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Ketones Are Produced From Quizlet

Bcii: Ketone Bodies

Bcii: Ketone Bodies

Sort The major site of formation of acetoacetate from fatty acids is the: a. adipose tissue. b. intestinal mucosa. c. kidney. d. liver. e. muscle. d. liver. Ketone bodies are formed in the liver and transported to the extrahepatic tissues mainly as: a. acetoacetyl-CoA. b. acetone. c. beta-hydroxybutyric acid. d. beta-hydroxybutyryl-CoA. e. lactic acid. b. acetone. Continue reading >>

Ketone Body Synthesis

Ketone Body Synthesis

Sort 1. Ketone body synthesis: Ketone bodies are x forms of lipid-based energy and consist mainly of x acid and its reduction product, x acid. β-hydroxybutyryl CoA and acetoacetyl CoA are x near the end of the β-oxidation scheme. x in an intermediate in the synthesis of acetoacetate from Acetyl CoA The primary site for formation of ketone bodies is x, with lesser activity in x. The entire process occurs within the x, beginning with condensation of two acetyl CoA molecules to make acetoacetyl CoA, as catalyzed by xase. Acetoacetyl CoA then condenses with another acetyl CoA to form β- hydroxymethylglutaryl coenzyme A (aka x). Cleavage of HMG CoA by HMG CoA xase yields acetoacetic acid and acetyl CoA. 1. Ketone body synthesis: Ketone bodies are water soluble forms of lipid-based energy and consist mainly of acetoacetic acid and its reduction product, β-hydroxybutyric acid. β-hydroxybutyryl CoA and acetoacetyl CoA are intermediates near the end of the β-oxidation scheme. HMG-CoA in an intermediate in the synthesis of acetoacetate from Acetyl CoA The primary site for formation of ketone bodies is liver, with lesser activity in kidney. The entire process occurs within the mitochondrial matrix, beginning with condensation of two acetyl CoA molecules to make acetoacetyl CoA, as catalyzed by β-ketothiolase. Acetoacetyl CoA then condenses with another acetyl CoA to form β- hydroxymethylglutaryl coenzyme A (aka HMG CoA). Cleavage of HMG CoA by HMG CoA Lyase yields acetoacetic acid and acetyl CoA. Acetoacetate Forms both D-β-Hydroxybutyrate and acetone In mitochondria a fraction of acetoacetate is reduced to D-β-hydroxybutyrate depending on the intramitochondrial x ratio. Some acetoacetate continually undergoes slow spontaneous nonx decarboxylation to acetone. In these pa Continue reading >>

Biochemistry

Biochemistry

Sort what is the regulation of the citric acid cycle The citric acid cycle is regulated mostly by substrate availability, product inhibition and by some cycle intermediates. • pyruvate dehydrogenase: is inhibited by its products, acetyl-CoA and NADH • citrate synthase: is inhibited by its product, citrate. It is also inhibited by NADH and succinyl-CoA (which signal the abundance of citric acid cycle intermediates). • isocitrate dehydrogenase and a-ketoglutarate dehydrogenase: like citrate synthase, these are inhibited by NADH and succinyl-CoA. Isocitrate dehydrogenase is also inhibited by ATP and stimulated by ADP. All aforementioned dehydrogenases are stimulated by Ca2+. This makes sense in the muscle, since Ca2+ release from the sarcoplasmic reticulum triggers muscle contraction, which requires a lot of energy. This way, the same "second messenger" activates an energy-demanding task and the means to produce that energy. What is the regulation of fatty acid metabolism Acyl-CoA movement into the mitochondrion is a crucial factor in regulation. Malonyl-CoA (which is present in the cytoplasm in high amounts when metabolic fuels are abundant) inhibits carnitine acyltransferase, thereby preventing acyl-CoA from entering the mitochondrion. Furthermore, 3-hydroxyacyl-CoA dehydrogenase is inhibited by NADH and thiolase is inhibited by acetyl-CoA, so that fatty acids wil not be oxidized when there are plenty of energy-yielding substrates in the cell. Explain in overview the metabolic reactions in the body that lead to the formation of ketone bodies (Ketogenesis). Ketogenesis is the process by which ketone bodies are produced as a result of fatty acid breakdown. Ketone bodies are produced mainly in the mitochondria of liver cells, and synthesis can occur in response to una Continue reading >>

