Fatty acid oxidation
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1. Fatty acid oxidation and synthesis involve complex multi-step pathways that occur in the cytoplasm and mitochondria. 2. Fatty acid oxidation via beta-oxidation breaks down fatty acids into acetyl-CoA units, requiring activation, transport into mitochondria, and four reaction cycles. 3. Fatty acid synthesis occurs primarily in the liver and involves production of acetyl-CoA and NADPH, conversion to malonyl-CoA, and fatty acid complex reactions to build palmitic acid from two-carbon units.
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The document describes lipid metabolism, including the digestion and absorption of lipids in the small intestine. Dietary lipids are emulsified by bile salts and broken down by pancreatic enzymes. The products of lipid digestion form micelles that enable absorption into the bloodstream. Once absorbed, fatty acids can be stored as triglycerides or undergo beta-oxidation to generate energy. Beta-oxidation involves activating fatty acids to acyl-CoA derivatives and transporting them into mitochondria, where they are broken down through repeated cycles to acetyl-CoA units.
Beta oxidation
The document discusses beta oxidation of fatty acids and its regulation. It covers:
1. The four steps of beta oxidation which occur in the mitochondria, involving oxidation, hydration, dehydrogenation, and thiolytic cleavage.
2. The role of carnitine in transporting fatty acids into the mitochondria for beta oxidation since fatty acids cannot pass through the mitochondrial membrane on their own.
3. Diseases related to defects in fatty acid oxidation pathways like Refsum disease and Zellweger syndrome.
Fatty acid synthesis:- Everything you need to know
Fatty acid synthesis occurs through a repeated cycle of condensation, reduction, dehydration, and reduction reactions. Acetyl-CoA is carboxylated to malonyl-CoA by the enzyme acetyl-CoA carboxylase, providing the two-carbon building blocks. The fatty acid synthase complex catalyzes the cycle of reactions, with the growing fatty acid chain attached to an acyl carrier protein. Typically 16 cycles produce palmitate, which is then released from the complex. Key cofactors include NADPH, ATP, biotin, and bicarbonate. Fatty acid synthesis takes place in the cytoplasm of tissues like liver, adipose, and lactating mammary
The de novo synthesis of fatty acid
The document summarizes the de novo synthesis of the fatty acid palmitic acid. It occurs in the cytosol using acetyl-CoA as a precursor. There are multiple steps: (1) acetyl-CoA and NADPH are produced, (2) acetyl-CoA is transported from mitochondria to cytosol by conversion to citrate, (3) citrate is degraded back to acetyl-CoA in the cytosol, (4) acetyl-CoA is carboxylated to malonyl-CoA by acetyl-CoA carboxylase, (5) the fatty acid synthase complex catalyzes repeated reactions using malonyl-CoA to eventually form the 16-carbon
Metabolismoflipids part 2
Fatty acids are synthesized in the liver and adipose tissue through three main stages: transport of acetyl-CoA into the cytosol, carboxylation of acetyl-CoA, and assembly of the fatty acid chain. Acetyl-CoA is converted to malonyl-CoA by acetyl-CoA carboxylase, then fatty acid chains are elongated through cycles of condensation, reduction, dehydration, and reduction using malonyl-ACP as the donor of additional two carbon units. When a 16-carbon palmitate chain is complete, it is released from the fatty acid synthase complex. Triacylglycerols and phospholipids are then synthesized from glycerol-
Beta oxidation & protein catabolism
1. Fatty acids from dietary triglycerides and adipose tissue are broken down through beta-oxidation in the mitochondria to produce acetyl-CoA, which feeds into the Krebs cycle.
2. Triglycerides must be emulsified to be digested and transported via chylomicrons in the bloodstream for use or storage.
3. Amino acids are broken down through transamination and the urea cycle to remove nitrogenous waste, while their carbon skeletons can be used for energy or biosynthesis as either glucogenic or ketogenic intermediates.
