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In a laboratory experiment, investigators feed two groups of rats two different fatty acids as their sole source of carbon for a month. The first group gets heptanoic acid (7:0), and the second gets octanoic acid (8:0). After the experiment, those in the first group are healthy and have gained weight, whereas those in the second group are weak and have lost weight as a result of losing muscle mass. What is the biochemical basis for this difference?

Short Answer

Expert verified
Heptanoic acid offers a metabolic advantage, leading to healthier, weight-gaining rats compared to those given octanoic acid, perhaps due to differences in energy efficiency and metabolism.

Step by step solution

01

Understanding the Fatty Acids

Heptanoic acid is a 7-carbon saturated fatty acid, while octanoic acid is an 8-carbon saturated fatty acid. Their roles as carbon sources in metabolism differ due to their structure and length.
02

Metabolism of Fatty Acids

Fatty acids are metabolized through a process called beta-oxidation, which occurs in the mitochondria. The breakdown leads to the production of acetyl-CoA molecules. The number of acetyl-CoA produced depends on the number of carbons in the fatty acid.
03

Energy Production Efficiency

Heptanoic acid (7:0) undergoes beta-oxidation, producing fewer acetyl-CoA molecules (3 molecules from full oxidation of 6 carbon atoms and 1 propionyl-CoA). Ample energy is generated for maintaining health and increasing weight. In contrast, octanoic acid (8:0) is also broken down through beta-oxidation, producing 4 acetyl-CoA molecules, which seems sufficient, but its metabolism may differ.
04

Interpreting Experimental Results

Since the rats fed with octanoic acid lose muscle mass and become weak, one plausible explanation is that octanoic acid, despite providing sufficient acetyl-CoA, does not support the same energy efficiency in tissues compared to heptanoic acid. It may also point towards differences in metabolic pathways or regulatory effects that are more favorable for heptanoic acid.

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Key Concepts

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

Beta-Oxidation
Beta-oxidation is the process by which fatty acids are broken down in the mitochondria to produce energy. This pathway involves the sequential removal of two-carbon units from fatty acids, resulting in the production of acetyl-CoA. It is named for the beta carbon that is oxidized to form a keto group, which then breaks the bond to release acetyl-CoA. This process continues until the entire fatty acid is converted into acetyl-CoA. Each cycle of beta-oxidation also generates electron carriers such as NADH and FADH₂, which are used in the electron transport chain to produce ATP, the energy currency of the cell.
Acetyl-CoA Production
Acetyl-CoA is a central molecule in metabolism, acting as an intersection between different biochemical pathways. It is produced not only from beta-oxidation but also from the breakdown of carbohydrates and some amino acids. When fatty acids are metabolized, the length of the fatty acid chain determines the number of acetyl-CoA units produced. For example, a 7-carbon fatty acid like heptanoic acid yields a different number of acetyl-CoA molecules than an 8-carbon fatty acid like octanoic acid. This difference in acetyl-CoA production can influence how efficiently an organism can produce energy from fatty acids.
Metabolic Pathways
The body's metabolism involves numerous pathways that work together to maintain energy balances and support physiological functions. These pathways are finely tuned and include those for the metabolism of carbohydrates, fats, and proteins. The entry of acetyl-CoA into the citric acid cycle is a crucial step in generating ATP, involving the oxidation of acetyl-CoA in a series of reactions. Depending on the body's needs, acetyl-CoA may also be diverted towards the synthesis of lipids or ketone bodies. Variations in these pathways can result in differences in energy efficiency, as seen in how the rats metabolized heptanoic and octanoic acids.
Energy Efficiency
Energy efficiency in metabolism refers to how well an organism can convert nutrients into usable energy. In the case of fatty acids, this depends on factors like the length of the carbon chain and the specific metabolic pathways involved. Heptanoic acid provides fewer acetyl-CoA molecules than octanoic acid during beta-oxidation, yet it seems to support more efficient energy production in the rats from the experiment. This suggests that factors other than just acetyl-CoA quantity, such as specific enzymatic efficiencies or tissue preferences for different substrates, play a role in determining overall energy efficiency.
Rat Experiment
The rat experiment illustrates how different fatty acids can lead to distinct physiological outcomes. By feeding rats heptanoic or octanoic acid exclusively, researchers observed that heptanoic acid supported better health and weight gain, while octanoic acid led to muscle loss and weakness. This experiment suggests that subtle differences in fatty acid metabolism can lead to significant physiological effects. It highlights the need to consider both the metabolic pathways involved and the context of nutritional intake when analyzing dietary sources. Such experiments are crucial for understanding how specific nutrients affect overall metabolism and energy balance in organisms.

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Most popular questions from this chapter

The activation of free palmitate to its coenzyme A derivative (palmitoyl-CoA) in the cytosol occurs before it can be oxidized in the mitochondrion. After adding palmitate and \(\left[{ }^{14} \mathrm{C}\right]\) coenzyme A to a liver homogenate, you find palmitoyl-CoA isolated from the cytosolic fraction is radioactive, but that isolated from the mitochondrial fraction is not. Explain.

An individual developed a condition characterized by progressive muscular weakness and aching muscle cramps. The symptoms were aggravated by fasting, exercise, and a high-fat diet. An homogenate of a skeletal muscle specimen from the patient oxidized added oleate more slowly than did control homogenates consisting of muscle specimens from healthy individuals. When the pathologist added carnitine to the patient's muscle homogenate, the rate of oleate oxidation equaled that in the control homogenates. Based on these results, the attending physician diagnosed the patient as having a carnitine deficiency. a. Why did added carnitine increase the rate of oleate oxidation in the patient's muscle homogenate? b. Why did fasting, exercise, and a high-fat diet aggravate the patient's symptoms? c. Suggest two possible reasons for the deficiency of muscle carnitine in this individual.

An investigator adds palmitate uniformly labeled with tritium \(\left({ }^{3} \mathrm{H}\right)\) to a specific activity of \(2.48 \times 10^{8}\) counts per minute \((\mathrm{cpm})\) per micromole of palmitate to a mitochondrial preparation that oxidizes it to acetyl-CoA. She then isolates the acetyl-CoA and hydrolyzes it to acetate. The specific activity of the isolated acetate is \(1.00 \times 10^{7} \mathrm{cpm} / \mu \mathrm{mol}\). Is this result consistent with the \(\beta\) oxidation pathway? Explain. What is the final fate of the removed tritium? (Note: Specific activity is a measure of the degree of labeling with a radioactive tracer expressed as radioactivity per unit mass. In a uniformly labeled compound, all atoms of a given type are labeled.)

Adding \(\left[3-{ }^{14} \mathrm{C}\right]\) propionate \(\left({ }^{14} \mathrm{C}\right.\) in the methyl group) to a liver homogenate leads to the rapid production of \({ }^{14} \mathrm{C}-l a b e l e d\) oxaloacetate. Draw a flowchart for the pathway by which propionate is transformed to oxaloacetate, and indicate the location of the \({ }^{14} \mathrm{C}\) in oxaloacetate.

Mutant Acetyl-CoA Carboxylase What would be the consequences for fat metabolism of a mutation in acetyl-CoA carboxylase that replaced the Ser residue normally phosphorylated by AMPK with an Ala residue? What might happen if the same Ser were replaced by Asp?

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