15.
Thyroxin is the major hormone produced by the thyroid gland. Rats may be
thyroidectomised (THX) either surgically or chemically. In an experiment designed to
investigate the relationship of the thyroid gland to metabolism (i.e. oxygen consumption)
and protein synthesis, following data were recorded. Experimental and control animals
were tested by measuring oxygen consumption in a respirometer for 1 hour and by
measuring incorporation of injected tritiated leucine (3H-Leu) in the liver. Post-injection,
rats were sacrificed at various time points and radioactivity in the liver was measured.
Based on the above description, which of the following control experiment should also be
performed to confirm the relationship of thyroxin to respiration and protein synthesis?
a. Inject untritiated leucine in the THX rats and take the measurements again
b. Inject untritiated leucine in the normal rats and take the measurements again
c. Inject Thyroxin in the THX rats and take the measurements again
d. Inject Thyroxin in the normal rats and take the measurements again
The correct control is option c. Inject Thyroxin in the THX rats and take the measurements again. This directly tests whether restoring thyroxin in thyroidectomized (THX) rats reverses the reduced oxygen consumption and protein synthesis, confirming a causal relationship between thyroxin and metabolism.
Introduction
Thyroxin is a major thyroid hormone that elevates metabolic rate, oxygen consumption, and protein turnover in mammals. In thyroidectomised rats (THX rats), removal of the thyroid gland lowers circulating thyroxin, reducing both 3H‑leucine incorporation in liver proteins and oxygen consumption, as shown by the experimental data in the question. Designing the right control experiment is essential to prove that these changes result specifically from thyroxin deficiency and not from unrelated surgical stress or other variables.
Understanding the experiment
In the given setup, normal rats with thyroid and THX rats are compared for:
-
3H‑Leucine incorporation in liver (mmoles/g/hr) – a measure of protein synthesis rate.
-
Oxygen consumption (ml/g/hr) – a measure of metabolic rate.
Normal rats show higher values for both parameters, whereas THX rats show reduced leucine incorporation and oxygen consumption, consistent with the loss of thyroxin. To confirm that thyroxin itself is responsible, an ideal control must restore thyroxin only in the THX rats and check whether the metabolic and protein synthesis parameters return toward normal.
Option (a): Inject untritiated leucine in THX rats
Statement: Inject untritiated leucine in the THX rats and take the measurements again.
-
The experiment measures protein synthesis using tritiated leucine (3H‑Leu), which is radioactive and detectable in the liver. Injecting unlabelled (untritiated) leucine would not provide a comparable readout of radioactivity and would change the specific activity of the leucine pool, confounding interpretation.
-
This manipulation does not address thyroxin levels; it alters only the tracer method. Therefore, it cannot test whether thyroxin deficiency per se causes reduced oxygen consumption and protein synthesis. Hence, option (a) is an inappropriate control.
Option (b): Inject untritiated leucine in normal rats
Statement: Inject untritiated leucine in the normal rats and take the measurements again.
-
As in option (a), switching from radioactive to non‑radioactive leucine in normal rats alters the detection method rather than the hormone status. This would eliminate or drastically reduce the radioactive signal, making results incomparable with the original 3H‑Leu data.
-
Again, thyroxin levels remain unchanged, so this option does not test whether the metabolic differences between normal and THX rats are due to thyroxin. It is therefore not a valid physiological control for the hormone–metabolism relationship.
Option (c): Inject Thyroxin in the THX rats (Correct)
Statement: Inject Thyroxin in the THX rats and take the measurements again.
-
THX rats are hypothyroid due to removal of their thyroid gland; their low thyroxin level explains the decreased oxygen consumption and protein synthesis. If thyroxin is the causal factor, administering exogenous thyroxin should restore metabolism toward normal values.
-
This is a classic hormone replacement control: by reversing the endocrine deficiency only in the experimental group (THX rats), one can show that the reduced 3H‑Leu incorporation and oxygen consumption are specifically due to absence of thyroxin, not to surgery, anesthesia, or other nonspecific factors. Because it directly tests the hypothesis, option (c) is the correct control experiment.
Option (d): Inject Thyroxin in the normal rats
Statement: Inject Thyroxin in the normal rats and take the measurements again.
-
Normal rats already possess functional thyroid glands and circulating thyroxin. Injecting additional hormone would push them toward hyperthyroid conditions, potentially increasing oxygen consumption and protein synthesis above normal.
-
While this might illustrate a dose–response effect, it does not restore a deficient state and therefore does not serve as a proper control to show that low values in THX rats are due to thyroxin deficiency. It addresses a different question (effect of excess thyroxin) and so is not the best control in this context.
Key takeaway
For questions on endocrine physiology and metabolic regulation, always look for a control that reverses the specific deficiency or manipulation in the experimental group. In this thyroxin–thyroidectomy–metabolism MCQ, injecting thyroxin into THX rats and repeating the measurements is the most direct way to confirm that thyroxin controls respiration and protein synthesis, making option (c) the correct answer.
