(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 \(\mathrm{CO}_{2}\) ?

Short Answer

Expert verified
One molecule of ethanol can generate 22 ATP equivalents. Per carbon atom, ethanol, with 11 ATP/C, is a better metabolic fuel than glucose, which has 3.67 ATP/C.

Step by step solution

01

Determine ATP generated from the oxidation of ethanol

The oxidation of one molecule of ethanol yield two molecules of acetate. Each acetate can be transformed into acetyl-CoA, which when enters the citric acid cycle produces 12 ATP. Two acetyl-CoA molecules are thus expected, hence, the total ATPs from the ethanol oxidation is \(2 * 12 = 24 ATP\). Note that the initial conversion of acetate to acetyl-CoA consumes one molecule of ATP for each acetate. Therefore, the Net ATP produced from ethanol is 22.
02

Determine ATP generated from the oxidation of glucose

One molecule of glucose (C6H12O6) gets oxidized to produce six molecules of \(CO_2\) which generates \(6 * 4 = 24 ATP\) theoretically. Since the initial steps of glycolysis consume 2 ATP, net ATP produced from the glucose is 22.
03

Compare the metabolic efficiency of glucose and ethanol

To compare the efficiency per carbon atom of both substances, we divide the number of ATPs generated by the number of carbon atoms. For glucose, it's \(\frac{22 ATP}{6 C} = 3.67 ATP/C\), for ethanol, it's \(\frac{22 ATP}{2 C} = 11 ATP/C\). Hence, ethanol is a better metabolic fuel per carbon atom compared to glucose.

Unlock Step-by-Step Solutions & Ace Your Exams!

  • Full Textbook Solutions

    Get detailed explanations and key concepts

  • Unlimited Al creation

    Al flashcards, explanations, exams and more...

  • Ads-free access

    To over 500 millions flashcards

  • Money-back guarantee

    We refund you if you fail your exam.

Over 30 million students worldwide already upgrade their learning with Vaia!

Key Concepts

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

Acetyl-CoA Formation
Understanding acetyl-CoA formation is critical when examining ethanol metabolism. Let's start with an essential process that occurs after ethanol consumption. The body converts ethanol into acetate. This acetate then combines with ATP (adenosine triphosphate), the primary energy currency of the cell, and CoASH (coenzyme A) to form acetyl-CoA, a pivotal molecule in metabolism.

In simple terms, the reaction is like exchanging currency; acetate trades with ATP and CoASH to 'purchase' a new form that's more usable for the body, which in this case is acetyl-CoA. This process consumes ATP, indicating an investment into the conversion that's needed before acetyl-CoA can enter the next metabolic stage. It's worthwhile to note that this step is akin to setting the stage before the main act of energy production begins.
Citric Acid Cycle
Once acetyl-CoA is formed, it's time for it to enter the 'metabolic stage show' known as the citric acid cycle, or Krebs cycle. Imagine this cycle as a complex machine in a factory. Acetyl-CoA is the raw material that goes in, and through a series of enzyme-controlled steps, it gets dismantled. The dismantling process releases carbon dioxide, but more importantly for energy production, it generates high-energy carriers like NADH and FADH2.

The citric acid cycle itself doesn't produce much ATP directly. However, it sets up the energy-rich molecules that are vital for the next phase, where the real power generation happens. Think of the citric acid cycle as a setup for the grand finale of energy production.
Oxidative Phosphorylation

Powering the Cellular Grid

With the stage set by the citric acid cycle, the performance can reach its climax through oxidative phosphorylation. This is the main power-generating step in the cell's energy production process. It's here that NADH and FADH2, the energetic molecules produced earlier, work to power the production of ATP.

The electron transport chain within the mitochondria takes the electrons from NADH and FADH2 and passes them along a series of 'electron accepting' complexes. As electrons flow through, they power the pumping of protons across the mitochondrial membrane, creating an energy store known as a proton gradient. This gradient is like a dam holding back water. The potential energy stored in this proton gradient is then converted into ATP as protons flow back through an enzyme called ATP synthase.
ATP Generation
In the grand scheme of cellular energy production, ATP generation is the final, most crucial step. The process involves the enzyme ATP synthase within the mitochondrial membrane, which acts similarly to a turbine in a hydroelectric power plant, converting flow energy into usable power — in our case, capturing the energy from the proton gradient into forming ATP.

ATP is the main source of energy for many cellular processes, from muscle contraction to nerve impulse propagation. Our bodies generate and use approximately our body weight in ATP every day, though only a small amount is present in the body at any moment. This incredible turnover underlines the efficiency and importance of ATP generation in our daily functioning.
Metabolic Fuel Efficiency

Assessing the Energy Yield

When considering the metabolic fuel efficiency of substances like glucose and ethanol, we're basically asking which gives us more bang for our buck. Measuring in 'ATP equivalents', we can compare how many ATP molecules can be generated from the breakdown of these fuels.

As demonstrated in the exercise provided, ethanol appears to be a better metabolic fuel per carbon atom because it produces more ATP per carbon when fully oxidized compared to glucose. It's a bit like comparing two types of fuel for cars; ethanol here would give you more miles per gallon (energy per carbon atom) than glucose if we assume that all conditions in the body are perfect for this comparison to hold true.

One App. One Place for Learning.

All the tools & learning materials you need for study success - in one app.

Get started for free

Most popular questions from this chapter

(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.)

(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?

a. Leptin was discovered when a congenitally obese strain of mice \((o b / o b \text { mice })\) was found to lack both copies of a gene encoding a peptide hormone produced mainly by adipose tissue. The peptide hormone was named leptin. Leptin is an anorexic (appetitesuppressing agent; its absence leads to obesity. Propose an experiment to test these ideas. b. A second strain of obese mice \((d b / d b\) mice ) produces leptin in abundance but fails to respond to it. Assuming the \(d b\) mutation leads to loss of function in a protein, what protein is likely to be nonfunctional or absent? How might you test your idea?

Would it be appropriate to call neuropeptide \(Y\) (NPY) the obesitypromoting hormone? What would be the phenotype of a mouse whose melanocortin-producing neurons failed to produce melanocortin? What would be the phenotype of a mouse lacking a functional MC3R gene? What would be the phenotype of a mouse lacking a functional leptin receptor gene?

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?

See all solutions

Recommended explanations on Chemistry Textbooks

View all explanations

What do you think about this solution?

We value your feedback to improve our textbook solutions.

Study anywhere. Anytime. Across all devices.

Sign-up for free