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MCAT Glycogen, Fasting, Hormones and Urea Cycle Practice Questions

By StudyStore · Published 2026-10-20 · 8 original questions · about 12 min

Eight free MCAT-style practice questions on insulin and glucagon signaling, glycogen metabolism, fasting and starvation, transamination, the urea cycle and metabolic hormones, with explanations.

Quick concept primer

Metabolism is regulated by a small number of hormones that switch pathways on and off. Insulin signals the fed state: it promotes glucose uptake, glycogen synthesis, fatty acid synthesis and protein synthesis. Glucagon (and epinephrine) signal the fasting or stressed state: via cAMP and protein kinase A they promote glycogen breakdown, gluconeogenesis and lipolysis. Cortisol acts more slowly and supports gluconeogenesis, protein breakdown and insulin resistance.

During fasting, liver glycogen supplies blood glucose first, then gluconeogenesis takes over (from lactate, glycerol and amino acids), and after several days the liver makes ketone bodies so the brain can spare muscle protein. Amino acid nitrogen is removed by transamination (using PLP, vitamin B6) and then disposed of as urea in the liver. Amino acid carbon skeletons enter central metabolism as glucogenic or ketogenic products.

Traps: muscle glycogen cannot raise blood glucose, and only two amino acids (leucine and lysine) are purely ketogenic.

8 practice questions

Try each question before opening the explanation. Click "Show answer and explanation" to check yourself. All questions are original and written for study practice.

Question 1

Glucagon binds its receptor on hepatocytes. Which sequence best describes the response in glycogen metabolism?

  1. Increased cAMP, activation of glycogen synthase and inhibition of phosphorylase
  2. Decreased cAMP, activated phosphatase, activation of glycogen synthase
  3. Increased cAMP, activated PKA, phosphorylation and activation of glycogen phosphorylase kinase, activation of glycogen phosphorylase, and inactivation of glycogen synthase
  4. Activation of tyrosine kinase receptors and stimulation of glycogen synthesis
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Answer: C. Increased cAMP, activated PKA, phosphorylation and activation of glycogen phosphorylase kinase, activation of glycogen phosphorylase, and inactivation of glycogen synthase

Glucagon acts through a G-protein-coupled receptor that raises cAMP and activates PKA. PKA phosphorylates phosphorylase kinase, which activates glycogen phosphorylase to degrade glycogen, and also phosphorylates glycogen synthase, which inactivates it. Both effects push the liver toward glucose release. Choice B describes the insulin response and choice D describes insulin receptor signaling.

Question 2

Why can glycogen stored in skeletal muscle NOT directly raise blood glucose concentration?

  1. Muscle lacks GLUT4
  2. Muscle cells lack glucose-6-phosphatase, so glucose-6-phosphate cannot be converted to free glucose and exported
  3. Muscle glycogen is a different molecule than liver glycogen
  4. Muscle cells lack glycogen phosphorylase
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Answer: B. Muscle cells lack glucose-6-phosphatase, so glucose-6-phosphate cannot be converted to free glucose and exported

Glycogenolysis in muscle yields glucose-1-phosphate, converted to glucose-6-phosphate, which is trapped inside the cell and used for glycolysis to fuel contraction. Liver expresses glucose-6-phosphatase, which removes the phosphate so glucose can leave through GLUT2. Muscle does have glycogen phosphorylase (choice D is false), and glycogen is chemically the same in both tissues.

Question 3

Blood measurements were taken from a healthy volunteer at three time points.

TimeGlucose (mM)InsulinGlucagonBeta-hydroxybutyrate (mM)
2 h after meal7.0highlow0.05
16 h fasted4.5lowhigh0.3
3 days fasted3.8very lowhigh3.0

What is the most likely benefit of the change seen at day 3?

  1. Ketone bodies are used by red blood cells, which then need less glucose
  2. The liver uses ketone bodies as its main fuel
  3. Ketone bodies allow the brain to meet part of its energy need, which reduces the amount of muscle protein broken down for gluconeogenesis
  4. Elevated ketone bodies increase insulin release, restoring glucose
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Answer: C. Ketone bodies allow the brain to meet part of its energy need, which reduces the amount of muscle protein broken down for gluconeogenesis

After several days of fasting, liver ketone production rises sharply. The brain takes up ketone bodies and replaces a large part of its glucose use, so less glucose must be made from amino acids, sparing muscle protein. Red blood cells have no mitochondria and cannot use ketones, the liver cannot use them either, and insulin remains low during fasting.

