The text has so far focused on the carbohydrates in the discussion of the generation and storage of metabolic energy.
The authors turn to the fatty acids as a fuel.
They explain why fats are the most concentrated energy stores.
The pathway of oxidation of fatty acids, which makes it available to the cell, is then presented.
The formation and role of the ketone bodies as acetyl transport molecules in circulation are discussed.
The text describes how the two acids are made.
An outline of the control of the oxidation and synthesis of fatty acids is provided.
The text ends this chapter with an introduction to the eicosanoid hormones.
A review of Chapter 12 will show you the structures of the fatty acids, the role of the lipids in the membranes, and the effect of the fatty acids on the structure of the membranes.
You should be able to complete the objectives once you have mastered this chapter.
The position of a double bond in a fatty acid can be specified by specifying the a, b, and w carbon atoms.
An overview of the synthesis and catabolism of fatty acids can be provided by listing the types of chemical reactions used.
It is appreciated that the albumin carries the fat from the adipocyte to other tissues.
There are three types of reactions carried out by cobalamin.
Provide the basis for the inability of animals to convert fat into sugar.
List the products of the committed step in the synthesis of fatty acid.
The sources of the NADPH are listed.
Give the systematic name, common name, and abbreviations for each of the four naturally occurring fatty acids.
The name and abbreviations of the compounds can be found in the D convention.
The position of the double bond is indicated by using the w convention.
The fatty acids should be placed in the order of the melting point.
Predict the residual acids from the oxidation of phenylpentanoic and phenyl hexanoic acids in a dog.
The phenyl rings and two of the methylene groups can't be metabolized.
Place the incomplete list of reactions in the proper order.
Indicate whether the following statement is true or false and explain your answer: after a meal rich in carbohydrates, acetyl CoA levels rise and ketone body synthesis increases.
D-Methylmalonyl CoA is converted to L-Methylmalonyl CoA.
Match the reactant or characteristic in the right column with the appropriate pathway in the left column.
The activities necessary to synthesise acetyl CoA and malonyl CoA are contained in the fatty acid synthase of mammals.
Oleate is the major product of the fatty acid synthase complex.
The undissociated form of the fatty acids is shown in question 2.
The order of e, c, a, b is determined by the content of double bonds of the C18 fatty acids.
Double bonds decrease intermolecular interactions and packing in the solid state.
The chain length, C16 versus C18, is what determines the order of (d) relative to (b).
The compound with the phenyl group would give rise to the acid.
phenylacetic acid would be degraded to phenylhexanoic acid.
The results suggested that the carbon atoms were being removed two at a time and that the fatty acids were being metabolized from the carboxyl terminus.
The oxidation of the b carbon atom was a likely step in the degradation.
The triacylglycerols have a high proportion.
The lower the amount of fat in the body, the higher the energy content (9 kcal/g) is.
On the basis of actual storage weight, triacylglycerols have six times more calories per gram than glycogen does.
The conversion of triacylglycerols into glyceraldehyde 3-phosphate can give rise to glucose.
The thioester linkage joins the fatty acid to CoA, which acts as a tag or handle by which the b-oxidation path can recognize, bind, and act on the saturated alkane chains of the fatty acids.
Since the thioester linkage is a high-energy bond, it can transfer the acyl group to carnitine, a reaction that is necessary to deliver the acyl group from the cytosol to the mitochondrial matrix for oxidation.
The large and negative value for the free energy of hydrolysis for acetyl CoA indicates that energy is required to synthesise it and that it can serve as an "activated" donor of acetyl groups.
The acyl group is transferred to the sulfhydryl group of CoA to form the thioester bond.
One acyl CoA is made from two ATPs.
The b-oxidation pathway is found in the matrix of the Mitochondrion.
CoA and its acyl derivatives are not allowed to pass through the mitochondria.
carnitine and its acyl derivatives can be shuttled across the inner mitochondria.
The acyl group is transferred from the matrix side to the inner side.
Two rounds of b oxidation are needed to produce 3 acetyl CoA.
2 FADH2 and 2 NADH molecule are produced by the two cycles.
Each acetyl CoA yields 10, each FADH2 produces 1.5, and each NADH makes 2.5.
