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Overview about Beta Oxidation of Fatty Acids.pptx

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Abdelrhman Abooda
Abdelrhman Abooda

Beta Oxidation of Fatty Acids

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Beta Oxidation of Fatty Acids
Fatty Acids • Fatty acids are the building blocks of the fat in our bodies and in the food we eat. During digestion, the body breaks down fats into fatty acids, which can then be absorbed into the blood. • Fatty acid molecules are usually joined together in groups of three, forming a molecule called a triglyceride.
Fatty Acid oxidation types • Oxidation of fatty acids occurs in multiple regions of the cell within the human body; the mitochondria, in which only beta-oxidation occurs; the peroxisome, where alpha- and beta-oxidation occur; and omega- oxidation, which occurs in the endoplasmic reticulum.
Beta-Oxidation • Beta-Oxidation may be defined as the oxidation of fatty acids on the beta- carbon atom. • This results in the sequential removal of a two carbon fragment, acetyl CoA.
Stages and tissues • Three stages • Activation of fatty acids occurring in the cytosol • Transport of fatty acids into mitochondria • Beta-Oxidation proper in the mitochondrial matrix • Fatty acids are oxidized by most of the tissues in the body. • Brain, erythrocytes and adrenal medulla cannot utilize fatty acids for energy requirement.
Fatty acid activation • Fatty acids are activated to acyl CoA by thiokinases or acyl CoA synthetases • The reaction occurs in two steps and requires ATP, coenzyme A and Mg2+ • Fatty acid reacts with ATP to form acyladenylate which then combines with coenzyme A to produce acyl CoA. • Two high energy phosphates are utilized, since ATP is converted to pyrophosphate (PPi). • The enzyme inorganic pyrophosphafase hydrolyses PPi to phosphate. • The immediate elimination of PPi makes this reaction totally irreversible.
Activation of fatty acid to Acyl CoA
- β Oxidation Proper • Each cycle of β -oxidation, liberating a two carbon unit-acetyl CoA, occurs in a sequence of four reactions 1 . Oxidation 2 . Hydration 3 . Oxidation 4 . Cleavage
1.Oxidation • Acyl CoA undergoes dehydrogenation by an FAD-dependent flavoenzyme, acyl CoA dehydrogenase. • A double bond is formed between α and β carbons (i.e., 2 and 3 carbons) 2.Hydration • Enoyl CoA hydratase brings • about the hydration of the double bond to form β -hydroxyacyl CoA.
3.Oxidation • β-Hydroxyacyl CoA dehydrogenase • catalyses the second oxidation and generates NADH. • The product formed is β-ketoacyl CoA. 4.Cleavage • The final reaction in β -oxidation is the liberation of a 2 carbon fragment, acetyl CoA from acyl CoA. • This occurs by a thiolytic cleavage catalysed by β-ketoacyl CoA thiolase (or thiolase).
Overview about Beta Oxidation of Fatty Acids.pptx
Overview about Beta Oxidation of Fatty Acids.pptx
Overview about Beta Oxidation of Fatty Acids.pptx
Regulation of Beta Oxidation During Fasting and Fed State • Fasting State: • Low Insulin, High Glucagon: • Insulin Levels: Insulin levels are low during fasting. • Glucagon Levels: Glucagon levels are elevated, signaling a need for increased energy production. • Activation of Hormone-Sensitive Lipase (HSL): • Fasting activates HSL: Hormone-sensitive lipase is activated in response to low insulin levels and high glucagon levels. • Lipolysis: HSL promotes the breakdown of triglycerides into fatty acids and glycerol in adipose tissue. • Transport of Fatty Acids into Mitochondria: • Carnitine Shuttle Activation: Fatty acids are transported into the mitochondria for beta-oxidation via the carnitine shuttle. • Carnitine Palmitoyltransferase-1 (CPT-1): CPT-1 activity increases, allowing fatty acids to enter the mitochondrial matrix.
Regulation of Beta Oxidation During Fasting and Fed State • Fed State: • High Insulin, Low Glucagon: • Insulin Dominance: Insulin levels are elevated during the fed state. • Glucagon Suppression: Glucagon levels decrease. • Inhibition of Hormone-Sensitive Lipase (HSL): • Insulin Effect on HSL: Insulin inhibits HSL, reducing lipolysis and the release of fatty acids from adipose tissue. • Decreased Fatty Acid Oxidation: • Inhibition of Beta-Oxidation Enzymes: Insulin inhibits AMPK, reducing the activation of enzymes involved in beta-oxidation. • Promotion of Lipogenesis: Insulin promotes lipogenesis (fatty acid synthesis) and storage of triglycerides.
Beta Oxidation Of fatty Acids Importance • Beta-oxidation is a significant source of metabolic energy during interprandial periods and high energy demand states, such as exercise. • In addition to glucose, many cell types rely on fatty acids as a source of energy. The fatty acid β-oxidation pathway is an evolutionarily well- conserved process of metabolizing fatty acids within the mitochondria to generate acetyl-coA and ATP.
Beta Oxidation Of fatty Acids Importance • Mitochondrial fatty acid β-oxidation disorders • Mitochondrial fatty acid β-oxidation disorders (FAODs) are a heterogeneous group of defects in fatty acid transport and mitochondrial β-oxidation. • They are inherited as autosomal recessive disorders and have a wide range of clinical presentations.
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Overview about Beta Oxidation of Fatty Acids.pptx