Question 4

Urea carries two nitrogen atoms. From which two sources do these nitrogen atoms enter the urea cycle?

  1. Two molecules of ammonium from glutamine
  2. Two nitrogen atoms from arginine's guanidino group only
  3. Free ammonium (via carbamoyl phosphate) and the amino group of aspartate
  4. The amino groups of glycine and serine
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Answer: C. Free ammonium (via carbamoyl phosphate) and the amino group of aspartate

Carbamoyl phosphate synthetase I combines ammonium (from glutamate dehydrogenase and glutaminase activity) with bicarbonate in the mitochondria to make carbamoyl phosphate, which donates the first nitrogen. In the cytosol, aspartate condenses with citrulline to form argininosuccinate and supplies the second nitrogen. Arginase then cleaves arginine into urea and ornithine, regenerating the carrier.

Question 5

In a transamination reaction catalyzed by alanine aminotransferase (ALT), alanine transfers its amino group to alpha-ketoglutarate. Which products and cofactor are involved?

  1. Pyruvate and glutamate, with pyridoxal phosphate (vitamin B6)
  2. Pyruvate and glutamine, with thiamine pyrophosphate
  3. Lactate and glutamate, with NAD+
  4. Oxaloacetate and aspartate, with biotin
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Answer: A. Pyruvate and glutamate, with pyridoxal phosphate (vitamin B6)

ALT shuttles the amino group from alanine to alpha-ketoglutarate, giving pyruvate (the keto acid) and glutamate (the new amino acid). All aminotransferases use pyridoxal phosphate, derived from vitamin B6, as the carrier of the amino group. Glutamate can then release ammonium by glutamate dehydrogenase or pass its nitrogen to aspartate for the urea cycle.

Question 6

Which amino acid is EXCLUSIVELY ketogenic, giving rise only to acetyl-CoA or acetoacetate and never to glucose?

  1. Alanine
  2. Leucine
  3. Aspartate
  4. Serine
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Answer: B. Leucine

Leucine and lysine are the only two purely ketogenic amino acids. Alanine and serine give pyruvate, and aspartate gives oxaloacetate, so all three are glucogenic. Phenylalanine, tyrosine, isoleucine and tryptophan can be both glucogenic and ketogenic, because they produce more than one type of breakdown product.

Question 7

Which statement about the hormones that regulate body mass is correct?

  1. Ghrelin is released by adipocytes and suppresses appetite
  2. Both hormones are made by the pancreas
  3. Leptin is released from adipose tissue and acts on the hypothalamus to decrease appetite, while ghrelin is released from the stomach and increases appetite
  4. Leptin is released from the stomach and stimulates appetite
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Answer: C. Leptin is released from adipose tissue and acts on the hypothalamus to decrease appetite, while ghrelin is released from the stomach and increases appetite

Leptin is an adipocyte hormone proportional to fat stores and acts on hypothalamic centers to reduce food intake. Ghrelin, from the empty stomach, rises before meals and stimulates hunger. Many people with obesity have high leptin levels but a blunted response, which is called leptin resistance.

Question 8

A patient with chronic excess cortisol (Cushing syndrome) is most likely to show which metabolic pattern?

  1. Hypoglycemia and increased muscle mass
  2. Hyperglycemia, muscle wasting, and increased gluconeogenesis
  3. Increased insulin sensitivity and weight loss
  4. Elevated ketone bodies with low blood glucose
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Answer: B. Hyperglycemia, muscle wasting, and increased gluconeogenesis

Cortisol raises blood glucose by stimulating gluconeogenic enzymes and by mobilizing amino acids from protein breakdown in muscle as substrate. It antagonizes insulin action in peripheral tissues, which leads to insulin resistance and hyperglycemia. Over time the result is muscle wasting, central fat redistribution and thin skin. These effects are opposite to choices A and C.

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Written by StudyStore from standard scientific facts as a study aid. These are not official exam questions and are not affiliated with or endorsed by any testing organization. Always check values against the reference provided with your exam or course.