A 45-year-old man is brought to the emergency department by ambulance after vomiting blood. The patient reports that he only ate a small snack the morning before and had not eaten anything for over 24 hours. At the hospital, the patient is stabilized. He is admitted to a surgical floor and placed on NPO with a nasogastric tube set to intermittent suction. He has been previously diagnosed with liver cirrhosis. An esophagogastroduodenoscopy (EGD) has been planned for the next afternoon. At the time of endoscopy, some pathways were generating glucose to maintain serum glucose levels. Which of the following enzymes catalyzes the irreversible biochemical reaction of this process?
Q2
An 11-year-old boy is brought to the emergency room with acute abdominal pain and hematuria. Past medical history is significant for malaria. On physical examination, he has jaundice and a generalized pallor. His hemoglobin is 5 g/dL, and his peripheral blood smear reveals fragmented RBC, microspherocytes, and eccentrocytes (bite cells). Which of the following reactions catalyzed by the enzyme is most likely deficient in this patient?
Q3
An investigator is conducting an experiment to study different pathways of glucose metabolism. He obtains cells cultured from various tissues to study the effect of increased extracellular glucose concentration. Following the incubation of these cells in 5% dextrose, he measures the intracellular fructose concentration. The concentration of fructose is expected to be highest in cells obtained from which of the following tissues?
Q4
An investigator is studying muscle tissue in high-performance athletes. He obtains blood samples from athletes before and after a workout session consisting of short, fast sprints. Which of the following findings is most likely upon evaluation of blood obtained after the workout session?
Q5
A 12-year-old boy and his siblings are referred to a geneticist for evaluation of a mild but chronic hemolytic anemia that has presented with fatigue, splenomegaly, and scleral icterus. Coombs test is negative and blood smear does not show any abnormal findings. An enzymatic panel is assayed, and pyruvate kinase is found to be mutated on both alleles. The geneticist explains that pyruvate kinase functions in glycolysis and is involved in a classic example of feed-forward regulation. Which of the following metabolites is able to activate pyruvate kinase?
Q6
You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?
Q7
What is the primary mechanism for glucose uptake in neurons?
Q8
To maintain blood glucose levels even after glycogen stores have been depleted, the body, mainly the liver, is able to synthesize glucose in a process called gluconeogenesis. Which of the following reactions of gluconeogenesis requires an enzyme different from glycolysis?
Q9
A 16-year-old teenager is brought to the emergency department after having slipped on ice while walking to school. She hit her head on the side of the pavement and retained consciousness. She was brought to the closest ER within an hour of the incident. The ER physician sends her immediately to get a CT scan and also orders routine blood work. The physician understands that in cases of stress, such as in this patient, the concentration of certain hormones will be increased, while others will be decreased. Considering allosteric regulation by hormones, which of the following enzymes will most likely be inhibited in this patient?
Q10
A newborn undergoing the standard screening tests is found to have a positive test for reducing sugars. Further testing is performed and reveals that the patient does not have galactosemia, but rather is given a diagnosis of fructosuria. What levels of enzymatic activity are altered in this patient?
Glycolysis in different tissues US Medical PG Practice Questions and MCQs
Question 1: A 45-year-old man is brought to the emergency department by ambulance after vomiting blood. The patient reports that he only ate a small snack the morning before and had not eaten anything for over 24 hours. At the hospital, the patient is stabilized. He is admitted to a surgical floor and placed on NPO with a nasogastric tube set to intermittent suction. He has been previously diagnosed with liver cirrhosis. An esophagogastroduodenoscopy (EGD) has been planned for the next afternoon. At the time of endoscopy, some pathways were generating glucose to maintain serum glucose levels. Which of the following enzymes catalyzes the irreversible biochemical reaction of this process?
A. Glucose-6-phosphate dehydrogenase
B. Glycogen phosphorylase
C. Enolase
D. Glyceraldehyde-3-phosphate dehydrogenase
E. Fructose-1,6-bisphosphatase (Correct Answer)
Explanation: ***Fructose-1,6-bisphosphatase***
- The scenario describes a patient in a fasting state for over 24 hours, during which **gluconeogenesis** is crucial for maintaining blood glucose levels.
