1) Fatty acids are oxidized through beta-oxidation in the mitochondria to generate acetyl-CoA units and energy in the form of ATP.
2) Beta-oxidation involves four steps - dehydrogenation, hydration, dehydrogenation, and thiolysis - that occur in a recurring cycle to shorten the fatty acid by two carbons each time.
3) Fatty acid oxidation provides the major source of energy during periods of fasting or low carbohydrate availability and yields substantial ATP through the electron transport chain.
Glycolysis is the metabolic pathway that converts glucose into pyruvate, generating a small amount of ATP. It occurs in the cytosol of cells and has three phases: energy investment, splitting of molecules, and energy generation. Glycolysis is regulated by three key enzymes - hexokinase, phosphofructokinase, and pyruvate kinase. It yields two ATP per glucose under anaerobic conditions when pyruvate is reduced to lactate, and eight ATP when pyruvate enters the citric acid cycle under aerobic conditions.
Pyruvate is converted to acetyl CoA by the pyruvate dehydrogenase (PDH) complex in the mitochondria. PDH is a multi-enzyme complex containing five coenzymes and three enzymes that catalyzes the oxidative decarboxylation of pyruvate. This generates acetyl CoA, NADH, and FADH2, with the NADH and FADH2 contributing to ATP production through oxidative phosphorylation. PDH activity is regulated by phosphorylation/dephosphorylation and end-product inhibition by acetyl CoA and NADH.
This document discusses fatty acid biosynthesis. It begins with an introduction to fatty acids, their types and functions. It then describes the localization and key steps of biosynthesis, which involves condensation, reduction, dehydration and reduction reactions. The main enzymes involved are acetyl-CoA carboxylase and fatty acid synthase. Biosynthesis occurs via fatty acid synthase and produces palmitate in 7 cycles. It is regulated differently in plants versus animals. Fatty acids have important structural and biological functions in both plants and animals.
This document summarizes the process of de novo fatty acid synthesis. It occurs in the cytosol of liver, kidney, adipose tissue, and lactating mammary glands. Acetyl-CoA is the starting material, which is transported from mitochondria to the cytosol via citrate. In the cytosol, fatty acid synthase complex catalyzes the reactions to produce palmitic acid (C16) through cycles of condensation, reduction, dehydration, and reduction. The process requires acetyl-CoA, malonyl-CoA, ATP, and NADPH as substrates and is regulated by enzymes and hormones.
This document summarizes gluconeogenesis, the process by which glucose is synthesized from non-carbohydrate precursors. It describes the major substrates and sites of gluconeogenesis, its importance during fasting, and how it resembles the reversed pathway of glycolysis. Key enzymes that bypass irreversible glycolysis steps are pyruvate carboxylase, phosphoenolpyruvate carboxykinase, and fructose-1,6-bisphosphatase. Gluconeogenesis is regulated by substrates, enzymes like pyruvate carboxylase, and hormones including glucagon and glucocorticoids.
This document provides information on beta-oxidation of fatty acids. It discusses the three stages of beta-oxidation: activation of fatty acids in the cytosol, transport into mitochondria via carnitine shuttle, and beta-oxidation in the mitochondrial matrix. The four reactions of each beta-oxidation cycle are also described: oxidation, hydration, oxidation, and cleavage. Deficiencies in beta-oxidation can cause conditions like sudden infant death syndrome.
The tricarboxylic acid (TCA) cycle is a series of enzyme-catalyzed reactions that forms a key part of aerobic respiration in cells. It was discovered by Hans Krebs in 1937 and is also known as the Krebs cycle or citric acid cycle. The cycle occupies a central position in metabolism, using acetate to generate carbon dioxide, reducing agents like NADH, and ATP through oxidative phosphorylation. It provides precursors for amino acid and nucleotide biosynthesis. The cycle is critical for generating the majority of a cell's energy needs through the complete oxidation of carbohydrates, fatty acids, and amino acids.
This document summarizes the process of fatty acid oxidation. It occurs in three stages: 1) beta-oxidation in the mitochondria breaks down fatty acids into acetyl-CoA units, producing NADH and FADH2. 2) The acetyl-CoA enters the citric acid cycle. 3) Electrons from NADH and FADH2 are used to power ATP synthesis via oxidative phosphorylation. Fatty acids are activated to fatty acyl-CoAs before beta-oxidation. Saturated, monounsaturated, and polyunsaturated fatty acids undergo this process with additional enzyme steps for unsaturated fatty acids. Beta-oxidation removes two carbons as acetyl-CoA in four enzyme
Glycolysis is the metabolic pathway that converts glucose into pyruvate, generating a small amount of ATP. It occurs in the cytosol of cells and has three phases: energy investment, splitting of molecules, and energy generation. Glycolysis is regulated by three key enzymes - hexokinase, phosphofructokinase, and pyruvate kinase. It yields two ATP per glucose under anaerobic conditions when pyruvate is reduced to lactate, and eight ATP when pyruvate enters the citric acid cycle under aerobic conditions.
Pyruvate is converted to acetyl CoA by the pyruvate dehydrogenase (PDH) complex in the mitochondria. PDH is a multi-enzyme complex containing five coenzymes and three enzymes that catalyzes the oxidative decarboxylation of pyruvate. This generates acetyl CoA, NADH, and FADH2, with the NADH and FADH2 contributing to ATP production through oxidative phosphorylation. PDH activity is regulated by phosphorylation/dephosphorylation and end-product inhibition by acetyl CoA and NADH.
This document discusses fatty acid biosynthesis. It begins with an introduction to fatty acids, their types and functions. It then describes the localization and key steps of biosynthesis, which involves condensation, reduction, dehydration and reduction reactions. The main enzymes involved are acetyl-CoA carboxylase and fatty acid synthase. Biosynthesis occurs via fatty acid synthase and produces palmitate in 7 cycles. It is regulated differently in plants versus animals. Fatty acids have important structural and biological functions in both plants and animals.
This document summarizes the process of de novo fatty acid synthesis. It occurs in the cytosol of liver, kidney, adipose tissue, and lactating mammary glands. Acetyl-CoA is the starting material, which is transported from mitochondria to the cytosol via citrate. In the cytosol, fatty acid synthase complex catalyzes the reactions to produce palmitic acid (C16) through cycles of condensation, reduction, dehydration, and reduction. The process requires acetyl-CoA, malonyl-CoA, ATP, and NADPH as substrates and is regulated by enzymes and hormones.
This document summarizes gluconeogenesis, the process by which glucose is synthesized from non-carbohydrate precursors. It describes the major substrates and sites of gluconeogenesis, its importance during fasting, and how it resembles the reversed pathway of glycolysis. Key enzymes that bypass irreversible glycolysis steps are pyruvate carboxylase, phosphoenolpyruvate carboxykinase, and fructose-1,6-bisphosphatase. Gluconeogenesis is regulated by substrates, enzymes like pyruvate carboxylase, and hormones including glucagon and glucocorticoids.
This document provides information on beta-oxidation of fatty acids. It discusses the three stages of beta-oxidation: activation of fatty acids in the cytosol, transport into mitochondria via carnitine shuttle, and beta-oxidation in the mitochondrial matrix. The four reactions of each beta-oxidation cycle are also described: oxidation, hydration, oxidation, and cleavage. Deficiencies in beta-oxidation can cause conditions like sudden infant death syndrome.
The tricarboxylic acid (TCA) cycle is a series of enzyme-catalyzed reactions that forms a key part of aerobic respiration in cells. It was discovered by Hans Krebs in 1937 and is also known as the Krebs cycle or citric acid cycle. The cycle occupies a central position in metabolism, using acetate to generate carbon dioxide, reducing agents like NADH, and ATP through oxidative phosphorylation. It provides precursors for amino acid and nucleotide biosynthesis. The cycle is critical for generating the majority of a cell's energy needs through the complete oxidation of carbohydrates, fatty acids, and amino acids.