The net yield is approximately 36 ATP because of the products of the reaction.
Oxaloacetate levels are high and acetyl CoA is condensation of oxaloacetate.
It is used for energy production.
acetyl CoA is abundant but oxaloacetate is low.
Choice (c) is correct because 3-hydroxybutyrate is in equilibrium with ace toacetate, the actual source of acetone.
ketone bodies are the form of acetyl units in blood.
A, c, d. Acyl CoA is involved in both synthesis and ox idation.
HCO3 is fixed to form a dicarboxylic acid.
This helps the condensation reactions with activated acyl groups to form an acetoacyl-ACP by releasing CO2
In order to form active sites at the interface of the subunits, the interactions of the different domains need to be made.
One is linked to the activated acetyl unit while the other is holding the acyl chain.
For a discussion about the correct answers, see pp.
6 acetyl CoA molecules are required for a C12:0 fatty acid.
One serves as a primer and five undergo condensation reactions as malonyl CoA derivatives.
Each malonyl CoA needs 1 ATP and 2 NADPH to be formed.
It is necessary for 5 ATP and 10 NADPH.
Acetyl CoA carboxylase is inactivated.
This effect is partially made up of citrate, which acts as an allosteric activator.
CHAPTER 22 of this enzyme is under the control of hormones and is dependent on aAMP not cAMP.
The acetyl CoA carboxylase is stimulated by high energy charge.
There are additional desaturations required.
Answer (c) is incorrect because the eicosanoid hormones exert local rather than global effects.
Answer (e) is correct because of the arachidonate.
The cyclooxygenase component of prostaglandin synthase is a part ofAspirin acetylates.
The inflammatory response is caused by prostaglandins, thromboxanes, and prostacyclin.
The fact that these systems exist in plants is important to animals.
See question 5 of the self-test.
In the a-oxidative decarboxylation of a free fatty acid, oxygen is used to oxidize it, which results in a shorter aldehyde.
The oxidation of the aldehyde to the acid is accomplished by the use of the electron acceptor, NAD+.
The oxidation of the fatty acid is caused by these steps being repeated.
The NADH generated through the oxidation of palmitate could be reoxidized in the electron transport chain.
Compare the yield of ATP generated by the oxidation of palmitate with that generated by the oxidation of the same fatty acid.
The products of the final round of oxidation are carbon dioxide and acetic acid.
Although most components of the diet contain unbranched chains, some plant tissues contain strontiums at odd numbered carbons in the acyl chain.
b oxidation can't break down these fatty acids.
The subject of study is the oxidation of long-chain alkanes, which are found in crude oil, because of concern about oil spills.
Alkane oxidation occurs in manybacteria.
An alkane is converted to a primary alcohol by using a monooxygenase.
Studies show that three more reactions are required for alcohol to oxidize.
A pathway for the conversion of a long-chain primary alcohol to a substrate that can undergo b oxidation is proposed.
You should include cofactors and electron acceptors.
Malonyl CoA, labeled with 14C in the methylene carbon, is used in excess in a system for the synthesis of palmitoyl CoA.
The structure of methylmalonyl CoA is shown below, which is an intermediate in the conversion of propionyl CoA to succinyl CoA.
This compound is similar to malonyl CoA.
High levels of methylmalonyl CoA are observed in people who are unable to convert propionyl CoA to succinyl CoA.
The majority of the fatty acids in the diet of animals are not even-numbered.
There are two reasons why this is possible.
There are li pases in the spherosome that convert triacylglycerol to monoacylglycerols.
Most of the glycerol is converted into free fatty acids in the plant cell.
Monoacylglycerols are converted to free fatty acids and glycerol by a lipase.
People who are concerned about their weight should pay attention to the amount of food they eat and the amount of calories they burn.
Less than five percent of the energy stored in the body is present as glycogen.
The b-oxidation pathway has a wide range of specificities for acyl chain lengths.
The synthesis of ketone bodies is carried out by the lyme.
Suppose a liver cell converts palmitic acid to acetoacetate and then exports it.
In culture, cells that are deficient can be isolated.