- **Fructose-1,6-bisphosphatase** is one of the key regulatory enzymes in gluconeogenesis, catalyzing an **irreversible reaction** that bypasses the phosphofructokinase-1 step of glycolysis.
*Glucose-6-phosphate dehydrogenase*
- This enzyme is involved in the **pentose phosphate pathway**, which generates NADPH and precursors for nucleotide synthesis.
- It does not directly participate in gluconeogenesis to produce glucose from non-carbohydrate sources.
*Glycogen phosphorylase*
- This enzyme is involved in **glycogenolysis**, the breakdown of glycogen into glucose-1-phosphate.
- While it releases glucose, the body's glycogen stores would likely be depleted after over 24 hours of fasting, making gluconeogenesis the primary pathway for glucose production.
*Enolase*
- Enolase is an enzyme in the glycolytic pathway, catalyzing the reversible conversion of 2-phosphoglycerate to phosphoenolpyruvate.
- It is not an enzyme of gluconeogenesis, nor does it catalyze an irreversible step in the glucose production process during fasting.
*Glyceraldehyde-3-phosphate dehydrogenase*
- This enzyme is also part of glycolysis, catalyzing the reversible oxidation and phosphorylation of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate.
- Like enolase, it is not an irreversible enzyme in gluconeogenesis that would be generating glucose under fasting conditions.
Question 2: An 11-year-old boy is brought to the emergency room with acute abdominal pain and hematuria. Past medical history is significant for malaria. On physical examination, he has jaundice and a generalized pallor. His hemoglobin is 5 g/dL, and his peripheral blood smear reveals fragmented RBC, microspherocytes, and eccentrocytes (bite cells). Which of the following reactions catalyzed by the enzyme is most likely deficient in this patient?
A. Glucose-1-phosphate + UTP → UDP-glucose + pyrophosphate
Explanation: ***D-glucose-6-phosphate + NADP+ → 6-phospho-D-glucono-1,5-lactone + NADPH + H+***
- This reaction is catalyzed by **glucose-6-phosphate dehydrogenase (G6PD)**, an enzyme critical for the production of **NADPH** in the **pentose phosphate pathway**.
- **NADPH** is essential for reducing **oxidative stress** in red blood cells. A deficiency in G6PD leads to increased susceptibility to hemolysis, especially under oxidative triggers like malaria, resulting in symptoms such as **acute hemolytic anemia**, jaundice, and specific morphological changes (e.g., **fragmented RBCs**, **microspherocytes**, and **eccentrocytes**, also known as **bite cells**).
*Glucose-1-phosphate + UTP → UDP-glucose + pyrophosphate*
- This reaction is catalyzed by **UDP-glucose pyrophosphorylase** and is important for **glycogen synthesis**.
- A deficiency in this enzyme would primarily affect glycogen metabolism and would not explain the **hemolytic anemia** or the characteristic red blood cell morphology seen in the patient.
*Glucose + ATP → Glucose-6-phosphate + ADP + H+*
- This reaction is catalyzed by **hexokinase**, the first committed step in **glycolysis**.
- While hexokinase deficiency can cause **hemolytic anemia**, it generally presents with chronic, moderate anemia and does not typically involve the specific red blood cell morphology (eccentrocytes/bite cells) associated with oxidative damage found in G6PD deficiency.
*D-glucose 6-phosphate → D-fructose-6-phosphate*
- This reaction is catalyzed by **phosphoglucose isomerase** (also known as phosphohexose isomerase) and is part of **glycolysis**.
- A deficiency in this enzyme would impair glycolysis and lead to **hemolytic anemia**, but its clinical presentation and RBC morphology differ from what is typically seen in G6PD deficiency, particularly the absence of oxidative stress markers like bite cells.
*Glucose-6-phosphate + H2O → glucose + Pi*
- This reaction is catalyzed by **glucose-6-phosphatase**, an enzyme found primarily in the liver and kidney, responsible for the final step in **gluconeogenesis** and glycogenolysis to release free glucose into the bloodstream.