Ketone Production Is The Result Of:

Ketone Production Is The Result Of:

Skip to content Learn vocabulary, terms, and more with flashcards, games, and other study tools. A ketone test can warn you of a serious diabetes complication called diabetic ketoacidosis (DKA). OBJECTIVE Insulin resistance is associated with mitochondrial dysfunction and decreased ATP synthesis. Standards Cyclohexanone, Benzophenone, and Benzaldehyde. Start studying Ketone Bodies. as surgery or a heart attack may result in ketone production. Diabetic Ketone Acidosis Herbal Remedies For Diabetic Wounds ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. ... dangerous and life-threatening levels of ketones can develop. Pruvit is a trusted health and wellness company with highly known ketone supplements and nutritional products. Ketosis is the physiological state where the concentration of ketone bodies in the blood is higher than normal. Ketostix and diabetes. In newborn infants, ketone production is activated by the high-fat content of milk. Ketone production is the result of quizlet. There are some health benefits to ketone bodies and ketogenesis as well. ... to determine if enough insulin is being given to turn off ketone production. 2,4-DNP Test for Aldehydes and Ketones. If you are looking for an amazing ketone supplement at an unbeatable price ... its ability to efficiently optimize ketone production. Check the result, which will display on the meter; This ketone product is whats referred to as an exogenous ketone. Ketone supplementation ... ketone production The term ketone bodies describes 3 molecules: acetoacetate, -hydroxybutyrate, and acetone. acidosis (pH 7.1) ... but rather to ketone body production 5. An Inconvenient Truth About Ketone Levels. ... Ketone production is the result of lipolysis (the breakdown of fat)not a direct caus Continue reading >>

Multiple Choice Questions- Lipid Metabolism (revision)- Set-2

Multiple Choice Questions- Lipid Metabolism (revision)- Set-2

1. Which of the following are the ketone bodies? a) Acetyl co A and Propionyl co A b) Lecithin and Lysolecithin c) Acetoacetate and Betahydroxy butyrate d) Pyruvate and lactate e) Succinyl co A and succinate 2. The enzyme ‘Thiolase’ catalyzes the conversion of- a) 2 Acetyl co A to Acetoacetyl co A b) Acetyl co A to Malonyl co A c) Fatty acid to Fatty Acyl co A d) Succinyl co A to succinate e) Propionyl co A to D- Methyl malonyl co A 3. In contrast to secondary bile salts, which of the following is characteristic of primary bile salts? a) Are hydroxylated at carbon 7 b) Have an oxidized side chain c) Form co A derivatives d) Can be conjugated to Glycine or Taurine e) Are reabsorbed in the intestine 4. Which of the following statements best describes the fatty acid synthase complex? a) Is a dimer of dissimilar subunits b) is composed of 7 different proteins c) Dissociates in to eight different proteins d) Catalyzes 8 different enzymatic steps e) Is composed of covalently linked enzymes 5. The end product of fatty acid synthesis in mammals is – a) Arachidonic acid b) Linoleic acid c) Stearic acid d) Palmitic acid e) Erucic acid 6. Which enzyme often mal functions in diseases associated with the symptoms of high blood triglyceride levels and Steatorrhea? a) Phospholipase D b) Lipoprotein lipase c) Thiokinase d) Acetyl co A carboxylase e) Pancreatic lipase 7. Which enzyme is an allosteric regulator of another enzyme on the list ? a) Acetyl co A carboxylase b) Pancreatic lipase c) Carnitine acyl transferase-1 d) Acetyl transacylase e) Keto acyl synthase 8. A new-born has severe respiratory problems. Over the next few days it is observed that the baby has severe muscle problems, demonstrates little development, and has neurological problems. A liver biopsy reveals a very Continue reading >>