  • 1. Beta Oxidation of Fatty Acids
  • 2. Fatty Acids • Fatty acids are the building blocks of the fat in our bodies and in the food we eat. During digestion, the body breaks down fats into fatty acids, which can then be absorbed into the blood. • Fatty acid molecules are usually joined together in groups of three, forming a molecule called a triglyceride.
  • 3. Fatty Acid oxidation types • Oxidation of fatty acids occurs in multiple regions of the cell within the human body; the mitochondria, in which only beta-oxidation occurs; the peroxisome, where alpha- and beta-oxidation occur; and omega- oxidation, which occurs in the endoplasmic reticulum.
  • 4. Beta-Oxidation • Beta-Oxidation may be defined as the oxidation of fatty acids on the beta- carbon atom. • This results in the sequential removal of a two carbon fragment, acetyl CoA.
  • 5. Stages and tissues • Three stages • Activation of fatty acids occurring in the cytosol • Transport of fatty acids into mitochondria • Beta-Oxidation proper in the mitochondrial matrix • Fatty acids are oxidized by most of the tissues in the body. • Brain, erythrocytes and adrenal medulla cannot utilize fatty acids for energy requirement.
  • 6. Fatty acid activation • Fatty acids are activated to acyl CoA by thiokinases or acyl CoA synthetases • The reaction occurs in two steps and requires ATP, coenzyme A and Mg2+ • Fatty acid reacts with ATP to form acyladenylate which then combines with coenzyme A to produce acyl CoA. • Two high energy phosphates are utilized, since ATP is converted to pyrophosphate (PPi). • The enzyme inorganic pyrophosphafase hydrolyses PPi to phosphate. • The immediate elimination of PPi makes this reaction totally irreversible.
  • 7. Activation of fatty acid to Acyl CoA
  • 8. - β Oxidation Proper • Each cycle of β -oxidation, liberating a two carbon unit-acetyl CoA, occurs in a sequence of four reactions 1 . Oxidation 2 . Hydration 3 . Oxidation 4 . Cleavage
  • 9. 1.Oxidation • Acyl CoA undergoes dehydrogenation by an FAD-dependent flavoenzyme, acyl CoA dehydrogenase. • A double bond is formed between α and β carbons (i.e., 2 and 3 carbons) 2.Hydration • Enoyl CoA hydratase brings • about the hydration of the double bond to form β -hydroxyacyl CoA.
  • 10. 3.Oxidation • β-Hydroxyacyl CoA dehydrogenase • catalyses the second oxidation and generates NADH. • The product formed is β-ketoacyl CoA. 4.Cleavage • The final reaction in β -oxidation is the liberation of a 2 carbon fragment, acetyl CoA from acyl CoA. • This occurs by a thiolytic cleavage catalysed by β-ketoacyl CoA thiolase (or thiolase).
  • 14. Regulation of Beta Oxidation During Fasting and Fed State • Fasting State: • Low Insulin, High Glucagon: • Insulin Levels: Insulin levels are low during fasting. • Glucagon Levels: Glucagon levels are elevated, signaling a need for increased energy production. • Activation of Hormone-Sensitive Lipase (HSL): • Fasting activates HSL: Hormone-sensitive lipase is activated in response to low insulin levels and high glucagon levels. • Lipolysis: HSL promotes the breakdown of triglycerides into fatty acids and glycerol in adipose tissue. • Transport of Fatty Acids into Mitochondria: • Carnitine Shuttle Activation: Fatty acids are transported into the mitochondria for beta-oxidation via the carnitine shuttle. • Carnitine Palmitoyltransferase-1 (CPT-1): CPT-1 activity increases, allowing fatty acids to enter the mitochondrial matrix.
  • 15. Regulation of Beta Oxidation During Fasting and Fed State • Fed State: • High Insulin, Low Glucagon: • Insulin Dominance: Insulin levels are elevated during the fed state. • Glucagon Suppression: Glucagon levels decrease. • Inhibition of Hormone-Sensitive Lipase (HSL): • Insulin Effect on HSL: Insulin inhibits HSL, reducing lipolysis and the release of fatty acids from adipose tissue. • Decreased Fatty Acid Oxidation: • Inhibition of Beta-Oxidation Enzymes: Insulin inhibits AMPK, reducing the activation of enzymes involved in beta-oxidation. • Promotion of Lipogenesis: Insulin promotes lipogenesis (fatty acid synthesis) and storage of triglycerides.
  • 16. Beta Oxidation Of fatty Acids Importance • Beta-oxidation is a significant source of metabolic energy during interprandial periods and high energy demand states, such as exercise. • In addition to glucose, many cell types rely on fatty acids as a source of energy. The fatty acid β-oxidation pathway is an evolutionarily well- conserved process of metabolizing fatty acids within the mitochondria to generate acetyl-coA and ATP.
  • 17. Beta Oxidation Of fatty Acids Importance • Mitochondrial fatty acid β-oxidation disorders • Mitochondrial fatty acid β-oxidation disorders (FAODs) are a heterogeneous group of defects in fatty acid transport and mitochondrial β-oxidation. • They are inherited as autosomal recessive disorders and have a wide range of clinical presentations.
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