This document summarizes the process of fatty acid oxidation. It occurs in three stages: 1) beta-oxidation in the mitochondria breaks down fatty acids into acetyl-CoA units, producing NADH and FADH2. 2) The acetyl-CoA enters the citric acid cycle. 3) Electrons from NADH and FADH2 are used to power ATP synthesis via oxidative phosphorylation. Fatty acids are activated to fatty acyl-CoAs before beta-oxidation. Saturated, monounsaturated, and polyunsaturated fatty acids undergo this process with additional enzyme steps for unsaturated fatty acids. Beta-oxidation removes two carbons as acetyl-CoA in four enzyme
Lipid metabolism involves the oxidation of fatty acids to produce energy. There are three main types of fatty acid oxidation: beta, alpha, and omega. Beta-oxidation occurs in the mitochondria and breaks down fatty acids into acetyl-CoA via a four-step process. Cholesterol is synthesized from acetyl-CoA in the liver through a series of reactions. Ketone bodies such as acetoacetate and beta-hydroxybutyrate are produced from acetyl-CoA in the liver during periods of low glucose and provide energy for other tissues. Lipoproteins such as chylomicrons, VLDL, LDL, and HDL are involved in transporting lipids between tissues.
Jayati Mishra presented on the de novo and salvage pathways of purines under the guidance of Pradip Hirapue. The presentation discussed:
1) The de novo pathway synthesizes purine nucleotides from simple precursors through a two-stage process forming IMP and then converting it to AMP or GMP.
2) The salvage pathway recycles purine bases and nucleosides obtained from the diet or cell turnover to form nucleotides.
3) Both pathways work together to synthesize the purine nucleotides needed for nucleic acid synthesis, with the salvage pathway playing a larger role in certain tissues.
1. Beta-oxidation is the process by which fatty acids are broken down in the mitochondria to produce acetyl-CoA, which enters the citric acid cycle.
2. It involves three main stages: activation of fatty acids in the cytosol, transport into the mitochondria via carnitine shuttle, and beta-oxidation within the mitochondrial matrix.
3. During beta-oxidation, fatty acid chains are shortened by two carbons in each cycle through four steps, producing acetyl-CoA and reducing equivalents like FADH2 and NADH that generate ATP through oxidative phosphorylation.
This file include these contents:
What is Triacylglycerol
Structure of triacylglycerol
Simple triacylglycerol
Mixed triacylglycerol
Biosynthesis of triacylglycerol
Utilization of triacylglycerol
Properties of triacylglycerol
Cholesterol is synthesized from acetyl-CoA in a multi-step process located in the endoplasmic reticulum and cytoplasm. HMG-CoA reductase catalyzes the rate-limiting step and is regulated by transcription, covalent modification, and competitive inhibitors like statins. Cholesterol is transported by LDL and HDL and is used for cell membrane structure, steroid hormone synthesis, or storage.
Biosynthesis of fatty acids occurs predominantly in the liver, kidney, adipose tissue and mammary glands. Acetyl CoA and NADPH provide the building blocks and reducing power for fatty acid formation. Fatty acid synthesis occurs in three stages: 1) Acetyl CoA and NADPH are produced in the mitochondria and cytosol, respectively; 2) Acetyl CoA is carboxylated to malonyl CoA by acetyl CoA carboxylase; 3) The fatty acid synthase complex catalyzes the reactions to elongate the fatty acid chain by two carbons at a time using malonyl CoA, producing a longer fatty acid with each cycle.
The document summarizes metabolism of triglycerides. Triglycerides are the preferred form for storing energy in the body as they do not require water for storage and have a high calorific value. Triglycerides are stored mainly in adipose tissue in the form of fat globules within adipocytes. Triglycerides are broken down into glycerol and fatty acids through hydrolysis by hormone-sensitive lipase and lipoprotein lipase. The released fatty acids are used for energy while glycerol can be reused or converted to glucose.
This document discusses fatty acid synthesis in the body. It begins by defining fatty acids and describing their roles in energy storage and as structural components of membranes. There are three systems for fatty acid synthesis: de novo synthesis in the cytoplasm, chain elongation in mitochondria, and chain elongation in microsomes. De novo synthesis occurs primarily in the liver and adipose tissues, starting from acetyl-CoA derived from glucose. This synthesis takes place in the cytoplasm and requires acetyl-CoA transport from mitochondria via citrate. The document then details the multi-step process of de novo fatty acid synthesis catalyzed by acetyl-CoA carboxylase and fatty acid synthase, and describes regulation of synthesis by products, hormones,
Lipid metabolism involves the breakdown and synthesis of fats and involves several processes. Fats are obtained through food or synthesized in the body from carbohydrates. Hormones signal the need for energy storage or release from fat cells. Fatty acids and glycerol are released from triglycerides and transported to tissues where the liver uses some for energy and resynthesizes others to be stored or used by muscles. Lipid metabolism occurs through several pathways including beta-oxidation of fatty acids, fatty acid synthesis, and cholesterol transport.
The document discusses amino acid metabolism. It begins by defining amino acids as derivatives of carboxylic acids with an amino group substitution. Amino acids are essential for building proteins and participate in many metabolic reactions. They are classified by the properties of their side chains. Protein digestion involves proteases in the stomach, pancreas, and small intestine that hydrolyze proteins into amino acids. Amino acids are absorbed into the blood and transported to tissues. Within cells, amino groups are transferred between amino acids and ketoacids in transamination reactions or removed as ammonia by deamination. The liver converts ammonia into less toxic urea via the urea cycle to prevent intoxication. Defects in the urea cycle can
1) Biological oxidation involves the conversion of energy from foods like carbohydrates and lipids into ATP through electron transport chain and oxidative phosphorylation in mitochondria.
2) The electron transport chain involves a series of protein complexes that transfer electrons from electron donors like NADH to final acceptor oxygen, creating a proton gradient that drives ATP synthesis.
3) Through the chemiosmotic hypothesis, the potential energy of the proton gradient is used by ATP synthase to phosphorylate ADP into ATP, coupling electron transport to oxidative phosphorylation.
Biological oxidation (part - III) Oxidative PhosphorylationAshok Katta
Biological oxidation (part - III) Oxidative Phosphorylation
- Mechanism of Oxidative Phosphorylation
-- Chemiosmotic theory
-P:O Ratio
Substrate Level Phosphorylation
Shuttle Systems for Oxidation of Extramitochondrial NADH
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
The pentose phosphate pathway, also known as the hexose monophosphate shunt, is an alternative metabolic pathway to glycolysis that occurs in the cytosol. It is a complex pathway that helps generate NADPH for fatty acid synthesis and glutathione for antioxidant activity, as well as synthesizing ribose-5-phosphate for nucleotide and nucleic acid formation. Glucose-6-phosphate enters the pathway and is oxidized through a two-phase process involving dehydrogenation using NADP+ instead of NAD+. Several intermediates are formed and rearranged before regenerating glucose-6-phosphate and glyceraldehyde-3-phosphate to complete the nonoxidative phase. Genetic defects in glucose-6
This document discusses the biosynthesis of purines and pyrimidines. It explains that purines and pyrimidines are synthesized through de novo and salvage pathways. The de novo pathway involves multiple enzyme-catalyzed steps to convert simple precursors into the complex purine and pyrimidine nucleotides. This includes converting ribose-5-phosphate into inosine monophosphate (IMP) through 10 steps for purine synthesis. IMP is then used to synthesize adenine monophosphate (AMP) and guanine monophosphate (GMP). The salvage pathway recovers bases and nucleotides from degraded DNA and RNA. Pyrimidine synthesis is described as simpler than purine synthesis.
The document discusses fatty acid synthesis. It begins by describing fatty acids and their roles in the body. It then covers the three main ways fatty acids are produced: diet, adipolysis, and de novo synthesis. The process of de novo synthesis occurs primarily in the liver, adipose tissue, and lactating mammary glands. It involves acetyl-CoA being carboxylated to malonyl-CoA by acetyl-CoA carboxylase. Fatty acid synthase then catalyzes the repeating cycles of condensation, reduction, dehydration, and reduction to elongate the fatty acid chain until a 16-carbon palmitate is produced. NADPH provides reducing equivalents for the reactions.