- A deficiency in glucose-6-phosphatase leads to **glycogen storage disease type I (Von Gierke's disease)**, characterized by **hypoglycemia**, **lactic acidosis**, and hepatomegaly, not hemolytic anemia.
Question 3: An investigator is conducting an experiment to study different pathways of glucose metabolism. He obtains cells cultured from various tissues to study the effect of increased extracellular glucose concentration. Following the incubation of these cells in 5% dextrose, he measures the intracellular fructose concentration. The concentration of fructose is expected to be highest in cells obtained from which of the following tissues?
A. Ovary
B. Retina
C. Myelin sheath
D. Kidney
E. Lens (Correct Answer)
Explanation: ***Lens***
- The **lens** is rich in the enzyme **aldose reductase**, which converts glucose to sorbitol, and then **sorbitol dehydrogenase** converts sorbitol to fructose via the **polyol pathway**.
- In a high-glucose environment, this pathway becomes highly active in the lens, leading to an increased production and accumulation of **fructose**, which can contribute to osmotic stress and cataract formation.
*Ovary*
- While other reproductive tissues can metabolize glucose, the **ovary** is not a primary site for significant fructose accumulation through the **polyol pathway** in response to elevated glucose.
- Its metabolic activity is more geared towards steroidogenesis and oocyte development rather than high fructose production from glucose.
*Retina*
- The **retina** contains some aldose reductase activity, and increased glucose can activate the **polyol pathway**, leading to sorbitol and fructose accumulation.
- However, the lens typically shows a more pronounced increase in fructose concentration due to its higher metabolic flux through this pathway and its susceptibility to osmotic damage.
*Myelin sheath*
- The **myelin sheath**, primarily composed of lipids, is part of the nervous system and is not known for significant **fructose production** via the **polyol pathway** in response to high glucose.
- Damage to myelin in diabetic conditions is often linked to other mechanisms like glycation and oxidative stress rather than direct fructose accumulation.
*Kidney*
- The **kidney** can utilize the **polyol pathway**, and conditions like **diabetic nephropathy** involve increased sorbitol and fructose production.
- However, the magnitude of fructose accumulation and its direct pathogenic role differ from that in the lens, where osmotic effects of polyols are particularly critical.
Question 4: An investigator is studying muscle tissue in high-performance athletes. He obtains blood samples from athletes before and after a workout session consisting of short, fast sprints. Which of the following findings is most likely upon evaluation of blood obtained after the workout session?
A. Decreased concentration of NADH
B. Increased concentration of H+ (Correct Answer)
C. Decreased concentration of lactate
D. Increased concentration of insulin
E. Increased concentration of ATP
Explanation: ***Increased concentration of H+***
- During **anaerobic metabolism** in high-intensity exercise like sprints, pyruvate is converted to **lactate** by **lactate dehydrogenase** to regenerate NAD+. This process produces H+, leading to a decrease in pH and an increase in H+ concentration in the blood.
- The accumulation of **hydrogen ions (H+)** contributes to metabolic acidosis, muscle fatigue, and the burning sensation experienced during intense exertion.
- Blood gas analysis would show **decreased pH** and **increased H+ concentration**.
*Decreased concentration of NADH*
- NADH is primarily an **intracellular metabolite** and is not typically measured in blood samples as it does not circulate freely in significant concentrations.
- Within muscle cells during anaerobic glycolysis, NADH is consumed by lactate dehydrogenase to convert pyruvate to lactate, regenerating NAD+ for continued glycolysis.
- This option is not a realistic blood finding from a clinical laboratory perspective.
*Decreased concentration of lactate*
- **High-intensity sprints** primarily rely on **anaerobic metabolism**, which rapidly produces **lactate** from pyruvate.
- Therefore, the concentration of lactate in the blood would significantly **increase** after such a workout, not decrease.
- Elevated blood lactate is a hallmark finding after intense anaerobic exercise.
*Increased concentration of insulin*
- **Insulin** levels typically **decrease** during exercise, especially high-intensity exercise, due to **sympathetic nervous system activation** and the body's need to mobilize glucose from liver glycogen and fatty acids.