Ketone Body Metabolism

Ketone Body Metabolism

Sort Scenario: Blood glucose levels decline due to starvation... Require: Tactic changes: Hormonal changes: Metabolic changes: Require: maintenance of blood glucose levels Tactic changes: - peripheral tissue glucose utilization + hepatic glucose production (gluconeogenesis) Hormonal changes: - insulin + glucagon + epinephrine and lipolytic hormones Metabolic changes: + lipolysis and ketogenesis for alternative fuels + hepatic beta oxidation to drive gluconeogenesis What substrates are required for gluconeogenesis to occur and how are these substrates replenished? Gluconeogenesis requires (1) C4 carbon sources and (2) high energy. -Carbon sources are replenished by glucogenic AA breakdown -Energy is replenished via beta oxidation of FA and oxidative phosphorylation -Acetyl CoA (produced by beta oxidation) promotes gluconeogenesis by activating pyruvate carboxylase (hormone required for gluconeogenesis) Continue reading >>

Multiple Choice Quiz

Multiple Choice Quiz

Please answer all questions A) pathways of chemical reactions that build compounds. C) the entire network of chemical processes involved in maintaining life and encompasses all of the sequences of chemical reactions that occur in the body. D) the process of photosynthesis. 4 As an antioxidant vitamin E or C can donate electrons to highly reactive compounds. These antioxidants then become 5 In metabolism, glucose is degraded to carbon dioxide and water. The carbon dioxide is produced in: 12 The action of the cytochromes in donating all the electrons that have moved down the chain to oxygen could be described as a C) fatty acids become many acetyl-CoA molecules. A) Fats must be broken down to glycerol and fatty acids before oxidation can occur. B) Fatty acids are oxidized stepwise into 2-carbon fragments. C) 2-carbon fragments of fatty acids enter the citric acid cycle to be oxidized. D) 2-carbon fragments from fatty acids can be used to synthesize glucose. A) Deficiencies of thiamin, riboflavin, and niacin may slow energy metabolism. B) The citric acid cycle begins when acetyl-CoA combines with citric acid to form oxaloacetic acid. C) Hydrogens released via the citric acid cycle are transported to the electron transport chain. D) In the electron transport system hydrogen reacts with oxygen and some of the energy is trapped as ATP. A) Glucose provides many more calories than fat on a per gram basis B) To maintain glycolysis it is necessary that fats provide the beginning fuel C) The entire pathway for fatty acid oxidation works best when carbohydrate is present. D) Carbohydrates provide all the ATP the cells need as long as fats provide the spark to start the whole process. A) removal of a protein from another protein molecule. C) removal of a carbon skeleton from a carbo Continue reading >>

Nutrition Ch. 7

Nutrition Ch. 7

Front Back .Wirisformula{ margin:0 !important; padding:0 !important; vertical-align:top !important;} Metabolism The sum total of all the chemcial reactions that go on in living cells. Energy metabolism includes all the reactions by which the body obtains and spends energy from food. Example: Nutrients provide the body with FUEL and follows them through a series of reactions that release energy from their chemical bonds. As the bonds break, they release energy in a controlled version of the process by which wood burns in a fire. Energy metabolism All of the chemical reactions through which the human body acquires and spends energy from food Anabolism Small compounds joined together to make largers ones; energy must be used in order to do this Ana = up Catabolism Larger compounds BROKEN down into smaller ones; energy is RELEASED kata = down Coupled reactions Energy released from the breakdown of a large compounds is used to drive other reactions ATP Adenosine triphosphate; energy currency of the body -- produced when large compounds are broken down ATP is used to make large compounds from smaller ones. Ribosomes Cellular machinery used to make proteins Mitochondria Where energy is derived from fat, CHO, protein via TCA cycle, electron transport chain Coenzyme Complex organic molecules that work with enzymes to facilitate the enzymes' activity. Many coenzymes have B vitamins as part of their structures. co = with Cofactor The general term for substances that facilitate enzyme action is cofactors; they include both organic coenzymes such as vitamins and inorganic substances such as minerals Enzymes Protein catalysts - proteins that facilitate chemical reactions without being changed in the process Metalloenzyme Enzymes that contain one or more minerals as part of their stru Continue reading >>