When compared with normal cells, they exhibit a slightly lower rate of synthesis.
It is very difficult to isolated cells without citrate lyase.
The linolenate can be synthesised from both the mitochondria and the reticular acyl-chain.
The b-oxidation pathway degraded the D10 bond.
Desert mammals can survive long periods of dry weather by consuming plants and seeds and generating water by metabolizing the fuels they provide.
Explain the reactions that lead to the formation of water.
You are looking at the mitochondria from the muscle cells of an infant who has a deficiency in one of the enzymes.
The rate of oxygen utilization is decreased when the mitochondria are incubated with linoleoyl CoA in the presence of palmitoyl CoA.
The levels of carnitine in the patient's blood and urine are low.
The net synthesis of pyruvate or oxaloacetate can't be done with acetyl CoA from fatty acid oxidation in mammals.
When 14C-labeled acetate is introduced into human tissue culture cells, it can convert to acetyl CoA.
Radioactive fatty acids can be used to label.
The lack of anidase that can introduce double bonds beyond the C-9 is what makes animals unable to synthesise linoleate and linolenate.
The eicosanoid hormones and a number of other needed fatty acids are produced by these unsaturated fatty acids.
The source of linoleate and linolenate is found in plants.
If 15 of the 16 carbons of palmitate are generated with one molecule of NADH, the yield of the molecule is 2.5 x 15.
The acetate molecule needs 2ATP to be activated.
The oxidation of acetyl CoA resulted in 10 ATP molecules.
The oxidation of a molecule of palmitate resulted in the creation of 45.5 molecules of ATP.
A single molecule of acetyl CoA and a single molecule of carbon dioxide would not be glucogenic.
The b carbon is blocked by the methyl group after oxidation.
The oxidation of a carbon in the palmitate derivative followed by decarboxylation of the molecule yields a fatty acid that has a methyl group at an even-numbered carbon.
The oxidation at the b carbon results in the generation of propionyl CoA and a shortened acyl derivative, lauroyl CoA.
Intermediates that can enter normal oxidative pathways can be created by the oxidation and decarboxylation of a branched-chain fatty acid.
The normal route for b oxidation inbacteria uses acyl CoA derivatives.
Two steps are needed to convert a primary alcohol to a free fatty acid.
The aldehyde is an intermediate in the conversion of a primary alcohol to a fatty acid.
The conversion of the free fatty acid to an acyl CoA derivative requires two equivalents of the acyl CoA.
Acyl CoA synthase is involved in the reaction.
Carbons 4 and 3 are not labeled because they are derived from acetyl CoA.
Carbons 15 and 16 of palmitate will be created by these two carbons.
C-2 of acetoacetyl-ACP is derived from the methylene carbon of malonyl-ACP.
When the second round of synthesis begins, butyryl-ACP condenses with a second molecule of methylene-labeled malonyl-ACP, which contributes C-1 and C-2 of the newly formed six-carbon ACP derivative.
C-2 and C-4 will be labeled.
Until palmitoyl-ACP is formed, chain extension continues.
Each even-numbered carbon atom will be labeled.
Carnitine acyltransferase I helps the transfer of long-chain fatty acids into the Mitochondrion.
Long-chain fatty acids are not available for cellular oxidation because of the failure to form such molecules.
In muscle, exercise or fast increases dependence on fat as a source of energy, so the inability to metabolize them can cause problems.
The formation of acyl carnitine is required by the cells.
If it is not possible to use fatty acids, they will remain in the cytosol, where their high concentrations cause cell enlargement and interfere with other functions.
Instead of exporting it to other cells, lymphatic cells must useglucose as a source of energy.
The rate of ketone body synthesis will be reduced because the failure to oxidize fatty acids will result in the use of acetyl CoA.
This will make the symptoms of hypoglycemia worse because the tissues that normally use ketone bodies as a source of energy will have to rely more onglucose.
Competition from malonyl CoA could cause a decrease in the rate of palmitoyl CoA synthesis, which could in turn lead to an increase in the concentration of acetyl CoA.
Malonyl CoA and methylmalonyl CoA could interfere with the transport of long-chain fatty acyl chains into the mitochondria.
