chapter 16 part 2 n.
Skip this Video
Download Presentation
Chapter 16 (Part 2)

Loading in 2 Seconds...

play fullscreen
1 / 24

Chapter 16 (Part 2) - PowerPoint PPT Presentation

  • Uploaded on

Chapter 16 (Part 2). Fatty acid Catabolism ( b -oxidation). Beta Oxidation of Fatty Acids. Process by which fatty acids are degraded by removal of 2-C units b -oxidation occurs in the mitochondria matrix The 2-C units are released as acetyl-CoA, not free acetate

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Chapter 16 (Part 2)' - iliana

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
chapter 16 part 2

Chapter 16 (Part 2)

Fatty acid Catabolism



Beta Oxidation of Fatty Acids

  • Process by which fatty acids are degraded by removal of 2-C units
  • b-oxidation occurs in the mitochondria matrix
  • The 2-C units are released as acetyl-CoA, not free acetate
  • The process begins with oxidation of the carbon that is "beta" to the carboxyl carbon, so the process is called"beta-oxidation"
fatty acids must first be activated by formation of acyl coa
Fatty acids must first be activated by formation of acyl-CoA
  • Acyl-CoA synthetase condenses fatty acids with CoA, with simultaneous hydrolysis of ATP to AMP and PPi
  • Formation of a CoA ester is expensive energetically
  • Reaction just barely breaks even with ATP hydrolysis DGo’ATP hydroysis = -32.3 kJ/mol, DGo’ Acyl-CoA synthesis +31.5 kJ/mol.
  • But subsequent hydrolysis of PPi drives the reaction strongly forward (DGo’ –33.6 kJ/mol)
import of acyl coa into mitochondria
Import of acyl-CoA into mitochondria
  • b-oxidation occurs in the mitochondria, requires import of long chain acyl-CoAs
  • Acyl-CoAs are converted to acyl-carnitines by carnitine acyltransferase.
  • A translocator then imports Acyl carnitine into the matrix while simultaneously exporting free carnitine to the cytosol
  • Acyl-carnitine is then converted back to acyl-CoA in the matrix
Deficiencies of carnitine or carnitine transferase or translocator activity are related to disease state
  • Symptons include muscle cramping during exercise, severe weakness and death.
  • Affects muscles, kidney, and heart tissues.
  • Muscle weakness related to importance of fatty acids as long term energy source
  • People with this disease supplement diet with medium chain fatty acids that do not require carnitine shuttle to enter mitochondria.
b oxidation
  • Strategy: create a carbonyl group on the -C
  • First 3 reactions do that; fourth cleaves the "-keto ester" in a reverse Claisen condensation
  • Products: an acetyl-CoA and a fatty acid two carbons shorter
b oxidation1
  • B-oxidation of palmitate (C16:0) yields 106 molecules of ATP
  • C 16:0-CoA + 7 FAD + 7 NAD+ + 7 H20 + 7 CoA  8 acetyl-CoA + 7 FADH2 + 7 NADH + 7 H+

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 acyl-CoA
  • Net yield = 106 ATPs

Acyl-CoA Dehydrogenase

  • Oxidation of the C-C bond
  • Mechanism involves proton abstraction, followed by double bond formation and hydride removal by FAD
  • Electrons are passed to an electron transfer flavoprotein, and then to the electron transport chain.

Enoyl-CoA Hydratase

  • aka crotonases
  • Adds water across the double bond
  • Uses substrates with trans-D2-and cis D2 double bonds (impt in b-oxidation of unsaturated FAs)
  • With trans-D2 substrate forms L-isomer, withcis D2 substrate forms D-isomer.
  • Normal reaction converts trans-enoyl-CoA to L--hydroxyacyl-CoA

Hydroxyacyl-CoA Dehydrogenase

  • Oxidizes the -Hydroxyl Group to keto group
  • This enzyme is completely specific for L-hydroxyacyl-CoA
  • D-hydroxylacyl-isomers are handled differently
  • Produces one NADH


  • Nucleophillic sulfhydryl group of CoA-SH attacks the b-carbonyl carbon of the 3-keto-acyl-CoA.
  • Results in the cleavage of the Ca-Cb bond.
  • Acetyl-CoA and an acyl-CoA (-) 2 carbons are formed
b oxidation of odd chain fatty acids
b-oxidation of odd chain fatty acids
  • Odd chain fatty acids are less common
  • Formed by some bacteria in the stomachs of rumaniants and the human colon.
  • b-oxidation occurs pretty much as w/ even chain fatty acids until the final thiolase cleavage which results in a 3 carbon acyl-CoA (propionyl-CoA)
  • Special set of 3 enzymes are required to further oxidize propionyl-CoA
  • Final Product succinyl-CoA enters TCA cycle
b oxidation of unsaturated fatty acids
b-oxidation of unsaturated fatty acids
  • b-oxidation occurs normally for 3 rounds until a cis-D3-enoyl-CoA is formed.
  • Acyl-CoA dehydrogenase can not add double bond between the a and b carbons.
  • Enoyl-CoA isomerase converts this to trans- 2 enoly-CoA
  • Now the b-oxidation can continue on w/ the hydration of the trans-D2-enoyl-CoA
  • Odd numbered double bonds handled by isomerase

Ketone Bodies

  • A special source of fuel and energy for certain tissues
  • Produced when acetyl-CoA levels exceed the capacity of the TCA cycle (depends on OAA levels)
  • Under starvation conditions no carbos to produced anpleorotic intermediates
  • Some of the acetyl-CoA produced by fatty acid oxidation in liver mitochondria is converted to acetone, acetoacetate and -hydroxybutyrate
  • These are called "ketone bodies"
  • Source of fuel for brain, heart and muscle
  • Major energy source for brain during starvation
  • They are transportable forms of fatty acids!

Re-utilization of

ketone bodies

Formation of

ketone bodies

ketone bodies and diabetes
Ketone Bodies and Diabetes
  • Lack of insulin related to uncontrolled fat breakdown in adipose tissues
  • Excess b-oxidation of fatty acids results in ketone body formation.
  • Can often smell acetone on the breath of diabetics.
  • High levels of ketone bodies leads to condition known as diabetic ketoacidosis.
  • Because ketone bodies are acids, accumulation can lower blood pH.

The Glyoxylate Cycle

  • A variant of TCA for plants and bacteria
  • Acetate-based growth - net synthesis of carbohydrates and other intermediates from acetate - is not possible with TCA
  • Glyoxylate cycle offers a solution for plants and some bacteria and algae
  • The CO2-evolving steps are bypassed and an extra acetate is utilized
  • Isocitrate lyase and malate synthase are the short-circuiting enzymes

Glyoxylate Cycle

  • Rxns occur in specialized organelles (glycoxysomes)
  • Plants store carbon in seeds as oil
  • The glyoxylate cycle allows plants to use acetyl-CoA derived from B-oxidation of fatty acids for carbohydrate synthesis
  • Animals can not do this! Acetyl-CoA is totally oxidized to CO2
  • Malate used in gluconeogenesis