Ketone Bodies

Ketone Bodies

Sort Ketone Bodies -->Represent 3 molecules that are formed when excess acetyl CoA cannot enter the TCA Cycle -->Represents 3 major molecules: 1)Acetoacetate 2)β-Hydroxybutyrate 3)Acetone -->Normal people produces ketones at a low rate -->Are only formed in the **LIVER**(by liver mitochondria) Reactions that lead to the formation of ketone bodies (***See pwrpt***) 1)2 Acetyl CoA molecules condense to form ***Acetoacetyl-CoA -->Is catalyzed by THIOLASE -->Represent the oppostie of thiolysis step in the oxidation of fatty acids -->Represent the parent compound of the 3 ketone bodies (2)Acetoacetyl CoA then reacts with another mol. of acetyl CoA to form **HMG-CoA* (3-hydroxy-3-methylglutaryl CoA) & *CoA** -->Reaction is catalyzed by **HMG-CoA Synthetase** -->HMG-CoA has 2 fates (can either progress to form ketone bodies OR can enter the pathway of CHOLESTEROL synthesis) -->Represent the **RATE-LIMITING STEP** in the synthesis of ketone bodies (3)HMG-CoA is cleaved to form **Acetoacetate**(First major ketone; represent ~20% of ketones) & another mol. of acetyl CoA -->Catalyzed by **HMG-CoA Lyase** (4) Acetoacetae can lead to the formation of β-hydroxybutyrate (~78% of ketone bodies) & Acetone (~2% of ketone bodies) via 2 separte reactions Interrelationships of the ketone bodies from Acetoacetate (1)Formation of β-hydroxybutyrate -->Acetoacetate will be reduced to form β-hyroxybutyrate in the mitochondrial matrix of the liver cell -->Is a REVERSIBLE RXN. -->Requires 1 mol of NADH (***Dependent on the NADH/NAD ratio inside the mitochondria) -->Catalyzed by β-hydroxybutyrate dehydrogenase (2)Formation of Acetone -->A slower, **spontaneous** decarboxylation to acetone -->In **DIABETIC KETOACIDOSIS, acetone imparts a characteristic smell to the patient's breath Features of Continue reading >>

Exam 3 Quizlet - Which Of The Following Is The Major...

Exam 3 Quizlet - Which Of The Following Is The Major...

Unformatted text preview: Which of the following is the major regulation point for transport of fatty acids into the mitochondria? carnitine acyltransferase I ?? The primary activation of triacylglycerol mobilization in adipocytes is through __________ of the enzyme ____________. phosphorylation; hormone sensitive lipase ?? Which of the following lipoproteins distributes dietary lipids? chylomicron ?? Which of the following statements regarding lipid digestion and absorption is true? The products of lipid digestion are resynthesized into triacylglycerols in intestinal epithelial cells. ?? The emulsification of fats: A. results in the formation of small fat droplets. B. depends upon the amphipathic structure of bile salts. C. results in the formation of micelles. A, B and C. results in the formation of small fat droplets. depends upon the amphipathic structure of bile salts. results in the formation of micelles. ?? In animals, the bulk of energy is stored as __________. triacylglycerols ?? Under fasting conditions, elevated glucagon will activate: hormone sensitive lipase ?? VLDL characteristic of which aproprotein: Apo B 100 ?? Which sphingolipid is a precursor for all other types of sphingolipids? Ceramide. ?? Which of the following is the regulated step of fatty acid synthesis in eukaryotes? Carboxylation of acetyl CoA. ?? The first step in fatty acid synthesis is the formation of ________ from acetyl CoA and carbon dioxide. malonyl CoA ?? The role of biotin in fatty acid biosynthesis is in ____________. malonyl CoA formation. ?? In chylomicro assembly which Apo protein is transferred from HDL? Apo CII ?? Regulation of acetylCoA carboxylase takes place on several levels. When glucose is low: Citrate levels are low ?? When the liver converts excess glucose into fatty a Continue reading >>

