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Chapter 27: Problem 18

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?

Short Answer

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Part A: An experiment could involve injecting ob/ob mice with leptin and monitoring for changes in appetite and body weight. If they eat less and lose weight, it confirms the role of leptin in appetite control and obesity prevention. Part B: In db/db mice, the protein likely to be defective or absent is the leptin receptor. This could be tested by examining the leptin receptors in these mice and potentially introducing functional leptin receptor genes to see if responsiveness to leptin is restored.

Step by step solution

01

Part A - Experiment Proposal to Test Effect of Leptin

To test the role of leptin in obesity, an experiment could be designed as follows: Obtain a group of typical mice (as a control group) and a group of ob/ob mice. Then, give leptin injections to the ob/ob mice while the control group is left untreated. Monitor the mice's behavior, specifically their feeding, and weigh them regularly to check changes in their body weight. If the ob/ob mice lose weight and eat less, it could be concluded that leptin indeed plays a role in appetite suppression and obesity prevention.
02

Part B - Identifying and Testing the Non-Functional Protein in db/db Mice

Assuming the db mutation leads to a loss of function in a protein, the defective protein is likely to be the leptin receptor, given that these mice produce leptin but do not respond to it. To test this hypothesis, examine the leptin receptors in these mice and compare them to normal mice. If the db/db mice have fewer receptors, non-functional receptors or no receptors at all, this would confirm that the leptin receptor is the protein affected by the db mutation. Further confirmation could be obtained by introducing functional leptin receptor genes into these mice to see if responsiveness to leptin is restored.

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Most popular questions from this chapter

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 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?

(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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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?
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