The pentose phosphate pathway (PPP), also known as the hexose monophosphate shunt (HMP) or phosphogluconate pathway, is an alternative glucose metabolism pathway to glycolysis. It is more complex than glycolysis and takes place in the cytosol. The PPP is important for generating NADPH for biosynthesis of fatty acids, steriods, and maintaining glutathione levels, as well as producing pentoses used in nucleic acid synthesis. The pathway contains oxidative and non-oxidative phases, with glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase being the regulatory enzymes controlled by NADPH and pentose levels.
This document summarizes the de novo synthesis of fatty acids. It discusses that fatty acid synthesis primarily occurs in the liver and lactating mammary glands using acetyl CoA, ATP, NADPH, Mn2+, and biotin. The first step is the production of cytosolic acetyl CoA from mitochondrial acetyl CoA. Acetyl CoA is then carboxylated to form malonyl CoA by acetyl CoA carboxylase. Fatty acid synthase is a multifunctional enzyme that catalyzes the remaining reactions. The major sources of NADPH required are the pentose phosphate pathway and conversion of malate to pyruvate in the cytosol. Palmitate, a 16 carbon
De novo synthesis of fatty acids (Biosynthesis of fatty acids)Ashok Katta
Synthesis of fatty acids in the body. Detailed pathway for de novo synthesis of fatty acids in the body including its energetic and regulation. also cover Multienzyme complex
Lipid metabolism involves the oxidation of fatty acids to produce energy. There are three main types of fatty acid oxidation: beta, alpha, and omega. Beta-oxidation occurs in the mitochondria and breaks down fatty acids into acetyl-CoA via a four-step process. Cholesterol is synthesized from acetyl-CoA in the liver through a series of reactions. Ketone bodies such as acetoacetate and beta-hydroxybutyrate are produced from acetyl-CoA in the liver during periods of low glucose and provide energy for other tissues. Lipoproteins such as chylomicrons, VLDL, LDL, and HDL are involved in transporting lipids between tissues.
Jayati Mishra presented on the de novo and salvage pathways of purines under the guidance of Pradip Hirapue. The presentation discussed:
1) The de novo pathway synthesizes purine nucleotides from simple precursors through a two-stage process forming IMP and then converting it to AMP or GMP.
2) The salvage pathway recycles purine bases and nucleosides obtained from the diet or cell turnover to form nucleotides.
3) Both pathways work together to synthesize the purine nucleotides needed for nucleic acid synthesis, with the salvage pathway playing a larger role in certain tissues.
1. Beta-oxidation is the process by which fatty acids are broken down in the mitochondria to produce acetyl-CoA, which enters the citric acid cycle.
2. It involves three main stages: activation of fatty acids in the cytosol, transport into the mitochondria via carnitine shuttle, and beta-oxidation within the mitochondrial matrix.
3. During beta-oxidation, fatty acid chains are shortened by two carbons in each cycle through four steps, producing acetyl-CoA and reducing equivalents like FADH2 and NADH that generate ATP through oxidative phosphorylation.
This file include these contents:
What is Triacylglycerol
Structure of triacylglycerol
Simple triacylglycerol
Mixed triacylglycerol
Biosynthesis of triacylglycerol
Utilization of triacylglycerol
Properties of triacylglycerol
Cholesterol is synthesized from acetyl-CoA in a multi-step process located in the endoplasmic reticulum and cytoplasm. HMG-CoA reductase catalyzes the rate-limiting step and is regulated by transcription, covalent modification, and competitive inhibitors like statins. Cholesterol is transported by LDL and HDL and is used for cell membrane structure, steroid hormone synthesis, or storage.
Biosynthesis of fatty acids occurs predominantly in the liver, kidney, adipose tissue and mammary glands. Acetyl CoA and NADPH provide the building blocks and reducing power for fatty acid formation. Fatty acid synthesis occurs in three stages: 1) Acetyl CoA and NADPH are produced in the mitochondria and cytosol, respectively; 2) Acetyl CoA is carboxylated to malonyl CoA by acetyl CoA carboxylase; 3) The fatty acid synthase complex catalyzes the reactions to elongate the fatty acid chain by two carbons at a time using malonyl CoA, producing a longer fatty acid with each cycle.
The document summarizes metabolism of triglycerides. Triglycerides are the preferred form for storing energy in the body as they do not require water for storage and have a high calorific value. Triglycerides are stored mainly in adipose tissue in the form of fat globules within adipocytes. Triglycerides are broken down into glycerol and fatty acids through hydrolysis by hormone-sensitive lipase and lipoprotein lipase. The released fatty acids are used for energy while glycerol can be reused or converted to glucose.
This document discusses fatty acid synthesis in the body. It begins by defining fatty acids and describing their roles in energy storage and as structural components of membranes. There are three systems for fatty acid synthesis: de novo synthesis in the cytoplasm, chain elongation in mitochondria, and chain elongation in microsomes. De novo synthesis occurs primarily in the liver and adipose tissues, starting from acetyl-CoA derived from glucose. This synthesis takes place in the cytoplasm and requires acetyl-CoA transport from mitochondria via citrate. The document then details the multi-step process of de novo fatty acid synthesis catalyzed by acetyl-CoA carboxylase and fatty acid synthase, and describes regulation of synthesis by products, hormones,
Lipid metabolism involves the breakdown and synthesis of fats and involves several processes. Fats are obtained through food or synthesized in the body from carbohydrates. Hormones signal the need for energy storage or release from fat cells. Fatty acids and glycerol are released from triglycerides and transported to tissues where the liver uses some for energy and resynthesizes others to be stored or used by muscles. Lipid metabolism occurs through several pathways including beta-oxidation of fatty acids, fatty acid synthesis, and cholesterol transport.
The document discusses amino acid metabolism. It begins by defining amino acids as derivatives of carboxylic acids with an amino group substitution. Amino acids are essential for building proteins and participate in many metabolic reactions. They are classified by the properties of their side chains. Protein digestion involves proteases in the stomach, pancreas, and small intestine that hydrolyze proteins into amino acids. Amino acids are absorbed into the blood and transported to tissues. Within cells, amino groups are transferred between amino acids and ketoacids in transamination reactions or removed as ammonia by deamination. The liver converts ammonia into less toxic urea via the urea cycle to prevent intoxication. Defects in the urea cycle can
1) Biological oxidation involves the conversion of energy from foods like carbohydrates and lipids into ATP through electron transport chain and oxidative phosphorylation in mitochondria.
2) The electron transport chain involves a series of protein complexes that transfer electrons from electron donors like NADH to final acceptor oxygen, creating a proton gradient that drives ATP synthesis.
3) Through the chemiosmotic hypothesis, the potential energy of the proton gradient is used by ATP synthase to phosphorylate ADP into ATP, coupling electron transport to oxidative phosphorylation.
Biological oxidation (part - III) Oxidative PhosphorylationAshok Katta
Biological oxidation (part - III) Oxidative Phosphorylation
- Mechanism of Oxidative Phosphorylation
-- Chemiosmotic theory
-P:O Ratio
Substrate Level Phosphorylation
Shuttle Systems for Oxidation of Extramitochondrial NADH
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
The pentose phosphate pathway, also known as the hexose monophosphate shunt, is an alternative metabolic pathway to glycolysis that occurs in the cytosol. It is a complex pathway that helps generate NADPH for fatty acid synthesis and glutathione for antioxidant activity, as well as synthesizing ribose-5-phosphate for nucleotide and nucleic acid formation. Glucose-6-phosphate enters the pathway and is oxidized through a two-phase process involving dehydrogenation using NADP+ instead of NAD+. Several intermediates are formed and rearranged before regenerating glucose-6-phosphate and glyceraldehyde-3-phosphate to complete the nonoxidative phase. Genetic defects in glucose-6
This document discusses the biosynthesis of purines and pyrimidines. It explains that purines and pyrimidines are synthesized through de novo and salvage pathways. The de novo pathway involves multiple enzyme-catalyzed steps to convert simple precursors into the complex purine and pyrimidine nucleotides. This includes converting ribose-5-phosphate into inosine monophosphate (IMP) through 10 steps for purine synthesis. IMP is then used to synthesize adenine monophosphate (AMP) and guanine monophosphate (GMP). The salvage pathway recovers bases and nucleotides from degraded DNA and RNA. Pyrimidine synthesis is described as simpler than purine synthesis.
