UPSC MainsBOTANY-PAPER-II201710 Marks
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Q23.

β-oxidation

How to Approach

This question requires a detailed explanation of β-oxidation, a crucial metabolic pathway. The answer should cover the steps involved, the location within the cell, the enzymes involved, the regulation of the process, and its significance. A clear, step-by-step description with relevant biochemical details is essential. Focus on the cyclical nature of the process and the products generated. Mentioning any associated disorders would add value.

Model Answer

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Introduction

β-oxidation is the catabolic process by which fatty acid molecules are broken down in the mitochondria and peroxisomes to generate acetyl-CoA, which can then be used in the citric acid cycle to produce energy. This pathway is vital for energy production, particularly during periods of fasting or prolonged exercise when glucose availability is limited. It’s a cyclical process that shortens the fatty acid chain by two carbon atoms with each turn, ultimately converting fats into a usable energy source. Understanding β-oxidation is fundamental to comprehending lipid metabolism and its role in maintaining energy homeostasis.

Overview of β-oxidation

β-oxidation is the primary pathway for the breakdown of fatty acids. It occurs primarily within the mitochondrial matrix in eukaryotes, although very long-chain fatty acids undergo initial oxidation in the peroxisomes. The process involves a series of four repeating enzymatic reactions that cleave two-carbon units from the carboxyl end of the fatty acid.

The Four Steps of β-oxidation

Each cycle of β-oxidation consists of the following four steps:

  1. Oxidation: Acyl-CoA dehydrogenase catalyzes the oxidation of acyl-CoA to trans-Δ2-enoyl-CoA, introducing a double bond between the α and β carbons. This reaction generates FADH2. Different acyl-CoA dehydrogenases exist for short, medium, and long-chain fatty acids.
  2. Hydration: Enoyl-CoA hydratase adds water across the double bond, forming L-β-hydroxyacyl-CoA.
  3. Oxidation: β-hydroxyacyl-CoA dehydrogenase oxidizes L-β-hydroxyacyl-CoA to β-ketoacyl-CoA, generating NADH.
  4. Thiolysis: β-ketothiolase cleaves β-ketoacyl-CoA, releasing acetyl-CoA and a shortened acyl-CoA molecule. This acyl-CoA then re-enters the cycle, repeating the four steps until the fatty acid is completely broken down.

Energetics of β-oxidation

The complete oxidation of one molecule of palmitic acid (a 16-carbon saturated fatty acid) yields:

  • 8 molecules of acetyl-CoA
  • 7 molecules of FADH2
  • 7 molecules of NADH

These coenzymes are then used in the citric acid cycle and oxidative phosphorylation to generate ATP. Approximately 106 ATP molecules are produced from the complete oxidation of one palmitic acid molecule (as of knowledge cutoff 2023).

Regulation of β-oxidation

β-oxidation is regulated by several factors:

  • Carnitine Shuttle: The transport of long-chain fatty acids into the mitochondrial matrix is mediated by the carnitine shuttle. This is a rate-limiting step and is regulated by malonyl-CoA, an intermediate in fatty acid synthesis. High levels of malonyl-CoA inhibit carnitine acyltransferase I, preventing fatty acid entry into the mitochondria.
  • Hormonal Control: Hormones like insulin, glucagon, and epinephrine influence β-oxidation. Insulin inhibits β-oxidation, while glucagon and epinephrine stimulate it.
  • NADH/NAD+ and FADH2/FAD ratios: High levels of NADH and FADH2 inhibit the dehydrogenases involved in β-oxidation, indicating sufficient energy levels.

Peroxisomal β-oxidation

Very long-chain fatty acids (longer than 22 carbons) are primarily oxidized in peroxisomes. Peroxisomal β-oxidation differs from mitochondrial β-oxidation in several ways:

  • The first step is catalyzed by acyl-CoA oxidase, which produces hydrogen peroxide (H2O2) as a byproduct.
  • Peroxisomal β-oxidation does not directly produce ATP.
  • The shortened acyl-CoA molecules produced in peroxisomes are then transported to the mitochondria for further oxidation.

Clinical Significance

Defects in β-oxidation can lead to various metabolic disorders, such as:

  • Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency: This is a common inherited metabolic disorder that prevents the breakdown of medium-chain fatty acids. It can cause hypoglycemia, lethargy, and even sudden death, particularly during periods of fasting.
  • Carnitine deficiency: This can impair the transport of fatty acids into the mitochondria, leading to energy deficits.

Conclusion

β-oxidation is a critical metabolic pathway for energy production from fatty acids. Its cyclical nature, regulated steps, and compartmentalization within mitochondria and peroxisomes ensure efficient and controlled lipid metabolism. Understanding the intricacies of this process is crucial for comprehending metabolic disorders and developing strategies to address them. Further research into the regulation and optimization of β-oxidation could offer potential therapeutic avenues for metabolic diseases and energy imbalances.

Answer Length

This is a comprehensive model answer for learning purposes and may exceed the word limit. In the exam, always adhere to the prescribed word count.

Additional Resources

Key Definitions

Acyl-CoA
A molecule composed of a fatty acid chain linked to coenzyme A, serving as the activated form of fatty acids for metabolism.
Malonyl-CoA
An intermediate in fatty acid synthesis that inhibits carnitine acyltransferase I, thereby regulating the entry of fatty acids into the mitochondria for β-oxidation.

Key Statistics

Approximately 70-80% of the body’s energy needs are met by the oxidation of fats during rest.

Source: Guyton and Hall Textbook of Medical Physiology (Knowledge cutoff 2023)

MCAD deficiency affects approximately 1 in 17,000 newborns.

Source: National Newborn Screening & Genetic Testing Program (Knowledge cutoff 2023)

Examples

Ketogenesis

During prolonged fasting or in uncontrolled diabetes, when glucose availability is limited, β-oxidation increases significantly. This leads to the production of ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone) as an alternative fuel source for the brain and other tissues.

Frequently Asked Questions

What is the role of carnitine in β-oxidation?

Carnitine acts as a shuttle to transport long-chain fatty acids across the inner mitochondrial membrane, where β-oxidation occurs. It forms acylcarnitine, which is then transported into the matrix by carnitine acyltransferase I and II.

Topics Covered

BiochemistryCell BiologyMetabolismEnergy ProductionFatty Acids