Nutrition Chapter 7

Nutrition Chapter 7

Sort Feasting eating in excess of energy needs metabolism favors fat formation - dietary fat to body fat is most direct and efficient conversion (carbohydrate and protein have other roles to fulfill before) fuel mix - depends on diet; carbohydrate and protein intakes influence fuel mix; increases in carbohydrate and protein intakes DISPLACE fat in the diet (more carbohydrate/protein and less fat) increase fat eaten DOES NOT enhance fat breakdown - does not respond to dietary fat intake! Transition from Feasting to Fasting after a meal (2-3 hours), glucose, glycerol, fatty acids used as needed, stored - fasting state draws on these stores (glycogen and fat are released/broken down) energy needed all the time! (sleeping) basal metabolism - cell's work to maintain life processes; 2/3 energy a person expends per day fasting (choice) vs. starving (no choice) - body cannot distinguish difference between them, forced to draw on reserves of carbohydrate and fat Fasting carbohydrate, fat, protein all eventually used as energy begins with release of glucose from liver's glycogen stores, fatty acids from adipose cells breakdown and acetyl CoA produced - Krebs cycle to produce energy (ATP) decrease blood glucose levels serve as signal - promotes further fat breakdown; release of amino acids from muscles Fatty Acids as Fuel good for now, but glucose is needed brain, nervous system, and RBC - primary source brain/nerve cells consume 1/2 total glucose used/day (50%) 1/4 of energy body uses at rest spent by brain RBC completely dependent on glucose, brain/nerve cells prefer glucose for energy Protein to the Rescue amino acids yielding pyruvate (to make glucose); breakdown of body proteins; amino acids that canoot make glucose used for energy by other cells; expensive way to make glucos Continue reading >>

Ketone Bodies

Ketone Bodies

Ketone bodies Acetone Acetoacetic acid (R)-beta-Hydroxybutyric acid Ketone bodies are three water-soluble molecules (acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone) that are produced by the liver from fatty acids[1] during periods of low food intake (fasting), carbohydrate restrictive diets, starvation, prolonged intense exercise,[2], alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus. These ketone bodies are readily picked up by the extra-hepatic tissues, and converted into acetyl-CoA which then enters the citric acid cycle and is oxidized in the mitochondria for energy.[3] In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids. Ketone bodies are produced by the liver under the circumstances listed above (i.e. fasting, starving, low carbohydrate diets, prolonged exercise and untreated type 1 diabetes mellitus) as a result of intense gluconeogenesis, which is the production of glucose from non-carbohydrate sources (not including fatty acids).[1] They are therefore always released into the blood by the liver together with newly produced glucose, after the liver glycogen stores have been depleted (these glycogen stores are depleted after only 24 hours of fasting)[1]. When two acetyl-CoA molecules lose their -CoAs, (or Co-enzyme A groups) they can form a (covalent) dimer called acetoacetate. Beta-hydroxybutyrate is a reduced form of acetoacetate, in which the ketone group is converted into an alcohol (or hydroxyl) group (see illustration on the right). Both are 4-carbon molecules, that can readily be converted back into acetyl-CoA by most tissues of the body, with the notable exception of the liver. Acetone is the decarboxylated form of acetoacetate which cannot be converted Continue reading >>