The document discusses fatty acid synthesis. It begins by describing fatty acids and their roles in the body. It then covers the three main ways fatty acids are produced: diet, adipolysis, and de novo synthesis. The process of de novo synthesis occurs primarily in the liver, adipose tissue, and lactating mammary glands. It involves acetyl-CoA being carboxylated to malonyl-CoA by acetyl-CoA carboxylase. Fatty acid synthase then catalyzes the repeating cycles of condensation, reduction, dehydration, and reduction to elongate the fatty acid chain until a 16-carbon palmitate is produced. NADPH provides reducing equivalents for the reactions.
The pentose phosphate pathway (PPP), also known as the hexose monophosphate shunt (HMP) or phosphogluconate pathway, is an alternative glucose metabolism pathway to glycolysis. It is more complex than glycolysis and takes place in the cytosol. The PPP is important for generating NADPH for biosynthesis of fatty acids, steriods, and maintaining glutathione levels, as well as producing pentoses used in nucleic acid synthesis. The pathway contains oxidative and non-oxidative phases, with glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase being the regulatory enzymes controlled by NADPH and pentose levels.
This document summarizes the de novo synthesis of fatty acids. It discusses that fatty acid synthesis primarily occurs in the liver and lactating mammary glands using acetyl CoA, ATP, NADPH, Mn2+, and biotin. The first step is the production of cytosolic acetyl CoA from mitochondrial acetyl CoA. Acetyl CoA is then carboxylated to form malonyl CoA by acetyl CoA carboxylase. Fatty acid synthase is a multifunctional enzyme that catalyzes the remaining reactions. The major sources of NADPH required are the pentose phosphate pathway and conversion of malate to pyruvate in the cytosol. Palmitate, a 16 carbon
De novo synthesis of fatty acids (Biosynthesis of fatty acids)Ashok Katta
Synthesis of fatty acids in the body. Detailed pathway for de novo synthesis of fatty acids in the body including its energetic and regulation. also cover Multienzyme complex
The liver is the largest organ in the body
It is located below the diaphragm in the right upper quadrant of the abdominal cavity and extended approximately from the right 5th rib to the lower border of the rib cage.
This document provides information about the glucose tolerance test (GTT), also known as the oral glucose tolerance test (OGTT). It defines the GTT as a standardized test used to diagnose diabetes mellitus in doubtful cases. The document outlines the indications for an OGTT as having symptoms of diabetes, inconclusive fasting blood sugar levels, pregnancy with excessive weight gain or history of large or miscarried babies. Contraindications are a confirmed diabetes diagnosis or using it for follow-up. Preparation involves a high carbohydrate diet before the test and fasting overnight. The test involves collecting fasting and 2-hour blood and urine samples after a glucose drink. Diagnosis of diabetes is made if fasting blood sugar is over 126 mg/dl or
Beta-oxidation is the process by which fatty acids are broken down in the mitochondria to generate acetyl-CoA molecules. Fatty acids first undergo activation to acyl-CoA derivatives in the cytosol before being transported into the mitochondrial matrix via the carnitine shuttle system. Inside the mitochondria, each cycle of beta-oxidation results in the sequential removal of two-carbon acetyl-CoA units from the fatty acid chain through a series of reactions: oxidation, hydration, oxidation, and thiolytic cleavage. This process continues until the fatty acid is completely broken down.
Fatty acid synthesis and degradation occur through different pathways. Synthesis takes place in the cytosol and requires NADPH and acetyl-CoA, adding two carbon units at a time from malonyl-CoA. Degradation occurs in the mitochondria using NADH and FADH2 to split acetyl-CoA units. Fatty acid synthesis is a multi-step process beginning with activation of acetyl-CoA followed by repeated elongation cycles using acetyl-ACP and malonyl-ACP substrates until palmitate is generated, then released by thioesterase.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
Lipids are a diverse group of compounds that are insoluble in water but soluble in organic solvents. They include fats, oils, waxes, sterols, and phospholipids. The document discusses the structure, function, and classification of various lipids. It describes simple lipids like triglycerides and waxes, as well as complex lipids including phospholipids. Phospholipids are important structural components of cell membranes and contain a phosphate group, alcohol, and fatty acids. Glycerophospholipids are the major class of phospholipids, with phosphatidylcholine, phosphatidylethanolamine, and others playing important roles in cells and tissues.
This document provides an overview of carbohydrate metabolism. It begins with definitions of nutrition and carbohydrates, discussing the classification and functions of carbohydrates. It then describes the major pathways involved in carbohydrate metabolism, including glycolysis, the citric acid cycle, gluconeogenesis, glycogenesis, and glycogenolysis. For each pathway, it outlines the key reactions and clinical aspects. It also discusses the roles of hormones in regulating carbohydrate metabolism and diseases related to defects in glycogen storage and metabolism. In summary, the document comprehensively reviews carbohydrate nutrition and the major catabolic and anabolic pathways involved in carbohydrate metabolism in the human body.
This document discusses intermediary carbohydrate metabolism, specifically glycolysis. It begins with an introduction to glycolysis, noting that it is the degradation of glucose into pyruvate through a series of 10 enzyme-catalyzed reactions. These reactions can occur aerobically, producing pyruvate, or anaerobically, producing lactate. The document then delves into the specific reactions, enzymes, and intermediates involved in both the preparatory and payoff phases of glycolysis. It also discusses the importance of 2,3-bisphosphoglycerate in red blood cells for regulating oxygen release from hemoglobin.
The document summarizes the process of beta-oxidation of fatty acids. It occurs in the mitochondrial matrix in four steps - oxidation, hydration, oxidation, and cleavage - resulting in the sequential removal of two-carbon acetyl-CoA units. Fatty acids are first activated to acyl-CoAs in the cytosol then transported into the mitochondria by the carnitine shuttle system to undergo beta-oxidation, generating acetyl-CoA, NADH, and FADH2. Defects in this process can cause various metabolic disorders like fatty acid oxidation disorders.
This document summarizes carbohydrate metabolism, including the absorption of monosaccharides, fate of absorbed sugars, pathways for glucose utilization, oxidation of glucose through glycolysis and the Krebs cycle, and glycogen metabolism. Key points include: monosaccharides are absorbed via simple diffusion, facilitated transport, or active transport; glucose is utilized through oxidation, storage, or conversion to other compounds; glycolysis occurs via two phases to generate ATP or lactate; the Krebs cycle further oxidizes pyruvate to generate more ATP; glycogen is synthesized from and broken down back to glucose to provide energy.
1. The document discusses different types of lipids including fatty acids, triglycerides, phospholipids, and steroids.
2. It explains the structures and properties of saturated and unsaturated fatty acids. Triglycerides are formed from glycerol and three fatty acids and are a major form of fat storage.
3. Phospholipids are a major component of cell membranes and contain a phosphate group. Cholesterol is an important sterol that is a component of cell membranes and precursor for other substances.
This document discusses several functions of lipids:
1. Lipids can be stored as an energy source, providing more potential for oxidation than glucose.
2. Lipids provide thermal insulation and mechanical protection for cells and tissues.
3. Lipids act as precursors for important signaling molecules like eicosanoids and platelet-activating factor (PAF) that regulate biological processes.