The synthesis and oxidation of fatty acids could be stopped by the use of methylmalonyl CoA.
Succinyl CoA can contribute net carbons to the citric acid cycle, which can lead to the creation of oxaloacetate.
Glycerol can be converted to sugar.
Even-numbered fatty acids can be used for net synthesis of glucose, whereas even-numbered ones cannot.
There are two of the three carbons of malonyl CoA in the acyl chain.
The resulting acid will have an even number of carbon atoms.
The initial condensation step with malonyl CoA can be used by certainbacteria.
The five-carbon acyl intermediate is extended in two-carbon units to yield an odd-numbered fatiguing acid.
In addition, high levels of this intermediate prevent carnitine acyltransferase I from entering the Mitochondrion.
A decrease in the concentration of malonyl CoA leads to a decrease in the rate of synthesis and an increase in the rate of oxidation.
If a molecule of FADH2 is equivalent in reducing power to NADH, then a molecule of the same molecule is required to synthesise a molecule.
If the two processes occur at the same time, there will be a net loss.
Glyoxysomes are no longer needed after leaf development.
The compound carnitine is not involved in the movement of acyl chains into the glyoxysome according to the observation.
Both ganelles and mitochondria oxidize acetyl CoA to CO2 and H2O, whereas the ganelles carry out b oxidation of fatty acids to acetyl CoA.
Carbohydrates that are consumed in excess of calories are converted to acetyl CoA, which in turn serves as a source of fat.
The primary storage form of energy in humans is triacylglycerols, which can be synthesised from both sugars and glycerol.
Excess calories are converted to fat.
Bicarbonate is a source of carbon dioxide that is used to make malonyl CoA.
Malonyl CoA is then used as a source of two-carbon units for the formation of acyl chain.
The synthesis of another molecule of malonyl CoA can be done with the rapid conversion of carbon dioxide to bicarbonate.
The carbon atom derived from bicarbonate can be used many times for the production of malonyl CoA, but it is never incorporated into the growing acyl chain, so it does not appear in palmitate.
As many as eight sets of enzymes would be required to carry out the oxidation of palmitate if each one could only operate on a specific type of CoA derivatives.
The b-oxidation pathway can use acyl CoA molecule of different chain lengths as the cell needs to synthesise fewer different enzymes to carry out the oxidation.
To synthesise acetoacetate from palmitate, the cells must oxidize the 16-carbon acyl chain, generating 8 molecule of acetyl CoA, which will in turn generate 4 molecule of acetoacetate.
Each molecule of palmitate is converted to acetyl CoA and produces a total of 7 NADH and FADH2 molecules.
There are 14 reduced cofactors.
The net yield of ATP per palmitate is 26.
The shuttle system transports two carbon units from the Mitochondrion to the cytosol.
The pentosephosphate pathway serves as a source of NADPH, so that the synthesis of fatty acid can continue even if malate is present.
The text says that malate can cross the mitochondria.
acetyl CoA from citrate in the cytosol is required to synthesise fatty acid.
The cells cannot grow and divide without the synthesis of acetyl CoA.
When a double bond at C-9 is available and a double bond at C-5 is available, a double bond at C-8 can be introduced.
Chains are followed by chain elongation to a 20-carbon derivative.
The 22-carbon acyl chain is the final reaction needed to yield clupanodonate.
Acyl chain with double bonds at C-13 and C-16 is possible if you shorten it to a 22-carbon chain.
The double bond at C-19 is needed to form clupanodonate.
Linoleate can't be used for the synthesis of clupanodonate.
The natural intermediate is formed by an acyl CoA dehydrogenase.
It would be hydrated by enoyl CoA hydratase.
The D3 double bond wouldn't be a good substitute for enoyl CoA hydratase.
The D2 configuration allows metabolism.
One less FADH2 would be formed since the double bond already exists in the fatty acids.
There would be 1.5 fewer ATP produced for each double bond.
These substances oxidize to create "energy-rich" electrons, which are used to reduce oxygen in the air.
In water generation, a molecule of water is generated during the formation of each ATP molecule.
The saturated carbon atoms of fatty acids make them a better source of electrons.