The_citric_acid_cycle[1].pdf
The citric acid cycle is the final stage of breaking down nutrients and occurs in the mitochondria. It uses acetyl-CoA molecules to produce carbon dioxide, hydrogen atoms, and ATP through a set of 8 enzyme-catalyzed reactions. First, pyruvate is converted to acetyl-CoA, which then feeds into the citric acid cycle to be oxidized and generate energy. The cycle is regulated by the energy levels of the cell and produces precursors for biosynthesis.
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Biochemistry_II_Ch._22_Fatty_Acid_Metabolism_Spring_2011.ppt
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De Novo Synthesis of fatty acids | Biosynthesis Of Fatty Acids |
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Fatty acid synthesis:- Everything you need to know
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Phospholipids
This document discusses lipids and phospholipids. It explains that lipids are insoluble in water and composed of fatty acids and glycerol. Phospholipids are produced when a phosphate group replaces a fatty acid in a triglyceride. Phospholipids form bilayers with hydrophilic heads facing out and hydrophobic tails packed inside. The document outlines the synthesis and degradation pathways of various phospholipids and their roles in cell membranes and signaling. Prostaglandins are also derived from arachidonic acid and mediate inflammatory responses.
Ketogenesis
During starvation and diabetes mellitus, acetyl-CoA from fatty acid oxidation takes an alternative route of forming ketone bodies in the liver mitochondria. This occurs via a multi-step process involving condensation, HMG-CoA production, lysis, reduction, and spontaneous decarboxylation. Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are utilized by extrahepatic tissues as fuel when glucose is unavailable. High glucagon and low insulin levels promote ketogenesis.
Metabolism of ketone bodies
This document discusses metabolism of ketone bodies during times of starvation and diabetes mellitus. It explains that when carbohydrates are unavailable, fatty acids are broken down to produce acetyl-CoA, which is then converted to ketone bodies - acetone, acetoacetate, and beta-hydroxybutyrate in the liver. These ketone bodies provide an alternative energy source for tissues like the brain. The document outlines the biochemical pathway and regulation of ketone body production.
Glycolysis
This document discusses glucose transporters, glycolysis, and the regulation of glycolysis. It provides the following key points:
- Glucose transporters facilitate the transport of glucose across plasma membranes into cells, as glucose cannot passively diffuse through the membrane.
- Glycolysis breaks down glucose to form pyruvate and produces 2 ATP molecules. Pyruvate can then be used for aerobic or anaerobic respiration to yield more energy.
- Three enzymes (hexokinase, phosphofructokinase, and pyruvate kinase) regulating the irreversible steps control glycolysis. Insulin promotes glycolysis while glucagon promotes gluconeogenesis.
Glycogen metabolism and it’s regulation
Glycogen is stored in the liver and muscles as a fuel reserve that can be easily mobilized to generate energy in the absence of oxygen. Glycogenesis is the process of glycogen synthesis from glucose, requiring enzymes like glycogen synthase. Glycogenolysis is the degradation of stored glycogen into glucose-6-phosphate and glucose by glycogen phosphorylase. The activities of glycogen synthase and phosphorylase are regulated by allosteric effectors and hormones like glucagon, epinephrine, and insulin to balance glycogen synthesis and breakdown. Genetic defects in glycogen metabolism can cause glycogen storage diseases.
Disorders of carbohydrate metabolism
This document discusses lactose intolerance, including its causes, symptoms, and diagnosis. Lactose intolerance is caused by a deficiency of the enzyme lactase, which breaks down lactose in the small intestine. Undigested lactose passes to the colon, where bacteria ferment it causing symptoms like bloating, diarrhea and nausea. The H2 breath test is an accurate way to diagnose lactose intolerance by measuring increased hydrogen levels in breath after ingesting lactose. Management involves taking lactase supplements, using lactose-reduced products, or limiting dairy.
