May 22, 2023
In the human body, fatty acids are oxidized in a variety of cell structures, including the mitochondria, where only beta-oxidation takes place, the peroxisome, where alpha- and beta-oxidation take place, and the endoplasmic reticulum, where omega-oxidation takes place.
When there is a high energy demand, such as during exercise, beta-oxidation is an important source of metabolic energy. Due to the release of circulating mediators like adrenaline and glucagon, which accelerate lipolysis, these metabolic circumstances cause the release of fatty acids from adipose tissue. When glycogen and gluconeogenic precursors are in short supply, this metabolic pathway meets a significant amount of the energy requirements of skeletal muscle, cardiac muscle, and kidneys. As a result, fatty acid oxidation offers a different, highly effective method of energy synthesis while also protecting muscles from catabolic deterioration. The body has to be cleansed of big, insoluble xenobiotic substances and lipid-based cellular components such sphingolipids and components of the plasma membrane.
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Fatty acids get oxidized in peroxisomes, mitochondria and nucleus. Very long-chain fatty acid gets oxidized in peroxisomes. Very short-chain fatty acid gets oxidized in Mitochondria. Short-chain, medium-chain, and long-chain fatty acids get oxidized in both Mitochondria, and peroxisome.
They are concerned with very long chain fatty acid oxidation. They are concerned with ether lipid (plasmalogen) synthesis and They are concerned with ⍺ oxidation of branched-chain fatty acids.
The carbon atom just before alpha carbon atom is ꞵ carbon atom. When the ꞵ carbon atom is oxidized, it is no more CH2. It becomes COOH (carboxyl group), I.e., we have pre-positioned the functional grp. Which will give us
CH3-CH2-CH2-COOH + CH3 - COOH
When the acetic acid gets attached to coA, we will call it acetyl CoA.
There are two carbon atoms .If there is n carbon containing fatty acid which undergoes ꞵ oxidation will always give n/2 Acetyl CoA because acetyl CoA contains 2 Carbon atoms Product of ꞵ oxidation of fatty acid is always acetyl-CoA molecules Peroxisome - the hydrogen peroxide generation due to ꞵ oxidation is peroxisome
|Fatty acids||Very short chain, short chain, medium chain and long chain fatty acids||Short chain, medium chain, long chain and Very long chain fatty acids|
|Type of Oxidation||ꞵ||ꞵ|
|Products||n/2 acetyl CoA||n/2 acetyl CoA|
The difference between mitochondrial oxidation and peroxisomal oxidation.:
When oxidation happens in Mitochondria, we remove the hydrogen atom from ꞵ carbon atom and give it to NAD and FAD, which further forms NADH and FADH2. When NADH and FADH2 go through an electron transfer chain, they give rise to ATP.
When oxidation happens in the peroxisome, we remove the hydrogen atom from ꞵ carbon atom and give it to the oxygen molecule. This then forms hydrogen peroxide (H2O2). To detoxify hydrogen peroxide, the peroxisome is equipped with catalase enzymes.
As soon as fatty acid gets into any cell, irrespective of the final fate of fatty acid, the 1st enzyme to act on this fatty acid will be acetyl CoA synthetase. This acetyl CoA synthetase uses 1 ATP which gets converted to AMP + PPI. This step uses two high energy phosphate and successfully converts fatty acid into acetyl CoA The purpose of acyl CoA synthetase is to trap fatty acid within the cell.Fatty acids are nonpolar substances. It can easily cross a cell membrane and get into cytoplasm. When entered in the cytoplasm, if we don't convert the fatty acid into any another form, the fatty acid concentration inside the cell becomes higher starts getting reflex across the membrane back into the circulation
Acyl CoA with carnitine gives acylcarnitine, and the enzyme is carnitine acyl transferase 1 (rate-limiting enzyme). Acyl carnitine crosses the inner mitochondrial membrane and enters the matrix. Once the acylcarnitine has entered the matrix if you retain the carrier the same carrier will put the acylcarnitine back into cytoplasm. Carnitine acyltransferase 2 releases the carnitine back and converts acylcarnitine to acyl CoA.
Steps of Phase I
Details of Phase 1 - Every Cycle
|Acyl CoA Dehydrogenase(co- enzyme: FAD)|
Ꞵ Hydroxyacyl CoA
dehydrogenase(co- enzyme: NAD)
|4 ATPs||Acetyl CoA|
The rate limiting enzyme of fatty acid oxidation is CPT1.
When 7 carbon-containing fatty acids are beta oxidized then on the first Cycle, the last two carbon atoms will come out as Acetyl CoA.
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To maintain blood glucose, we must Stimulate gluconeogenesis to support gluconeogenesis; there should be peripheral lipolysis. In starvation, where there is no insulin when there are excess counter-regulatory hormones, they stimulate hormone-sensitive lipase. During starvation, there is an increase in free fatty acid levels in the serum. The free fatty acid and glycerol, when in the liver, the glycerol will be used as a substrate for gluconeogenesis, and the fatty acid will be oxidized to provide the necessary energy for gluconeogenesis. During starvation, the Acetyl CoA produced can't go under the citric cycle because it requires oxaloacetate, but all the oxaloacetate is used to produce gluconeogenesis. Then the accumulated Acetyl CoA condenses to form ketone bodies.
In diabetics, there is absolute insulin deficiency there is peripheral lipolysis. Lipolysis is inevitable by insulin. In diabetes, there is excessive peripheral lipolysis, leading to the formation of glycerol and fatty acids. Therefore, a person loses weight wherever there is the aggression of insulin resistance.
The fatty acid and glycerol, when in the liver the glycerol, will be used as a substrate for gluconeogenesis. Gluconeogenesis is possible in insulin resistance because glucagon is hyperactive, and the fatty acid will be oxidized to provide the necessary energy for gluconeogenesis. The Acetyl CoA produced can't go under the citric cycle because it requires oxaloacetate, but all the oxaloacetate is used to produce gluconeogenesis. Then the accumulated Acetyl CoA condenses to form ketone bodies conversion of acetyl CoA to ketone bodies:
Whenever acetyl CoA accumulates, two molecules of acetyl CoA condenses each other in the presence of thiolase to form Acetyl acetyl CoA. Then this acetyl acetyl CoA reacts with another molecule of acetyl CoA in the presence of HMG CoA synthase to form HMG CoA Then the enzyme HMG CoA lyase takes of one acetyl CoA which gets recycled back, and that is how HMG CoA then it gets into first ketone body which is Acetoacetate. Acetoacetate On spontaneous decarboxylation forms acetone.In the presence of ꞵ hydroxybutyrate dehydrogenase forms ꞵ hydroxybutyrate using 1 NADH
This is everything that you need to know about fatty acid oxidation for your biochemistry preparation. For more interesting and informative blog posts like this download the PrepLadder App and keep reading our blog!
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