Ketogenesis

Ketogenesis

Ketogenesis pathway. The three ketone bodies (acetoacetate, acetone, and beta-hydroxy-butyrate) are marked within an orange box Ketogenesis is the biochemical process by which organisms produce a group of substances collectively known as ketone bodies by the breakdown of fatty acids and ketogenic amino acids.[1][2] This process supplies energy to certain organs (particularly the brain) under circumstances such as fasting, but insufficient ketogenesis can cause hypoglycemia and excessive production of ketone bodies leads to a dangerous state known as ketoacidosis.[3] Production[edit] Ketone bodies are produced mainly in the mitochondria of liver cells, and synthesis can occur in response to an unavailability of blood glucose, such as during fasting.[3] Other cells are capable of carrying out ketogenesis, but they are not as effective at doing so.[4] Ketogenesis occurs constantly in a healthy individual.[5] Ketogenesis takes place in the setting of low glucose levels in the blood, after exhaustion of other cellular carbohydrate stores, such as glycogen.[citation needed] It can also take place when there is insufficient insulin (e.g. in type 1 (but not 2) diabetes), particularly during periods of "ketogenic stress" such as intercurrent illness.[3] The production of ketone bodies is then initiated to make available energy that is stored as fatty acids. Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle; i.e. if activity in TCA cycle is low due to low amo Continue reading >>

Fatty Acid Oxidation, Ketone Body Production

Fatty Acid Oxidation, Ketone Body Production

Sort Draw a simple diagram linking glycolysis, the TCA cycle, triglyceride breakdown and triglyceride synthesis as seen in the liver. Include some of the major substrates, intermediates, and products such as glycerol, DHAP, fatty acyl CoA, malonyl CoA and acetyl CoA. (be able to do this...) Outline the 4 steps involved in the synthesis of triglycerides from glycerol-3-phosphate and activated fatty acids. 1 fatty acid, linked to Acetyl-CoA, is added to glycerol-3-phosphate via an acyltransferase enzyme. The product here is a glycerol backbone with one R group attached (lysophosphatidic acid). Another fatty acid is added to lysophophatidic acid via a different acyltransferase enzyme, creating a molecule with a glycerol backbone and two fatty acids (phosphatidic acid). The phosphate group remaining on the final carbon of the glycerol backbone is removed by a phosphatase enzyme (making diacylglycerol), in order for... The third and final fatty acid to be added by a third acyltransferase enzyme, creating the end triacylglycerol product. Describe how fatty acids are mobilized from adipose tissue. Triacylglycerols are stored in adipocytes (fat storage cells). When fatty acids are needed by the body for energy, hormones (including epinephrine) are produced and bind to their appropriate receptors. This leads to the adenylate cyclase enzyme catalyzing the production of cAMP from ATP. A cAMP-dependent protein kinase then has the effect of activating hormone-sensitive lipase via phosphorylation. Now, this lipase is able to cleave one fatty acid from the triacylglycerol. Further removal of fatty acids is able to occur through the action of diacylglycerol- and monoacylglycerol-specific enzymes. Outline the pathway for activation and transport of the fatty acids to the mitochondrion f Continue reading >>

Oxidation Of Fatty Acids And Ketone Bodies

Oxidation Of Fatty Acids And Ketone Bodies

Sort What is different about Beta oxidation of FA with double bonds? 1. Additional enzymes are required for oxidation of unsaturated fatty acids. 2. In a β-oxidation cycle involving a double bond, only three ATPs are produced. 3. To calculate ATP production for oxidation of an unsaturated fatty acid, subtract 2 ATP for each double bond. 9 acetyl-CoA= 9x12= 108 ATP 8 cycle 5x8= 40 148 2 double bond -2x2= -4 Total =144 ATP (no need to subtract 2 ATP for activation) How are VLCFA oxidized? VLCFAs (some LCFAs) are oxidized in peroxisomes by reactions similar to mitochondrial β-oxidation. However, peroxisomes do not have electron transport chain and oxidative phosphorylation, thus peroxisomal fatty acid oxidation does not produce ATP. VLCFAs are shortened to short- and median-chain fatty acid CoAs, which are converted to What are the symptoms of classical CPTII deficiency? -Most common of carnitine metabilosm Symptoms: -adolescent-adult onset -recurrent acute myoglobinuria precipitated by prolonged exercise or fasting -weak -hypoglycemic -hypoketosis -lipid deposits in skeletal muscle -Creratine phosphokinase (CPK) and long chain acycarnitines are elevated in the blood If infantile: -CPT ,10% normal -hypoglycemia -severe hypoketosis -hepatomegaly -cardiomyopathy Continue reading >>

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