- Exercise promotes glucose uptake through **insulin-independent mechanisms** (GLUT4 translocation via AMP-activated protein kinase).
- Increased insulin would be counterproductive during intense exercise when glucose mobilization is needed.
*Increased concentration of ATP*
- ATP does not circulate in blood in measurable concentrations as a typical laboratory finding.
- Within muscle cells, ATP is rapidly **consumed** during intense exercise to fuel muscle contraction.
- While cells work to maintain ATP levels through anaerobic glycolysis and the creatine phosphate system, net ATP does not accumulate in the blood.
Question 5: A 12-year-old boy and his siblings are referred to a geneticist for evaluation of a mild but chronic hemolytic anemia that has presented with fatigue, splenomegaly, and scleral icterus. Coombs test is negative and blood smear does not show any abnormal findings. An enzymatic panel is assayed, and pyruvate kinase is found to be mutated on both alleles. The geneticist explains that pyruvate kinase functions in glycolysis and is involved in a classic example of feed-forward regulation. Which of the following metabolites is able to activate pyruvate kinase?
A. Fructose-1,6-bisphosphate (Correct Answer)
B. Alanine
C. ATP
D. Glucose-6-phosphate
E. Glyceraldehyde-3-phosphate
Explanation: ***Fructose-1,6-bisphosphate***
- **Fructose-1,6-bisphosphate** is a potent **allosteric activator** of pyruvate kinase. This is an example of **feed-forward activation**, where a product of an early irreversible step in glycolysis (catalyzed by phosphofructokinase-1) activates a later enzyme (pyruvate kinase) in the pathway.
- This activation ensures that substrates for the later steps of glycolysis are rapidly utilized when earlier steps are highly active, matching the rate of metabolite flow and increasing the overall efficiency of glycolysis for energy production.
*Alanine*
- **Alanine** is an **inhibitor** of pyruvate kinase, not an activator. It serves as an indicator of a high cellular energy state and ample amino acid supply.
- High levels of alanine signal the cell that there is sufficient energy and building blocks, thus **shutting down** glycolysis at the pyruvate kinase step to conserve glucose for other needs like glycogen synthesis.
*ATP*
- **ATP** (adenosine triphosphate) is an **allosteric inhibitor** of pyruvate kinase. High ATP levels signal a high energy state in the cell.
- When the cell has sufficient energy, ATP binds to a regulatory site on pyruvate kinase, reducing its activity and **slowing down glycolysis** to prevent overproduction of ATP.
*Glucose-6-phosphate*
- **Glucose-6-phosphate** is an intermediate in glycolysis but does not directly activate pyruvate kinase. It can act as an allosteric inhibitor of hexokinase, the first enzyme in glycolysis, but not pyruvate kinase.
- Its accumulation typically signifies a **backup** in the glycolytic pathway (e.g., due to downstream inhibition), leading to a *reduction* in overall glucose flux rather than a direct activation of pyruvate kinase.
*Glyceraldehyde-3-phosphate*
- **Glyceraldehyde-3-phosphate** is an intermediate in glycolysis, but it does not directly activate pyruvate kinase. It is a substrate for glyceraldehyde-3-phosphate dehydrogenase.
- While its presence indicates active glycolysis, it does not exert a specific allosteric regulatory effect on pyruvate kinase in the way fructose-1,6-bisphosphate does.
Question 6: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?
A. Norepinephrine causes increased glucose absorption within the intestines.
B. Without epinephrine, insulin cannot act on the liver.
C. Peripheral tissues require epinephrine to take up glucose.
D. Epinephrine increases liver glycogenolysis. (Correct Answer)
E. Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.
Explanation: ***Epinephrine increases liver glycogenolysis.***
- **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy.
- It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**.
*Norepinephrine causes increased glucose absorption within the intestines.*
- **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress.
- Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine.
*Without epinephrine, insulin cannot act on the liver.*
- **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**.
- Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it.
*Peripheral tissues require epinephrine to take up glucose.*
- **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**.
- Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress.
*Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.*
- Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**.
- This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.
