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Chapter 27: Problem 13

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.

Short Answer

Expert verified
Daily leptin injections into ob/ob mice might decrease their food intake, increase fatty acid oxidation, and decrease their body weight. Leptin therapy might not be successful in overweight humans as they often suffer from leptin resistance, i.e. their bodies do not respond to leptin properly, even though leptin levels are high.

Step by step solution

01

Understanding Leptin Role

Leptin is a hormone that is produced by the body's fat cells and is crucial in regulating energy balance by inhibiting hunger. So, ob/ob mice with a defective leptin gene would lack this inhibition of hunger leading to excess eating, lower rate of fatty acid oxidation and increased body weight.
02

Effects of Leptin injections

Based on leptin's role, giving ob/ob mice daily leptin injections can be predicted to decrease their food intake, increase fatty acid oxidation (which is the process of breaking down fats for energy), and thus, decrease their body weight.
03

Leptin therapy in Humans

The reason why leptin therapy might not have significant success in overweight individuals could be that obesity in humans is often not caused by leptin deficiency but rather, leptin resistance. This is a state where the body has high levels of leptin but does not respond to it properly. Hence, increasing leptin levels in the body further through injections might not necessarily result in a decrease in body weight.

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Most popular questions from this chapter

(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?

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

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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