This document provides an overview of carbohydrate metabolism. It begins with an introduction to nutrition and carbohydrates, discussing the classification and functions of carbohydrates. It then describes the major metabolic pathways involved in carbohydrate metabolism, including glycolysis, the citric acid cycle, gluconeogenesis, and others. For each pathway, it provides details on the reactions, enzymes involved, energy production, and some clinical aspects. It also discusses the role of hormones in carbohydrate metabolism and dental aspects. The document concludes with a summary and references section.
The document summarizes key concepts related to cellular respiration. It discusses the four main stages: glycolysis, formation of acetyl-CoA, the citric acid cycle, and the electron transport chain. Glycolysis breaks down glucose into pyruvate, generating a small amount of ATP. In later stages, pyruvate fully oxidizes, producing much more ATP through oxidative phosphorylation as electrons are passed through the electron transport chain. The fate of pyruvate depends on whether oxygen is present, determining whether aerobic or anaerobic respiration occurs.
The citric acid cycle (TCA cycle) is a series of chemical reactions used by all aerobic organisms to generate energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins. The cycle consists of 8 steps: 1) conversion of pyruvic acid to acetyl-CoA, 2) citrate synthase catalyzes the formation of citric acid, 3) isocitrate dehydrogenase and other enzymes catalyze additional reactions, generating NADH, FADH2, and GTP to fuel ATP synthesis. The net result is the oxidation of acetyl-CoA to carbon dioxide to generate between 36-38 ATP.
explains the palmitate synthesis- which is most common FA stored in Adipose tissue , elongation system and Desaturation system, compares oxidation with synthesis.
A fatty acid contains a long hydrocarbon chain and a terminal carboxylate group. The hydrocarbon chain may be saturated (with no double bond) or may be unsaturated (containing double bond).
Free fatty acids also called unesterified (UFA) or nonesterified (NEFA) fatty acids are fatty acids that are in the unesterified state.
In plasma, longer-chain FFA are combined with albumin, and in the cell they are attached to a fatty acid-binding protein.
Shorter-chain fatty acids are more watersoluble and exist as the un-ionized acid or as a fatty acid anion.
By these means, free fatty acids are made accessible as a fuel in other tissues.
This document provides information on the digestion, absorption, and metabolism of lipids. It discusses how dietary lipids are broken down by lipases in the mouth, stomach, and small intestine. Pancreatic lipase plays a major role in digesting triglycerides into fatty acids and monoacylglycerides. These products are absorbed via micelles in the small intestine and resynthesized into triglycerides for transport to the liver and peripheral tissues. The document also outlines the pathways of beta-oxidation of fatty acids in mitochondria, ketogenesis in the liver from fatty acids, and utilization of ketone bodies by extrahepatic tissues.
This document discusses lipid metabolism, including the mobilization and breakdown of triglycerides through lipolysis. Triglycerides are hydrolyzed into fatty acids and glycerol. Fatty acids undergo beta-oxidation in the mitochondria to produce acetyl-CoA for energy production, while glycerol is converted to glycerol-3-phosphate and enters glycolysis. The document also describes the synthesis of triglycerides from fatty acids and glycerol-3-phosphate in the liver and adipose tissue. It outlines the steps of beta-oxidation, where fatty acids are broken down into two-carbon fragments to generate acetyl-CoA.
This document discusses lipid metabolism. It covers the following topics in 3 sentences or less each:
- Beta oxidation of fatty acids, which occurs in the mitochondria through a series of reactions to break down fatty acids into acetyl-CoA.
- Formation and utilization of ketone bodies in the liver from acetyl-CoA produced during fatty acid breakdown, and their use as energy sources in other tissues.
- De novo synthesis of fatty acids like palmitate from acetyl-CoA and malonyl-CoA in the cytosol, involving a fatty acid synthase complex and NADPH reducing equivalents.
This ppt has been presented as seminar in Department of Biochemistry ,C.C.S. university, Meerut.in front of all faculty members for the detailed discussion on this topic. Hope this will help you to go through the concept in an easy manner.
The document discusses lipid metabolism and the relationships between lipid and carbohydrate metabolism. It covers the digestion and absorption of lipids in the stomach and small intestine. Lipids are broken down into fatty acids and monoacylglycerols by pancreatic lipases. These products are combined into micelles to be absorbed. The fatty acids and glycerol are further metabolized. Glycerol is converted to dihydroxyacetone phosphate and fatty acids undergo beta-oxidation in the mitochondria to produce acetyl-CoA. Acetyl-CoA contributes to ATP production through the citric acid cycle. Ketone bodies are produced when acetyl-CoA levels are high due to fatty acid breakdown. Ketone bodies can be used for
This document provides an overview of lipid metabolism. It discusses β-oxidation of fatty acids, formation and utilization of ketone bodies, de novo fatty acid synthesis, the biological significance of cholesterol and its conversion to bile acids, steroid hormones and vitamin D. It also covers disorders of lipid metabolism like hypercholesterolemia and atherosclerosis. The key points are: β-oxidation breaks down fatty acids in the mitochondria, ketone bodies are energy sources formed from acetyl-CoA, and cholesterol is essential for cell membranes and is a precursor for other steroids.
Fatty acid metabolism is a complex multi-step process that occurs in different cellular locations. Triglycerides are first hydrolyzed by lipases to release fatty acids. The fatty acids are then bound to coenzyme A and transported into the mitochondrial matrix using carnitine. Inside the mitochondria, the fatty acids undergo beta-oxidation where they are broken down in a cycle of reactions that cleave two carbon units at a time, producing acetyl-CoA. If fatty acid breakdown outpaces the citric acid cycle, ketone bodies like acetoacetate can be produced from acetyl-CoA. Acetoacetate is an important energy source for tissues like the heart and kidney.
The document discusses lipid metabolism, including β-oxidation of fatty acids, formation and utilization of ketone bodies, de novo synthesis of fatty acids, and disorders of lipid metabolism such as hypercholesterolemia, atherosclerosis, fatty liver and obesity. It provides details on the multi-step processes of β-oxidation of fatty acids, ketogenesis, fatty acid synthesis, and cholesterol conversion to bile acids and steroid hormones. Disorders are discussed in relation to abnormalities in lipid metabolism and risk factors.
Lipid metabolism involves the breakdown and storage of fats. Key processes include beta-oxidation of fatty acids in the mitochondria, ketogenesis in the liver during fasting or diabetes, and de novo synthesis of fatty acids like palmitic acid. Cholesterol is important for cell membranes and can be converted to bile acids, steroid hormones like estrogen and testosterone, and vitamin D. Disorders of lipid metabolism include hypercholesterolemia, atherosclerosis, fatty liver disease, and obesity.
Lipid metabolism involves the breakdown and storage of fats. Key processes include beta-oxidation of fatty acids in the mitochondria, ketogenesis in the liver during fasting or starvation, and de novo synthesis of fatty acids like palmitic acid. Cholesterol is important for cell membranes and can be converted to bile acids, steroid hormones like estrogen and testosterone, and vitamin D. Disorders of lipid metabolism include hypercholesterolemia, atherosclerosis, fatty liver disease, and obesity.
It mainly contains metabolism of saturated and unsaturated fats. It also contains utilisation of cholesterol after degradation in body i.e. synthesis of bile acids, Vit. D, steroid hormone etc. It also describe synthesis of ketone bodies and utilisation.
oxidation of alpha, beta fatty acid and unsaturated fatty acid mariagul6
This document summarizes fatty acid oxidation through beta-oxidation. It discusses how fatty acids are broken down into acetyl-CoA in the mitochondria, generating energy in the form of ATP. Key points covered include the carnitine shuttle transport system, reactions of beta-oxidation, and oxidation of odd-chain and unsaturated fatty acids. Deficiencies in carnitine or the carnitine shuttle enzymes can impair fatty acid breakdown.
