Warning: foreach() argument must be of type array|object, bool given in /var/www/html/web/app/themes/studypress-core-theme/template-parts/header/mobile-offcanvas.php on line 20

A young rat maintained on a diet deficient in methionine fails to thrive unless choline is included in the diet. Explain.

Short Answer

Expert verified
The young rat thrives with choline because it provides essential methyl groups, compensating for a methionine deficiency.

Step by step solution

01

Understanding the Problem

To begin, let's understand the problem. Methionine is an essential amino acid, meaning it must be obtained from the diet because the body cannot synthesize it. Choline is a nutrient that can be synthesized in the body but may require methionine for its synthesis. The question focuses on why a rat's health would improve when choline is added to a methionine-deficient diet.
02

Role of Methionine

Methionine is crucial for numerous biological functions such as protein synthesis, and it is a precursor to important molecules like homocysteine and S-adenosylmethionine (SAM), which is involved in methylation reactions. Since the rat's diet is deficient in this amino acid, many of these processes are likely disrupted, impacting the rat's ability to thrive.
03

Role of Choline

Choline plays an important role as a precursor in the biosynthesis of the neurotransmitter acetylcholine, and as part of the structure of cell membranes. Although rats can produce choline, the synthesis relies on available methyl groups, often derived from methionine. In the absence of methionine, endogenous choline production may be insufficient.
04

Linking Choline and Methionine

In the absence of sufficient methionine, introducing choline directly into the diet may partially compensate for the lack of available methyl donors. Choline can donate methyl groups in various metabolic reactions, supporting vital processes that would otherwise be hindered by a methionine deficiency. This dietary supplementation allows the young rat to thrive even in the absence of methionine.
05

Conclusion and Final Explanation

Adding choline to the diet of the methionine-deficient rat supports growth by providing essential methyl groups needed for critical biosynthetic pathways. This supplementation compensates for the methionine deficiency by allowing some processes to continue that would depend on the availability of methionine.

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.

Essential Amino Acids
Essential amino acids are building blocks of proteins that our bodies cannot produce on their own. Because of this, they must be obtained from dietary sources. Methionine is one of these essential amino acids and plays a vital role in various physiological processes. If an animal, like a young rat, is deprived of methionine, several essential biological pathways can be disrupted.
  • Methionine is crucial for protein synthesis. Without enough methionine, the body might struggle to create the proteins it needs to function.
  • It is also a precursor to essential compounds involved in metabolic reactions. For instance, methionine contributes to the production of homocysteine and S-adenosylmethionine (SAM), which are vital for methylation reactions—a process that regulates gene expression and protein function.

When methionine is deficient in the diet, including other aids like choline may help to mitigate the challenges a deficiency brings.
Methionine Metabolism
Methionine metabolism is an important biochemical pathway that ensures our bodies can produce necessary compounds and perform essential functions. Once consumed in the diet, methionine is not used directly but is converted into other molecules that serve as methyl donors.
  • This metabolism starts with methionine being converted into S-adenosylmethionine (SAM), a powerful methyl donor involved in numerous biological reactions like DNA methylation.
  • In the absence of sufficient methionine, these reactions are at risk, potentially affecting growth, development, and overall health.
  • Metabolic routes involving methionine also lead to the production of homocysteine, which must be recycled or eliminated efficiently to prevent health issues.

Without enough methionine, other dietary components must come to the rescue to help maintain these vital pathways, like adding choline to the diet.
Choline Supplementation
Choline is an essential nutrient that serves many roles in the body, including brain function and cellular structure. Even though the body can synthesize choline, this process leans heavily on the availability of methyl groups, typically derived from methionine.
  • Choline is a precursor to acetylcholine, a neurotransmitter necessary for memory and muscle control.
  • It is also significant in the formation and maintenance of cell membranes due to its incorporation into phospholipids.
  • In circumstances where methionine is deficient, as with our young rat example, the body’s ability to synthesize adequate choline is compromised.

Supplementing the diet with choline can help offset the shortage of methyl groups, thereby supporting metabolic activities even when methionine is lacking. This supplementation not only aids critical pathways but also helps in maintaining normal function under conditions where methionine is not sufficiently available from the diet.

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

Patients treated with a statin drug generally exhibit a dramatic lowering of serum cholesterol. However, the amount of the enzyme HMG-CoA reductase present in cells can increase substantially. Suggest a simple explanation for this effect.

Using your knowledge of fatty acid biosynthesis, provide an explanation for the two experimental observations. a. A biochemist adds uniformly labeled \(\left[{ }^{14} \mathrm{C}\right]\) acetyl-CoA to a soluble liver fraction, which yields palmitate uniformly labeled with \({ }^{14} \mathrm{C}\). b. In a second experiment, the biochemist adds a trace of uniformly labeled \(\left.{ }^{[14} \mathrm{C}\right]\) acetyl-CoA in the presence of an excess of unlabeled malonyl-CoA to a soluble liver fraction, which yields palmitate labeled with \({ }^{14} \mathrm{C}\) only in C-15 and C-16.

The formation of a thioester of acetoacetate is catalyzed by fatty acid synthase during fatty acid synthesis, and by acetyl-CoA acetyltransferase in the first step of cholesterol biosynthesis. Both are Claisen condensations. However, in fatty acid synthesis, malonyl-CoA forms in an earlier step so that decarboxylation facilitates the condensation. In the cholesterol biosynthesis pathway, the condensation occurs between two acetyl-CoA molecules, and no decarboxylation occurs to facilitate the reaction. Suggest a reason why the thermodynamic augmentation of decarboxylation is needed in fatty acid synthesis, but not in the first steps of cholesterol biosynthesis.

A researcher has prepared a solution that contains all the enzymes and cofactors necessary for fatty acid biosynthesis from added acetyl-CoA and malonyl-CoA. a. She then adds \(\left[2-{ }^{2} \mathrm{H}\right]\) acetyl-CoA (labeled with deuterium, the heavy isotope of hydrogen) and an excess of unlabeled malonyl- CoA as substrates. How many deuterium atoms incorporate into every molecule of palmitate? What are their locations? Explain. b. In a separate experiment, the researcher adds unlabeled acetyl-CoA and \(\left[2-{ }^{2} \mathrm{H}\right]\) malonyl-CoA as substrates. How many deuterium atoms incorporate into every molecule of palmitate? What are their locations? Explain.

After a person has ingested large amounts of sucrose, the body transforms the glucose and fructose that exceed caloric requirements to fatty acids for triacylglycerol synthesis. This fatty acid synthesis consumes acetyl-CoA, ATP, and NADPH. How do cells produce acetyl-CoA, ATP, and NADPH from glucose?

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