Cholesterol & atherosclerosis
Cholesterol is a lipid that is essential for cell membrane structure and hormone production. It is synthesized through a metabolic pathway and regulated at the rate-limiting step by HMG-CoA reductase. High cholesterol levels can lead to atherosclerosis, a hardening of the arteries due to plaque buildup. Plaque forms when cholesterol builds up in artery walls as macrophages take up cholesterol and become foam cells. Over time, plaque can narrow arteries and risk blockages leading to heart attacks and other problems. Risk factors for high cholesterol and atherosclerosis include diet, obesity, smoking, and other lifestyle and genetic factors.
atherosclerosis
The document discusses atherosclerosis, which is a disease characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids and other materials within the inner layer of arterial walls. This buildup forms atherosclerotic plaques that protrude into the arterial lumen. Major risk factors for atherosclerosis include increasing age, male gender, family history, genetic abnormalities, hyperlipidemia, hypertension, cigarette smoking, and diabetes. The consequences of atherosclerosis include heart attacks, strokes, aortic aneurysms, and peripheral vascular disease. Prevention involves lifestyle changes while treatment focuses on controlling risk factors and surgical interventions if needed.
regulation of cholesterol synthesis
Regulation of cholesterol synthesis occurs primarily at the HMG-CoA reductase step through competitive inhibition by statins, feedback inhibition by downstream products, covalent modification by hormones like glucagon and insulin, and sterol-mediated regulation of gene transcription. Cholesterol levels are also controlled by transport in lipoproteins and uptake by tissues, and influenced by diet, lifestyle factors, and certain medical conditions that can raise or lower serum cholesterol concentration.
Aromatic amino acids
Tryptophan metabolism involves several steps. First, tryptophan is converted to 5-hydroxytryptophan by tryptophan hydroxylase, an early and rate-limiting step. 5-hydroxytryptophan is then decarboxylated by aromatic L-amino acid decarboxylase to produce serotonin. Serotonin can then be further metabolized through several pathways.
cholesterol synthesis
This document summarizes key information about cholesterol:
- Cholesterol is a constituent of cell membranes and is necessary for synthesizing steroid hormones, bile salts, and vitamin D. Abnormal cholesterol metabolism can lead to cardiovascular disease.
- Cholesterol maintains stability and stiffness of cell membranes and is responsible for neurotransmitter and vitamin D synthesis. It is also involved in synthesizing hormones like aldosterone.
- Cholesterol biosynthesis is a complex process where carbon atoms come from acetyl-CoA and occurs in five stages, forming HMG CoA, mevalonate, isoprenoid units, squalene, and finally cholesterol.
- Cholesterol can be exported to tissues via LDL, converted to bile acids
Ammonia metabolism
Ammonia is produced through the metabolism of amino acids and nitrogenous compounds and exists as NH4+ ions at physiological pH. It is transported and stored as glutamine, which can be converted back to ammonia and glutamate. The liver plays a key role in ammonia disposal through the urea cycle, where ammonia and aspartate are converted to urea and fumarate in a 5-step process. Elevated ammonia is toxic and can cause neurological issues if not properly eliminated as urea through the kidneys. Genetic defects in the urea cycle can lead to hyperammonemia.
Vit a + vit k
Vitamin K plays an important role in blood clotting by activating clotting factors in the coagulation cascade. It exists in multiple forms, with vitamin K1 derived from plants and vitamin K2 produced by bacteria. Vitamin K is absorbed in the intestine and transported to the liver via chylomicrons, where it is stored and distributed to tissues bound to lipoproteins. A deficiency can impair clotting and cause bleeding, while vitamin K is also involved in bone mineralization, cell growth regulation, and preventing cardiovascular disease.
Vitamin A and D
Vitamin A is a fat-soluble vitamin that exists in multiple forms including retinol, retinal, and retinoic acid. It plays important roles in vision, gene transcription, epithelial cell maintenance, reproduction, and immune function. Deficiency can cause night blindness, dry eyes, skin issues, and even blindness. Toxicity from excess intake is also possible. The body carefully regulates vitamin A levels through absorption in the intestine, storage in the liver, and transport to tissues as needed.