Metabolism of Lipids PT.pdf explanation for presentationArmiyahuAlonigbeja
This document provides an overview of lipid metabolism. It discusses the classification of lipids and lipoprotein systems. The major pathways discussed include the oxidation and synthesis of fatty acids, metabolism of unsaturated fatty acids, metabolism of acylglycerols, degradation of phospholipids, and cholesterol synthesis. Key aspects of lipid metabolism covered are the beta-oxidation of fatty acids, biosynthesis of fatty acids from acetyl-CoA, and the role of the liver in producing ketone bodies from fatty acids.
Beta-oxidation occurs in the mitochondrial matrix and involves the breakdown of fatty acids into acetyl-CoA units. It occurs in four stages: 1) activation of fatty acids into acyl-CoA in the cytoplasm, 2) transport of acyl-CoA into the mitochondria via carnitine shuttle, 3) beta-oxidation cycles within the mitochondria that sequentially cleave two-carbon acetyl-CoA units from the fatty acid, and 4) oxidation of acetyl-CoA by the citric acid cycle to generate ATP. Most tissues can break down fatty acids via beta-oxidation except the brain, red blood cells, and adrenal medulla.
Fatty acids have four main functions in the body: as building blocks for cell membranes, as targeting molecules to direct proteins, as fuel molecules stored as triglycerides, and as messenger molecules. Fatty acids provide more energy than carbohydrates and proteins when broken down, yielding about 9000 calories per gram compared to 4000 calories per gram for carbohydrates and proteins. The breakdown of fatty acids is a complex multi-step process involving hydrolysis by lipases, activation with coenzyme A, transport into mitochondria via carnitine, and step-wise breakdown removing two carbon groups at a time to form acetyl-CoA. If acetyl-CoA levels are too high, ketone bodies like aceto
Recombinant DNA technology allows for the creation of novel gene combinations not found in nature. Genes can be inserted into host cells and replicated. This technology is used in research, medicine, agriculture, and industry. In medicine, it enables production of insulin, growth factors, vaccines, and gene therapy. It is also used for genetic mapping, disease diagnosis, forensics, and prenatal testing. In agriculture, it improves crop yields and develops pest/drought resistance. Industry utilizes it to produce enzymes, additives, sugars, and chemicals.
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The document discusses 16 clinical case studies presented by Dr. Namrata Chhabra involving patients' medical histories, laboratory results, and biochemical abnormalities. For each case, Dr. Chhabra asks students to provide diagnoses based on the evidence and explain the underlying biochemical defects or mechanisms. The cases cover topics like diabetes, acid-base imbalances, enzyme deficiencies, and vitamin deficiency disorders.
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(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
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𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
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2. FATTY ACIDS
A fatty acid contains a long hydrocarbon chain and
a terminal carboxylate group. The hydrocarbon
chain may be saturated (with no double bond) or
may be unsaturated (containing double bond).
Fatty acids can be obtained from-
Diet
Adipolysis
De novo synthesis
10/19/2012 Biochemistry For Medics 2
3. FUNCTIONS OF FATTY
ACIDS
Fatty acids have four major physiological roles.
1) Fatty acids are building blocks of
phospholipids and glycolipids.
2) Many proteins are modified by the covalent
attachment of fatty acids, which target them to
membrane locations
3) Fatty acids are fuel molecules. They are stored
as triacylglycerols. Fatty acids mobilized from
triacylglycerols are oxidized to meet the energy
needs of a cell or organism.
4) Fatty acid derivatives serve as hormones and
intracellular messengers e.g. steroids, sex
hormones and prostaglandins.
10/19/2012 Biochemistry For Medics 3
4. TRIGLYCERIDES
Triglycerides are a highly
concentrated stores of energy
because they
are reduced and anhydrous.
The yield from the complete oxidation
of fatty acids is about 9 kcal g-1 (38 kJ
g-1)
Triacylglycerols are nonpolar, and are
stored in a nearly anhydrous form,
whereas much more polar proteins
and carbohydrates are more highly
10/19/2012 Biochemistry For Medics 4
5. TRIGLYCERIDES V/S GLYCOGEN
A gram of nearly anhydrous fat stores
more than six times as much energy
as a gram of hydrated glycogen, which
is likely the reason that triacylglycerols
rather than glycogen were selected in
evolution as the major energy reservoir.
The glycogen and glucose stores provide
enough energy to sustain biological
function for about 24 hours, whereas the
Triacylglycerol stores allow survival
for several weeks.
10/19/2012 Biochemistry For Medics 5
6. PROVISION OF DIETARY
FATTY ACIDS
Most lipids are
ingested in the
form of
triacylglycerols,
that must be
degraded to fatty
acids for
absorption
across the
intestinal
epithelium.
o Free fatty acids and monoacylglycerols obtained by digestion of
dietary triglycerides are absorbed by intestinal epithelial cells.
o Triacylglycerols are resynthesized and packaged with other lipids and
apoprotein B-48 to form chylomicrons, which are then released into the
lymph system.
10/19/2012 Biochemistry For Medics 6
7. PROVISION OF FATTY ACIDS
FROM ADIPOSE TISSUE
The triacylglycerols are degraded to fatty acids and glycerol by hormone
sensitive lipase.The released fatty are transported to the energy-requiring
tissues.
10/19/2012 Biochemistry For Medics 7
8. TRANSPORTATION OF
FREE FATTY ACIDS
Free fatty acids—also called unesterified (UFA) or
nonesterified (NEFA) fatty acids—are fatty acids
that are in the unesterified state.
In plasma, longer-chain FFA are combined
with albumin, and in the cell they are attached to
a fatty acid-binding protein.
Shorter-chain fatty acids are more water-
soluble and exist as the un-ionized acid or as a
fatty acid anion.
By these means, free fatty acids are made
accessible as a fuel in other tissues.
10/19/2012 Biochemistry For Medics 8
9. TYPES OF FATTY ACID
OXIDATION
Fatty acids can be oxidized by-
1) Beta oxidation- Major mechanism, occurs in the
mitochondria matrix. 2-C units are released as
acetyl CoA per cycle.
2) Alpha oxidation- Predominantly takes place in
brain and liver, one carbon is lost in the form of
CO2 per cycle.
3) Omega oxidation- Minor mechanism, but
becomes important in conditions of impaired beta
oxidation
4) Peroxisomal oxidation- Mainly for the trimming
of very long chain fatty acids.
10/19/2012 Biochemistry For Medics 9
10. BETA OXIDATION
Overview of beta oxidation
A saturated acyl Co A is degraded by a
recurring sequence of four reactions:
1) Oxidation by flavin adenine
dinucleotide (FAD)
2) Hydration,
3) Oxidation by NAD+, and
4) Thiolysis by Co ASH
10/19/2012 Biochemistry For Medics 10
11. BETA OXIDATION
The fatty acyl chain is shortened by
two carbon atoms as a result of these
reactions,
FADH2, NADH, and acetyl Co A are
generated.
Because oxidation is on the β carbon
and the chain is broken between the α
(2)- and β (3)-carbon atoms—hence
the name – β oxidation .
10/19/2012 Biochemistry For Medics 11
12. ACTIVATION OF FATTY
ACIDS
Fatty acids must first be converted to an active
intermediate before they can be catabolized. This
is the only step in the complete degradation of a
fatty acid that requires energy from ATP. The
activation of a fatty acid is accomplished in
two steps-
10/19/2012 Biochemistry For Medics 12
13. TRANSPORT OF FATTY ACID IN
TO MITOCHONDRIAL MATRIX
Fatty acids are activated on the outer mitochondrial
membrane, whereas they are oxidized in the mitochondrial
matrix.
Activated long-chain fatty acids are transported across the
membrane by conjugating them to carnitine, a zwitterionic
alcohol.