Question 7: What is the primary mechanism for glucose uptake in neurons?
A. GLUT1
B. GLUT2
C. GLUT3 (Correct Answer)
D. GLUT4
Explanation: ***GLUT3***
- **GLUT3** is the primary glucose transporter in **neurons** and has a **high affinity** for glucose.
- This high affinity ensures that neurons can continuously take up glucose, even when blood glucose levels are relatively low, to meet their significant energy demands.
*GLUT1*
- **GLUT1** is abundant in **red blood cells** and at the **blood-brain barrier**, where it provides basal glucose transport to many cell types.
- While present in the brain, it is primarily responsible for glucose transport across the **blood-brain barrier** into the interstitial fluid, not directly into neurons as the main mechanism.
*GLUT2*
- **GLUT2** has a **low affinity** and **high capacity** for glucose, primarily found in the **liver, pancreatic beta cells, kidney, and intestine**.
- Its role is to sense high glucose levels and transport large amounts of glucose accordingly, which is not characteristic of neuronal glucose uptake.
*GLUT4*
- **GLUT4** is the **insulin-sensitive** glucose transporter, predominantly found in **adipose tissue** and **skeletal muscle**.
- Its translocation to the cell membrane is stimulated by insulin, a mechanism not central to neuronal glucose uptake.
Question 8: To maintain blood glucose levels even after glycogen stores have been depleted, the body, mainly the liver, is able to synthesize glucose in a process called gluconeogenesis. Which of the following reactions of gluconeogenesis requires an enzyme different from glycolysis?
A. Fructose 1,6-bisphosphate --> Fructose-6-phosphate (Correct Answer)
B. Glyceraldehyde 3-phosphate --> 1,3-bisphosphoglycerate
C. 2-phosphoglycerate --> 3-phosphoglycerate
D. Dihydroxyacetone phosphate --> Glyceraldehyde 3-phosphate
E. Phosphoenolpyruvate --> 2-phosphoglycerate
Explanation: ***Fructose 1,6-bisphosphate --> Fructose-6-phosphate***
- This reaction in gluconeogenesis is catalyzed by **fructose 1,6-bisphosphatase**, which is distinct from **phosphofructokinase-1** that catalyzes the reverse reaction in glycolysis.
- This step is one of the three **irreversible steps** in glycolysis that must be bypassed by different enzymes in gluconeogenesis to ensure the unidirectional flow of the pathway.
*Glyceraldehyde 3-phosphate --> 1,3-bisphosphoglycerate*
- This reaction is catalyzed by **Glyceraldehyde 3-phosphate dehydrogenase** in both glycolysis and gluconeogenesis, as it is a **reversible step**.
- In gluconeogenesis, the equilibrium is shifted towards the formation of glyceraldehyde 3-phosphate due to the low concentration of products.
*2-phosphoglycerate --> 3-phosphoglycerate*
- This is a reversible isomerization reaction catalyzed by **phosphoglycerate mutase** in both glycolysis and gluconeogenesis.
- No unique enzyme is required for gluconeogenesis at this step.
*Dihydroxyacetone phosphate --> Glyceraldehyde 3-phosphate*
- This reversible interconversion between these two triose phosphates is catalyzed by **triose phosphate isomerase** in both pathways.
- These molecules are in equilibrium and can be readily converted from one to the other.
*Phosphoenolpyruvate --> 2-phosphoglycerate*
- This is a reversible reaction catalyzed by **enolase** in both glycolysis and gluconeogenesis.
- No distinct enzyme is needed for this step in gluconeogenesis.
Question 9: A 16-year-old teenager is brought to the emergency department after having slipped on ice while walking to school. She hit her head on the side of the pavement and retained consciousness. She was brought to the closest ER within an hour of the incident. The ER physician sends her immediately to get a CT scan and also orders routine blood work. The physician understands that in cases of stress, such as in this patient, the concentration of certain hormones will be increased, while others will be decreased. Considering allosteric regulation by hormones, which of the following enzymes will most likely be inhibited in this patient?
