(Integrates with Chapter \(23 .\) ) Assuming each NADH is worth 3 ATP, each \(\mathrm{FADH}_{2}\) is worth \(2 \mathrm{ATP}\), and each NADPH is worth \(4 \mathrm{ATP}\) How many ATP equivalents are produced when one molecule of palmitoyl-CoA is oxidized to 8 molecules of acetyl-CoA by the fatty acid \(\beta\) -oxidation pathway? How many ATP equivalents are consumed when 8 molecules of acetyl-CoA are transformed into one molecule of palmitoyl-CoA by the fatty acid biosynthetic pathway? Can both of these metabolic sequences be metabolically favorable at the same time if \(\Delta G\) for ATP synthesis is \(+50 \mathrm{kJ} / \mathrm{mol}\) ?

Short Answer

Expert verified
The ATP equivalents produced via \(\beta\)-oxidation of Palmitoyl-CoA are 35. The ATP equivalents consumed in the biosynthesis of Palmitoyl-CoA from Acetyl-CoA are 16. No, both metabolic pathways cannot be favorable at the same time because they are opposites in the energy generation and consumption process.

Step by step solution

01

Calculation of ATP equivalents produced via \(\beta\)-oxidation

One cycle of \(\beta\)-oxidation of fatty acid produces 1 FADH2, 1 NADH, and 1 Acetyl-CoA. Palmitoyl-CoA has 16 carbons, so it goes through 7 cycles of \(\beta\)-oxidation to produce 8 Acetyl-CoA, which gives 7 FADH2 and 7 NADH. Considering each FADH2 and NADH is worth \(2 \mathrm{ATP}\) and \(3 \mathrm{ATP}\) respectively, the total ATP equivalent produced would be \((7 \times \mathrm{FADH}_{2} \times 2)+(7 \times \mathrm{NADH} \times 3) = 35 \mathrm{ATP}\)
02

Calculation of ATP equivalents consumed in fatty acid biosynthesis

One molecule of Acetyl-CoA requires 2 ATP equivalents to be transformed into palmitoyl-CoA (fatty acid synthesis). Thus, 8 molecules of acetyl-CoA will consume \(8 \times 2 = 16 \mathrm{ATP}\) equivalents.
03

Determining the metabolic favorability

\(\Delta G\) for ATP synthesis is given as \(+50 \mathrm{kJ} / \mathrm{mol}\). It is an endothermic process meaning energy-consuming. High \(\Delta G\) values indicate that the reaction is not spontaneously favorable. Since \(\beta\)-oxidation of palmitoyl-CoA generates ATP and fatty acid biosynthesis consumes ATP, these two pathways are opposites. Therefore, they cannot both be favorable at the same time.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Fatty Acid Beta-Oxidation
Fatty acid beta-oxidation is a multistep process that breaks down fatty acids to produce energy. This process occurs in the mitochondria of cells and is a crucial way our bodies utilize the energy stored in fats. During beta-oxidation, fatty acids are progressively broken down into two-carbon units, resulting in the formation of acetyl-CoA, NADH, and FADH2.

An example using palmitoyl-CoA, which has 16 carbons, demonstrates the process: palmitoyl-CoA undergoes 7 cycles of beta-oxidation to produce 8 acetyl-CoA, 7 NADH, and 7 FADH2. These products then lead to the creation of ATP. The NADH and FADH2 created during these cycles enter the electron transport chain, where they are further processed to generate a significant amount of ATP. It is a classic example of how our body efficiently manages energy resources.
ATP Equivalents in Metabolism
Understanding ATP equivalents in metabolism is essential for gauging how much energy is produced or used by different biochemical processes. ATP, or adenosine triphosphate, serves as the energy currency of the cell. Other molecules like NADH, FADH2, and NADPH are also involved in energy transfer but are converted to ATP equivalents for easier comparison of the energy they can yield.

For instance, in the mitochondrial electron transport chain, each NADH can yield 3 ATP, and each FADH2 can yield 2 ATP. This conversion provides a clearer picture of the total energy yield from different pathways. The ATP equivalents generated during fatty acid beta-oxidation or consumed during fatty acid biosynthesis are vital for understanding the balance of energy in cells and whether a process is energetically favorable.
Fatty Acid Biosynthesis
On the flip side of beta-oxidation is fatty acid biosynthesis, which is the anabolic pathway for creating fatty acids. This process takes place in the cytoplasm and requires energy input in the form of ATP. Unlike beta-oxidation, biosynthesis aims to synthesize larger molecules from smaller ones, which is a biosynthetic or 'building-up' process.

Considering acetyl-CoA as the building block, it takes 2 ATP equivalents for the conversion of one acetyl-CoA into fatty acid, such as palmitoyl-CoA. This denotes the energy-consuming nature of biosynthesis. To build a molecule of palmitoyl-CoA from acetyl-CoA, a substantial amount of ATP is utilized, contrasting the energy yield of the beta-oxidation pathway.