Carbohydrates with carbons at the alcohol level of oxidation or at the aldehyde level of oxidation provide fewer electrons during terminal oxidation.
Plants with a high percentage of fats are a better source of water than seeds.
The molecule's weight is 255 g mol-1.
The number of moles of water produced by the oxidation of palmitate is calculated.
The text on page 610 shows that palmitoyl CoA oxidation gives 7 FADH2, 7 NADH, and 8 acetyl CoA molecule.
The text on page 478 shows that oxidation of acetyl CoA in the citric acid cycle yields 3 NADH, 1 FADH2, and 1 GTP, equivalent to 1 ATP, utilizing 2 water molecule.
The 8 acetyl CoA molecule produced from palmitoyl CoA gives 24 NADH, 8 FADH2, and 8 ATP equivalents.
31 NADH and 15 FADH2 are the reduced electron carriers from the oxidative process.
When NADH is taken out of the electron transport chain and FADH2 is taken out, 2.5 and 1.5 ATP are produced.
One water is gained for every pair of e- oxidation.
The total number of water molecules produced is 146, and the net water produced is (146 + 23) + 123 moles of water per mole of palmitate.
The water's weight is 18.0 g mol-1.
The amount of palmitoyl CoA is equivalent to 0.12 mole of palmitate.
The oxidation of a C16 fatty acid leads to the formation of acetyl CoA.
The net number of carbons entering and leaving the cycle is zero because Acetyl CoA is oxidation to two CO2 in the citric acid cycle.
Net carbons are not available to enter the pathway.
The carbon compound is an intermediate in the citric acid cycle.
Two extra carbons are added to the gluconeogenic pathway by Succinyl CoA.
High levels of citrate signal that ade quate carbon atoms are available for synthesis of palmitoyl CoA.
The rate of glycolysis is decelerating.
Increased production of malonyl CoA leads to stimulation of the synthesis of fatty acid.
The transport of citrate from the matrix to the cytosol is important because the two acetyl CoA carboxylases are located in the cytosol.
A lack of 2,4-dienoyl CoA reductase is the most likely deficiency.
The carnitine derivatives of the 2,4-dienoyl CoA are found in blood and urine, and there is evidence that they accumulate in the Mitochondrion.
The formation of carnitineadienoate allows the acyl molecule to be moved into the circulation.
Mitochondria from the patient function normally, taking up oxygen as they carry out oxidation of various substrates.
The absence of the reductase molecule allows only a limited number of rounds of b oxidation to occur before the 2,4-dienoyl molecule is formed.
There are difficulties in providing energy for muscle contraction if there is no muscle tone.
A virtual deficiency of carnitine can be caused by cells being esterified to decadienoate molecules.
Under these conditions, the cell's ability to transport other long-chain fatty acids is limited.
There is less available for muscular activity because of the impairment of fatty acid oxidation.
Limit linoleate in the diet is an immediate strategy for dealing with this disorder.
linoleate is a starting point for many of the other eicosanoid hormones.
It is necessary to limit the amount of linoleate in the diet of a person with a reductase deficiency.
Direct synthesis from 14C-acetate or b oxidation of radioactive fatty acids can be used to generate Radioactive acetyl CoA.
During the first pass through the cycle, neither of the two carbons that enter citrate from acetate is removed as carbon dioxide.
The carbon from 14C-methyl-labeled acetate shows up in C-2 and C-3 of oxaloacetate because of the symmetry of the molecule.
The conversion of oxaloacetate to phosphoenolpyruvate yields apep labeled at C-2 or C3.
The formation of glyceraldehyde 3-phosphate and its isomer dihydroxyacetonephosphate gives two different types of molecule.
fructose 1,6-bisphosphate is radioactively labeled at carbons 1, 2, 5, and 6.
The four carbons will be labeled with the same compound.
The label will have been incorporated, but no net synthesis will have taken place.
The need for a kinase and a dehydrogenase is when glycerol enters glycolysis.
Chapter 16 explains how to convert dihydroxyacetone phosphate to pyruvate.
41/2 acetoacetyl CoA + 41/2 H2O 41/2 acetoacetate + 41/2 H+ + 41/2 CoA 3.
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