A. Glucose-6-phosphatase
B. Fructose 1,6-bisphosphatase
C. Pyruvate carboxylase
D. Phosphofructokinase (Correct Answer)
E. Glycogen phosphorylase
Explanation: ***Phosphofructokinase***
- In a stress state, **cortisol** and **epinephrine** levels are elevated, leading to increased **gluconeogenesis** and **glycogenolysis** to provide rapid energy.
- **Allosteric inhibition** of PFK-1 occurs through multiple mechanisms:
- **ATP** and **citrate** (high energy signals) act as direct **allosteric inhibitors** of PFK-1
- **Glucagon** (elevated during stress) indirectly inhibits PFK-1 by reducing levels of **fructose-2,6-bisphosphate**, a potent allosteric activator
- This inhibition of glycolysis spares glucose for critical organs like the brain and heart.
*Glucose-6-phosphatase*
- This enzyme catalyzes the final step of **gluconeogenesis** and **glycogenolysis**, converting G6P to free glucose.
- During stress, its activity is **stimulated** to increase blood glucose levels, not inhibited.
*Fructose 1,6-bisphosphatase*
- This enzyme plays a key role in **gluconeogenesis**, a process vital for maintaining glucose homeostasis during stress.
- Its activity would be **upregulated** to produce glucose, rather than inhibited.
*Pyruvate carboxylase*
- This enzyme initiates **gluconeogenesis** by converting pyruvate to oxaloacetate in the mitochondria.
- During stress, its activity is **stimulated** by elevated acetyl-CoA (an allosteric activator), not inhibited.
*Glycogen phosphorylase*
- This enzyme is responsible for **glycogenolysis**, the breakdown of glycogen into glucose-1-phosphate.
- Its activity is **stimulated** by stress hormones (epinephrine and glucagon) through cAMP-mediated phosphorylation, ensuring rapid glucose availability.
Question 10: A newborn undergoing the standard screening tests is found to have a positive test for reducing sugars. Further testing is performed and reveals that the patient does not have galactosemia, but rather is given a diagnosis of fructosuria. What levels of enzymatic activity are altered in this patient?
A. Hexokinase decreased; fructokinase decreased
B. Hexokinase unchanged; fructokinase unchanged
C. Hexokinase increased; fructokinase increased
D. Hexokinase increased; fructokinase decreased
E. Hexokinase unchanged; fructokinase decreased (Correct Answer)
Explanation: ***Hexokinase unchanged; fructokinase decreased***
- **Essential fructosuria** is caused by a deficiency in **fructokinase**, the enzyme responsible for the first step of fructose metabolism (fructose → fructose-1-phosphate).
- This results in **decreased or absent fructokinase activity**, leading to fructose accumulation in blood and urine (positive reducing sugar test).
- **Hexokinase activity remains unchanged** - there is no upregulation or compensatory increase in hexokinase. The enzyme maintains its normal baseline activity.
- Essential fructosuria is a **benign, asymptomatic condition** with no metabolic stress, so no compensatory enzyme changes occur.
- The small amount of fructose that needs metabolism can be handled by normal baseline hexokinase activity (hexokinase has broad substrate specificity).
*Hexokinase decreased; fructokinase decreased*
- While **fructokinase is decreased** in essential fructosuria, hexokinase activity is not decreased.
- Hexokinase is a constitutively expressed glycolytic enzyme whose activity does not change in this benign condition.
*Hexokinase unchanged; fructokinase unchanged*
- This is incorrect because **fructokinase activity is specifically decreased** in essential fructosuria, which is the defining enzymatic defect of the condition.
- The decreased fructokinase activity causes fructose to accumulate and appear in the urine.
*Hexokinase increased; fructokinase increased*
- **Fructokinase is decreased, not increased** - an increase would prevent the fructose accumulation characteristic of this condition.
- Hexokinase activity does not increase as essential fructosuria causes no metabolic stress requiring compensation.
*Hexokinase increased; fructokinase decreased*
- While **fructokinase is decreased** in essential fructosuria, hexokinase activity does not increase.
- This is a benign condition with no compensatory enzyme upregulation - hexokinase maintains normal baseline activity levels.
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