Vitamin b12
Vitamin B12, also known as cobalamin, is essential for normal cell metabolism and blood cell formation. It contains a cobalt ion at its core and different attachments to the cobalt determine the type of B12. The main sources are animal products. B12 requires intrinsic factor for absorption in the ileum. A deficiency can cause megaloblastic anemia and neurological problems due to impaired DNA synthesis and methylation reactions. Pernicious anemia is a type of B12 deficiency caused by a lack of intrinsic factor.
glycogen metabolism
This document summarizes the process of gluconeogenesis. It begins by defining gluconeogenesis as the production of glucose from non-carbohydrate precursors when sufficient carbohydrates are not available from diet or glycogen reserves. The major sites are the liver and kidney. The key substrates that enter gluconeogenesis after conversion to pyruvate or later intermediates are listed as lactate, glucogenic amino acids, glycerol, and propionyl CoA. The document then describes the individual pathways for each substrate and explains how gluconeogenesis bypasses the irreversible steps of glycolysis through specific enzymes. It concludes by discussing the regulation and significance of maintaining glucose production through gluconeogenesis.
HMP Shunt
The document summarizes key aspects of the hexose monophosphate pathway (HMP pathway or pentose phosphate pathway). It describes the pathway's location in the cytosol and key tissues where it is active. The oxidative and non-oxidative phases of the pathway and their reactions are outlined. Regulation of the pathway by NADPH concentration is mentioned. The significance of the pathway is that it generates pentoses and NADPH, which is important for biosynthesis and antioxidant reactions. Deficiencies in the pathway can cause hemolytic anemia.
Folic acid
Folic acid is a B vitamin found in green leafy vegetables and whole grains. It is required for DNA synthesis and cell division. The biologically active form is tetrahydrofolate, which carries single carbon groups and is involved in reactions like purine synthesis. Deficiency can cause megaloblastic anemia during pregnancy or infancy due to impaired DNA synthesis. It is also associated with increased homocysteine levels and neural tube defects if deficiency occurs during pregnancy. While folic acid supplements can treat deficiency, they should not be given to cancer patients as it may increase abnormal cell growth and division.
Folate
Folic acid is essential for one carbon metabolism and the synthesis of DNA, RNA, and proteins. Rich sources include green leafy vegetables and yeast. Deficiency can cause megaloblastic anemia and fetal neural tube defects. It is caused by inadequate intake, increased need during pregnancy, malabsorption, medications, and B12 deficiency trapping folate. Symptoms include fatigue, sore tongue, and neurological issues. Diagnosis involves blood tests of folate, B12, and homocysteine levels. Treatment is oral folic acid supplementation.
Carbohydrate metabolism
This document provides information on carbohydrate metabolism and various pathways involved including glycolysis, the citric acid cycle, and pyruvate dehydrogenase complex. It discusses:
- The key roles of glucose and glycogen in carbohydrate metabolism
- The three phases of glycolysis and production of ATP
- Conversion of pyruvate to lactate under anaerobic conditions
- Regulation of key enzymes in glycolysis
- Significance of glycolysis in various tissues and diseases
- The citric acid cycle and its importance in energy production
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Fatty acid oxidation
- 1. FATTY ACID OXIDATION AND FATTY ACID SYNTHESIS Presented by Shabnam Dixit Simarjot Kaur Simran Kaur Simran Tangri SimranpreetKaur Simranpreet Kaur
- 2. FATTY ACID OXIDATION The fatty acids in the body are mostly oxidised by β-oxidation may be defined as the oxidation of fatty acids on the β-carbon atom. This results in sequential removal of two carbon fragment, acetyl CoA .
- 3. β-OXIDATION • It is known as β-oxidation because the oxidation and splitting of two-carbon units occur at β- carbon atom. • It involves three stages Ø Fatty acid activation Ø Transport acyl CoA into mitochondria Ø β-oxidation proper
- 4. Fatty Acid Activation • Reaction occurs in two steps • Activated by thiokinases or acyl CoA synthetases • It requires ATP, coenzyme and Mg+2
- 5. Transport of Acyl CoA into Mitochondria • A specialised Carnitine carrier system operates to transport activated fatty acids from cytosol to the mitochondria ØAcyl group of acyl CoA is transferred to carnitine catalysed by carnitine acyltranferse 1 ØAcyl-carnitine is transported across the membrane to mitochondrial matrix by a specific carrier protein. ØCarnitine acyl transferase2 converts acyl- carnitine to acyl-CoA.
