rehbrcke, Nuthetal, Germany Affiliation Department of Bioinformatics, School of Biology and Pharmaceutics, Friedrich Schiller University of Jena, Jena, Germany In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans The question whether fatty acids can be converted into glucose in humans has a long standing tradition in biochemistry, and the expected answer is No. Using recent advances in Systems Biology in the form of large-scale metabolic reconstructions, we reassessed this question by performing a global investigation of a genome-scale human metabolic network, which had been reconstructed on the basis of experimental results. By elementary flux pattern analysis, we found numerous pathways on which gluconeogenesis from fatty acids is feasible in humans. On these pathways, four moles of acetyl-CoA are converted into one mole of glucose and two moles of CO2. Analyzing the detected pathways in detail we found that their energetic requirements potentially limit their capacity. T Continue reading >>