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Most popular questions from this chapter

Strenuous muscle exertion (as in the 100 -meter dash) rapidly depletes ATP levels. How long will 8 m \(M\) ATP last if 1 gram of muscle consumes \(300 \mu\) mol of ATP per minute? (Assume muscle is \(70 \%\) water.) Muscle contains phosphocreatine as a reserve of phosphorylation potential. Assuming [phosphocreatine] \(=40 \mathrm{m} M,[\text { creatine }]=4 \mathrm{m} M,\) and \(\left.\Delta G^{\circ \prime} \text { (phosphocreatine }+\mathrm{H}_{2} \mathrm{O} \rightleftharpoons \text { creatine }+\mathrm{P}_{\mathrm{i}}\right)=-43.3 \mathrm{kJ} / \mathrm{mol}\) how low must [ATP] become before it can be replenished by the reaction: phosphocreatine \(+\mathrm{ADP} \rightleftharpoons \mathrm{ATP}+\) creatine? [Remember \(\Delta G^{\circ \prime}\) (ATP hydrolysis) \(=-30.5 \mathrm{kJ} / \mathrm{mol} .\)]

(Integrates with Chapters \(18 \text { and } 22 .)\) The reactions catalyzed by PFK and FBPase constitute another substrate cycle. PFK is AMP activated; FBPase is AMP inhibited. In muscle, the maximal activity of PFK (mmol of substrate transformed per minute) is ten times greater than FBPase activity. If the increase in [AMP] described in problem 5 raised PFK activity from \(10 \%\) to \(90 \%\) of its maximal value but lowered FBPase activity from \(90 \%\) to \(10 \%\) of its maximal value, by what factor is the flux of fructose- 6 - \(P\) through the glycolytic pathway changed? (Hint: Let PFK maximal activity = 10, FBPase maximal activity \(=1 ;\) calculate the relative activities of the two enzymes at low \([\mathrm{AMP}]\) and at high \([\mathrm{AMP}] ;\) let \(J,\) the flux of \(\mathrm{F}\) - 6 -P through the substrate cycle under any condition, equal the velocity of the PFK reaction minus the velocity of the FBPase reaction.)

The Human Biochemistry box, The Metabolic Effects of Alcohol Consumption, points out that ethanol is metabolized to acetate in the liver by alcohol dehydrogenase and aldehyde dehydrogenase: $$\begin{array}{r} \mathrm{CH}_{3} \mathrm{CH}_{2} \mathrm{OH}+\mathrm{NAD}^{+} \rightleftharpoons \mathrm{CH}_{3} \mathrm{CHO}+\mathrm{NADH}+\mathrm{H}^{+} \\\ \mathrm{CH}_{3} \mathrm{CHO}+\mathrm{NAD}^{+}+\mathrm{H}_{2} \mathrm{O} \rightleftharpoons \mathrm{CH}_{3} \mathrm{COO}^{-}+\mathrm{NADH}+2 \mathrm{H}^{+} \end{array}$$ These reactions alter the NAD \(^{+} /\) NADH ratio in liver cells. From your knowledge of glycolysis, gluconeogenesis, and fatty acid oxidation, what might be the effect of an altered \(\mathrm{NAD}^{+} / \mathrm{NADH}\) ratio on these pathways? What is the basis of this effect?

(Integrates with Chapters 19 and \(20 .\) ) Acetate produced in ethanol metabolism can be transformed into acetyl-CoA by the acetyl thiokinase reaction: $$\text { Acetate }+\mathrm{ATP}+\mathrm{CoASH} \longrightarrow \text { acetyl-CoA }+\mathrm{AMP}+\mathrm{PP}_{\mathrm{i}}$$ Acetyl-CoA then can enter the citric acid cycle and undergo oxidation to \(2 \mathrm{CO}_{2}\). How many ATP equivalents can be generated in a liver cell from the oxidation of one molecule of ethanol to \(2 \mathrm{CO}_{2}\) by this route, assuming oxidative phosphorylation is part of the process? (Assume all reactions prior to acetyl-CoA entering the citric acid cycle occur outside the mitochondrion.) Per carbon atom, which is a better metabolic fuel, ethanol or glucose? That is, how many ATP equivalents per carbon atom are generated by combustion of glucose versus ethanol to \(\mathrm{CO}_{2}\) ?

(Integrates with Chapters 3,18 , and \(22 .\) ) The conversion of PEP to pyruvate by pyruvate kinase (glycolysis) and the reverse reaction to form PEP from pyruvate by pyruvate carboxylase and PEP carboxykinase (gluconeogenesis) represent a so-called substrate cycle. The direction of net conversion is determined by the relative concentrations of allosteric regulators that exert kinetic control over pyruvate kinase, pyruvate carboxylase, and PEP carboxykinase. Recall that the last step in glycolysis is catalyzed by pyruvate kinase: \(P E P+A D P \rightleftharpoons\) pyruvate \(+\) ATP The standard free energy change is \(-31.7 \mathrm{kJ} / \mathrm{mol}\). a. Calculate the equilibrium constant for this reaction. b. If \([\mathrm{ATP}]=[\mathrm{ADP}],\) by what factor must [pyruvate] exceed [PEP] for this reaction to proceed in the reverse direction? The reversal of this reaction in eukaryotic cells is essential to gluconeogenesis and proceeds in two steps, each requiring an equivalent of nucleoside triphosphate energy: c. The \(\Delta G^{\circ}\) ' for the overall reaction is \(+0.8 \mathrm{kJ} /\) mol. What is the value of \(K_{\mathrm{eq}} ?\) d. Assuming [ATP] = [ADP], [GTP] = [GDP], and Pi \(=1 \mathrm{m} M\) when this reaction reaches equilibrium, what is the ratio of \([\mathrm{PEP}] /[\text { pyruvate }]\) e. Are both directions in the substrate cycle likely to be strongly favored under physiological conditions?

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