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Chapter 27: Problem 15

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?

Short Answer

Expert verified
Ethanol metabolism reduces the NAD+/NADH ratio potentially disrupting glycolysis, gluconeogenesis, and fatty acid oxidation based on its role in maintaining a balance in these processes. This can lead to hypoglycaemia and accumulation of fatty acids, potentially causing health issues like fatty liver.

Step by step solution

01

Understand the role of the NAD+/NADH ratio in the metabolic processes

NAD+ is a coenzyme that plays a significant role in oxidation-reduction reactions in metabolism. It is involved in both glycolysis and gluconeogenesis, helping to oxidize glucose in the former and reduce pyruvate in the latter. The ratio of NAD+ to NADH is important in maintaining the balance between these processes.
02

Link the NAD+/NADH ratio to glycolysis, gluconeogenesis, and fatty acid oxidation

In glycolysis, glucose is broken down, releasing energy, and NAD+ is reduced to NADH. In gluconeogenesis, the reverse process happens, and glucose is formed, NADH is oxidised to NAD+. For fatty acid oxidation, NAD+ is also needed to be reduced to NADH. Therefore, the NAD+/NADH ratio is crucial in regulating these metabolic pathways.
03

Analyze the impact of ethanol metabolism on the NAD+/NADH ratio

The metabolism of ethanol by the liver consumes NAD+ and produces NADH, thereby lowering the NAD+/NADH ratio. Under normal conditions, glycolysis, gluconeogenesis, and fatty acid oxidation are all balanced by the ratio of NAD+ to NADH. Disturbing this balance by consuming ethanol can disrupt these cycles. This could potentially lead to an accumulation of glucose causing hypoglycaemia, and accumulation of fatty acids leading to fatty liver.
04

Complete the answer

The alteration of the NAD+/NADH ratio by the metabolism of ethanol can disrupt important pathways such as glycolysis, gluconeogenesis, and fatty acid oxidation, potentially leading to health complications. This effect is based on the role that the NAD+/NADH ratio plays in balancing these processes.

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Most popular questions from this chapter

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

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?

(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 \(+50 \mathrm{kJ} / \mathrm{mol}\) ?

The existence of leptin was revealed when the ob/ob genetically obese strain of mice was discovered. These mice have a defective leptin gene. Predict the effects of daily leptin injections into \(o b / o b\) mice on food intake, fatty acid oxidation, and body weight. Similar clinical trials have been conducted on humans, with limited success. Suggest a reason why this therapy might not be a miracle cure for overweight individuals.

(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.)
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