Carnitine (ß-hydroxy-Υ-trimethyl ammonium butyrate),
(CH3)3N+—CH2—CH(OH)—CH2—COO–, is widely distributed
and is particularly abundant in muscle. Carnitine is obtained
from foods, particularly animal-based foods, and via
endogenous synthesis. 10/19/2012 Biochemistry For Medics 13
14. ROLE OF CARNITINE
1) The acyl group is to the hydroxyl group of
carnitine to form acyl carnitine. This reaction is
catalyzed by carnitine acyl transferase I
2) Acyl carnitine is then shuttled across the inner
mitochondrial membrane by a translocase.
3) The acyl group is transferred back to CoA on
the matrix side of the membrane. This reaction,
which is catalyzed by carnitine acyl transferase
II.
Finally, the translocase returns carnitine to the
cytosolic side in exchange for an incoming acyl
carnitine
10/19/2012 Biochemistry For Medics 14
16. STEPS OF BETA
OXIDATION
Step-1
Dehydrogenation-
The first step is the
removal of two
hydrogen atoms from
the 2(α)- and 3(β)-
carbon atoms,
catalyzed by acyl-
CoA
dehydrogenase and
requiring FAD. This
results in the
formation of Δ2-trans-
enoyl-CoA and
10/19/2012 Biochemistry For Medics 16
17. STEPS OF BETA
OXIDATION
Electrons from the FADH2 prosthetic group of
the reduced acyl CoA dehydrogenase are
transferred to electron-
transferring flavoprotein (ETF).
ETF donates electrons to ETF: ubiquinone
reductase, an iron-sulfur protein.
Ubiquinone is thereby reduced to ubiquinol,
which delivers its high-potential electrons to the
second proton-pumping site of the respiratory
chain.
10/19/2012 Biochemistry For Medics 17
18. STEPS OF BETA
OXIDATION
Step-2- Hydration
Water is added to saturate
the double bond and form
3-hydroxyacyl-CoA,
catalyzed by Δ 2-enoyl-CoA
hydratase.
10/19/2012 Biochemistry For Medics 18
19. STEPS OF BETA
OXIDATION
Step-3-
dehydrogenation-
The 3-hydroxy derivative
undergoes further
dehydrogenation on the
3-carbon catalyzed by
L(+)-3-hydroxyacyl-
CoA dehydrogenase to
form the corresponding
3-ketoacyl-CoA
compound. In this case,
NAD+ is the coenzyme
involved.
10/19/2012 Biochemistry For Medics 19
20. STEPS OF BETA
OXIDATION
Step-4-
Thiolysis-
3-ketoacyl-CoA is
split at the 2,3-
position
by thiolase (3-
ketoacyl-CoA-
thiolase), forming
acetyl-CoA and a
new acyl-CoA two
carbons shorter
than the original
acyl-CoA
molecule.
10/19/2012 Biochemistry For Medics 20
21. STEPS OF BETA
OXIDATION
The acyl-CoA
formed in the
cleavage reaction
reenters the
oxidative pathway
at reaction 2.
Since acetyl-
CoA can be
oxidized to
CO2 and water via
the citric acid
cycle the
complete
oxidation of fatty
acids is achieved
10/19/2012 Biochemistry For Medics 21
22. BETA OXIDATION
The overall reaction can be represented as
follows-
10/19/2012 Biochemistry For Medics 22
23. BETA OXIDATION- ENERGY
YIELD
Energy yield by the complete oxidation of one
mol of Palmitic acid-
The degradation of palmitoyl CoA (C16-acyl Co A)
requires seven reaction cycles. In the seventh cycle,
the C4-ketoacyl CoA is thiolyzed to two molecules of
acetyl CoA.
106 (129 As per old concept) ATP are produced
by the complete oxidation of one mol of Palmitic
acid. 10/19/2012 Biochemistry For Medics 23
24. BETA OXIDATION- ENERGY
YIELD
2.5 ATPs per NADH = 17.5
1.5 ATPs per FADH2 = 10.5
10 ATPs per acetyl-CoA = 80
Total = 108 ATPs
2 ATP equivalents (ATP AMP + PPi
PPi 2 Pi)
consumed during activation of palmitate to
Palmitoyl CoA
Net Energy output- 108-2 = 106 ATP
10/19/2012 Biochemistry For Medics 24
25. DISORDERS ASSOCIATED
WITH IMPAIRED BETA
OXIDATION
1) Deficiencies of carnitine or carnitine
transferase or translocase
Symptoms include muscle cramps during
exercise, severe weakness and death.
Muscle weakness related to importance of
fatty acids as long term energy source
Hypoglycemia and hypo ketosis are common
findings
Diet containing medium chain fatty acids is
recommended since they do not require carnitine
shuttle to enter mitochondria.
10/19/2012 Biochemistry For Medics 25
26. DISORDERS ASSOCIATED
WITH IMPAIRED BETA
OXIDATION
2) Jamaican Sickness- Jamaican vomiting
sickness is caused by eating the unripe fruit of
akee tree, which contains the toxin hypoglycin,
that inactivates medium and short-chain acyl-
CoA dehydrogenases, inhibiting β oxidation and
thereby causing hypoglycemia.
3) Dicarboxylic aciduria is characterized by-
i) Excretion of C6–C10 -dicarboxylic acids and
ii) Nonketotic hypoglycemia which is caused
by lack of mitochondrial medium chain acyl-
CoA dehydrogenases.
10/19/2012 Biochemistry For Medics 26
27. DISORDERS ASSOCIATED
WITH IMPAIRED BETA
OXIDATION
4) Acute fatty liver of pregnancy
Manifests in the second half of pregnancy, usually
close to term, but may also develop in the
postpartum period.
The patient developed symptoms of hepatic
dysfunction at 36 weeks of gestation.
Short history of illness, hypoglycemia, liver failure,
renal failure, and coagulopathy are observed.
Diagnosis is made based on an incidental finding of
abnormal liver enzyme levels.
Affected patients may become jaundiced or
develop encephalopathy from liver failure, usually
reflected by an elevated ammonia level.
Profound hypoglycemia is common.
10/19/2012 Biochemistry For Medics 27
28. BETA OXIDATION OF ODD
CHAIN FATTY ACIDS
Fatty acids with an odd number of carbon atoms are
oxidized by the pathway of β-oxidation, producing
acetyl-CoA, until a three-carbon (propionyl-CoA)
residue remains. This compound is converted to
Succinyl-CoA, a constituent of the citric acid cycle
The propionyl residue from an odd-chain fatty acid is
the only part of a fatty acid that is glucogenic. Acetyl
CoA cannot be converted into pyruvate or Oxaloacetate
in animals. 10/19/2012 Biochemistry For Medics 28
29. BETA OXIDATION OF
UNSATURATED FATTY ACIDS
In the oxidation of unsaturated fatty acids,
most of the reactions are the same as those for
saturated fatty acids, only two additional
enzymes an isomerase and a reductase are
needed to degrade a wide range of unsaturated
fatty acids.
Energy yield is less by the oxidation of
unsaturated fatty acids since they are less
reduced.
Per double bonds 2 ATP are less formed,
since the first step of dehydrogenation to
introduce double bond is not required, For Medics
10/19/2012 Biochemistry as the 29
30. BETA OXIDATION OF
Palmitoleoyl Co A undergoes
UNSATURATED FATTY of degradation,
three cycles ACIDS
which are carried out by the
same enzymes as in the
oxidation of saturated fatty acids.
The cis- Δ 3-enoyl CoA formed
in the third round is not a
substrate for acyl CoA
dehydrogenase.
An isomerase converts this
double bond into a trans- Δ 2
double bond.
The subsequent reactions are
those of the saturated fatty acid
oxidation pathway, in which
the trans- Δ 2-enoyl CoA is a 30
10/19/2012 Biochemistry For Medics
31. BETA OXIDATION OF POLY
UNSATURATED FATTY ACIDS
10/19/2012 Biochemistry For Medics 31
32. BETA OXIDATION OF POLY
UNSATURATED FATTY ACIDS
A different set of enzymes is required for the oxidation of
Linoleic acid, a C18 polyunsaturated fatty acid with cis-Δ
9 and cis-Δ12 double bonds .