- 6. ØThe carnitine released returns to cytosol for reuse.
- 7. β-Oxidation Proper • It occurs in sequence of four reactions. ØOxidation ØHydration ØOxidation ØCleavage
- 9. Energetics of β-oxidation • Palmitoyl CoA undergoes 7 cycles of β-oxidation to yield 8 acetyl CoA
- 10. SIDS –a disorder due to blockade in β- oxidation • Sudden infant death syndrome • Frequency 1 in 10000 births • Deficiency of medium chain acyl CoA dehydrogenase
- 11. Jamaican Vomiting Sickness • It is caused by eating unripe ackee fruit which contains toxic amino acid hypoglycine A. • Hypoglycine A inhibits acyl CoA dehydrogenase, thus β-oxidation is blocked. • Characterised by hypoglycemia , vomiting, convulsions, coma and death.
- 12. OXIDATION OF ODD CHAIN FATTY ACIDS
- 13. Inborn errors of Propionate metabolism • Methyl Malonic Acidemia ØAccumulation of methyl malonic acid followed by excretion in urine ØCauses severe metabolic acidosis ØDamages CNS retards growth
- 14. α-Oxidation of Fatty Acids • It is a process by which fatty acids are oxidised by removing carbon atoms one at a time from carboxyl end. • Process occurs in endoplasmic reticulum, does not require CoA. • Does not require energy.
- 15. Refsum’s Disease • Metabolic error due lack of phytanic acid α oxidase. • Phytanic acid accumulates in the body. • Patient presents neuropathy and cerebral ataxia. • Characteristic shortening of fourth toe.
- 17. BIOSYNTHESIS OF FATTY ACIDS • De Novo Synthesis occurs in liver ,kidney, adipose tissue , brain, and mammary glands. • This pathway operates in cytoplasm. • It occurs in three stages- ØProduction of acetyl CoA and NADPH ØConversion of acetyl CoA to malonyl CoA ØReactions of fatty acid synthase complex
- 18. Production of Acetyl CoA and NADPH
- 19. Formation of Malonyl CoA • Enzyme used for conversion is acetyl CoA carboxylase. • It is ATP dependent reaction and requires biotin for CO2 fixation.
- 20. Reaction of Fatty Acid Complex • It occurs in series of steps ØCarboxylation of acetyl CoA ØThree carbon and two carbon units are added ØCondensation ØReduction ØDehydration ØSecond reduction ØPalmitic acid is released
- 22. Regulation of Fatty Acids • Availability of substrate Fatty acid synthesis occurs carbohydrates is abundant and level of fatty acid is low. • Acetyl CoA carboxylase Phosphorylation inactivates acetyl CoA carboxylase.AMP activates this phosphorylation while ATP inhibits it.
- 23. • Hormonal influence Insulin promotes fatty acid synthesis and glucagon inhibits it. • Availability of NADPH The reducing equivalents for fatty acid synthesis are provided by NADPH which comes from citrate transport or HMP shunt.
- 24. Fatty Acid Synthase Complex • Multi enzyme complex • Dimer composed of two identical subunits • Each subunits contain 3 domains with 7 enzymes
- 26. First Domain or condensing Unit • Enzymes involved ØBeta -keto acyl synthase or condensing enzyme(CE) ØAcetyl transferase(AT) ØMalonyl transacylase(MT)
- 27. Second domain or Reduction Unit • It contains ØDehydratase(DH) ØEnoyl reductase(ER) ØBeta –keto acyl reductase(KR) ØAcyl carrier protein(ACP)
- 28. Third Domain 0r Releasing Unit • It contains ØThioestrase(TE) or de acylase ØIt is involved in release of palmitate synthesised
- 29. Significance of FAS Complex • One gene codes all the enzymes so all enzymes are in equimolar concentration • Intermediates of the reaction can easily interact with active sites of the enzyme • FAS complex offers great efficiency