The cis- Δ 3 double bond formed after three rounds of β
oxidation is converted into a trans- Δ 2 double bond by
isomerase.
The acyl CoA produced by another round of β oxidation
contains a cis- Δ 4 double bond. Dehydrogenation of this
species by acyl CoA dehydrogenase yields a 2,4-
dienoyl intermediate, which is not a substrate for the next
enzyme in the β -oxidation pathway.
This impasse is circumvented by 2,4-dienoyl CoA
reductase, an enzyme that uses NADPH to reduce the
2,4-dienoyl intermediate to trans-D 3-enoyl CoA.
cis-Δ 3-Enoyl CoA isomerase then converts trans- Δ 3-
enoyl CoA into the trans- Δ 2 form, a customary
intermediate in the beta-oxidation pathway. For Medics
10/19/2012 Biochemistry 32
33. MINOR PATHWAYS OF
FATTY ACID OXIDATION
1) α- Oxidation- Oxidation occurs at C-2 instead
of C-3 , as in β oxidation
2) ω- Oxidation – Oxidation occurs at the
methyl end of the fatty acid molecule.
3) Peroxisomal fatty acid oxidation- Occurs for
the chain shortening of very long chain fatty
acids.
10/19/2012 Biochemistry For Medics 33
34. α- OXIDATION OF FATTY ACIDS
Takes place in the microsomes of brain and
liver,
Involves decarboxylation process for the
removal of single carbon atom at one time with
the resultant production of an odd chain fatty
acid that can be subsequently oxidized by beta
oxidation for energy production.
It is strictly an aerobic process.
No prior activation of the fatty acid is required.
The process involves hydroxylation of the
alpha carbon with a specific α-hydroxylase that
requires Fe++ and vitamin C/FH4 as cofactors.
10/19/2012 Biochemistry For Medics 34
35. BIOLOGICAL SIGNIFICANCE OF
ALPHA OXIDATION
α- Oxidation is most suited for the oxidation of
phytanic acid, produced from dietary phytol, a
constituent of chlorophyll of plants.
Phytanic acid is a significant constituent of milk
lipids and animal fats.
Normally it is metabolized by an initial α-
hydroxylation followed by dehydrogenation and
decarboxylation.
Beta oxidation can not occur initially because of the
presence of 3- methyl groups, but it can proceed
after decarboxylation.
The whole reaction produces three molecules of
propionyl co A, three molecules of Acetyl co A,
and one molecule of iso butyryl co A .
10/19/2012 Biochemistry For Medics 35
36. Phytanic acid
is oxidized by
Phytanic acid
α oxidase (α-
hydroxylase
enzyme) to
yield CO2 and
odd chain fatty
acid Pristanic
acid that can
be
subsequently
oxidized by
beta oxidation.
10/19/2012 Biochemistry For Medics 36
37. BIOLOGICAL SIGNIFICANCE OF
ALPHA OXIDATION
2)The hydroxy fatty acids produced as
intermediates of this pathway like Cerebronic
acid can be used for the synthesis of
cerebrosides and sulfatides
3) Odd chain fatty acids produced upon
decarboxylation in this pathway, can be used for
the synthesis of sphingolipids and can also
undergo beta oxidation to form propionyl co
A and Acetyl co A. The number of acetyl co A
depend upon the chain length. Propionyl co A is
converted to Succinyl co A to gain entry in to
TCA cycle for further oxidation.
10/19/2012 Biochemistry For Medics 37
38. CLINICAL SIGNIFICANCE
OF ALPHA OXIDATION
Refsum's disease (RD)-is a neurocutaneous
syndrome that is characterized biochemically by
the accumulation of phytanic acid in plasma and
tissues. Patients with Refsum disease are
unable to degrade phytanic acid because of a
deficient activity of Phytanic acid oxidase
enzyme catalyzing the first step of phytanic acid
alpha-oxidation.
Peripheral polyneuropathy, cerebellar
ataxia, retinitis pigmentosa, and Ichthyosis
(rough, dry and scaly skin) are the major
clinical components. The symptoms evolve
slowly and insidiously from childhood through
adolescence and early adulthood.
10/19/2012 Biochemistry For Medics 38
39. OMEGA OXIDATION OF
FATTY ACIDS
Involves hydroxylation and occurs in the
endoplasmic reticulum of many tissues.
Hydroxylation takes place on the methyl carbon
at the other end of the molecule from the carboxyl
group or on the carbon next to the methyl end.
It uses the “mixed function oxidase” type of
reaction requiring Cytochrome P450, O2 and
NADPH, as well as the necessary enzymes.
Hydroxy fatty acids can be further oxidized to a
dicarboxylic acid via sequential reactions of
Alcohol dehydrogenase and aldehyde
dehydrogenases.
The process occurs primarily with medium chain
fatty acids. 10/19/2012 Biochemistry For Medics 39
40. OMEGA OXIDATION OF
FATTY ACIDS
Dicarboxylic
acids so
formed can
undergo beta
oxidation to
produce
shorter chain
dicarboxylic
acids such as
Adipic
acids(C6)
and succinic
acid (C4).
10/19/2012 Biochemistry For Medics 40
41. SIGNIFICANCE OF OMEGA
OXIDATION
The microsomal (endoplasmic reticulum, ER)
pathway of fatty acid ω-oxidation represents a
minor pathway of overall fatty acid oxidation.
However, in certain pathophysiological states,
such as diabetes, chronic alcohol
consumption, and starvation, the ω-oxidation
pathway may provide an effective means for the
elimination of toxic levels of free fatty acids.
10/19/2012 Biochemistry For Medics 41
42. PEROXISOMAL OXIDATION OF VERY
LONG CHAIN FATTY ACIDS
In peroxisomes, a flavoprotein dehydrogenase
transfers electrons to O2 to yield H2O2 instead of
capturing the high-energy electrons as FADH2,
as occurs in mitochondrial beta oxidation.
Catalase is needed to convert the hydrogen
peroxide produced in the initial reaction into
water and oxygen.
Subsequent steps are identical with their
mitochondrial counterparts,
They are carried out by different isoform of the
enzymes.
10/19/2012 Biochemistry For Medics 42
43. PEROXISOMAL OXIDATION OF VERY
LONG CHAIN FATTY ACIDS
The specificity of the peroxisomal enzymes is for
longer chain fatty acids. Thus peroxisomal enzymes
function to shorten the chain length of relatively long
chain fatty acids to a point at which beta oxidation
can be completed in mitochondria.
10/19/2012 Biochemistry For Medics 43
44. SIGNIFICANCE OF
PEROXISOMAL OXIDATION
Peroxisomal reactions include chain
shortening of very long chain fatty acids,
dicarboxylic acids, conversion of cholesterol
to bile acids and formation of ether lipids.
The congenital absence of functional
peroxisomes, an inherited defect , causes
Zellweger syndrome.
10/19/2012 Biochemistry For Medics 44
45. ZELLWEGER SYNDROME
Zellweger syndrome, also
called cerebrohepatorenal syndrome is a rare,
congenital disorder (present at birth),
characterized by the reduction or absence of
Peroxisomes in the cells of the liver, kidneys,
and brain.
The most common features of Zellweger
syndrome include vision
disturbances, prenatal growth failure, lack of
muscle tone, unusual facial characteristics,
mental retardation, seizures, and an inability
to suck and/or swallow.
10/19/2012 Biochemistry For Medics 45
46. ZELLWEGER SYNDROME
The abnormally high levels of VLCFA( Very
long chain fatty acids ), are most diagnostic.
There is no cure for Zellweger syndrome, nor
is there a standard course of treatment.
Most treatments are symptomatic and
supportive.
Most infants do not survive past the first 6
months, and usually succumb to respiratory
distress, gastrointestinal bleeding, or liver
failure.
10/19/2012 Biochemistry For Medics 46