The Genetic Cause: The Broken GULO Gene
The inability to convert glucose to vitamin C is not a matter of choice or diet, but a genetic flaw shared by a specific group of animals, including humans. The entire process of vitamin C synthesis from glucose in most mammals relies on four key enzymes. The final step, however, requires a functional L-gulonolactone oxidase (GULO) enzyme. Unfortunately, in certain species, the gene responsible for producing this enzyme (also called GULO) has undergone mutations, resulting in a non-functional pseudogene.
As a consequence of this genetic defect, the final step in the synthesis pathway cannot be completed. The body can convert glucose into the precursor compound, but without the active GULO enzyme, it cannot produce the final ascorbic acid. For these animals, vitamin C, or ascorbic acid, is a true vitamin—an essential nutrient that must be obtained from external sources through their diet.
A Shared Evolutionary History
The loss of the functional GULO gene has occurred independently in several unrelated lineages over evolutionary history. This is a fascinating example of convergent evolution, where different species develop the same biological trait or deficiency. For instance, the mutation in primates occurred approximately 63 million years ago, while the defect in guinea pigs is estimated to be around 14 million years old. These separate events suggest that the loss of this metabolic function was not lethal and could be sustained if the diet provided a sufficient and consistent source of vitamin C.
The Vitamin C Biosynthesis Pathway
The conversion of glucose to vitamin C (ascorbic acid) is a multi-step process in animals that can synthesize it. The pathway involves several enzymatic reactions, which can be summarized as follows:
- Initial Steps: Glucose is converted through several enzymatic steps, leading to the formation of UDP-glucuronic acid.
- Intermediate Steps: UDP-glucuronic acid is further processed, eventually yielding L-gulonic acid.
- Lactone Formation: The L-gulonic acid is converted into L-gulonolactone.
- Final Step (GULO Dependent): L-gulonolactone is oxidized by the L-gulonolactone oxidase (GULO) enzyme to produce ascorbic acid.
Animals with a non-functional GULO gene, such as humans and guinea pigs, can complete all the steps up to the formation of L-gulonolactone, but the critical final oxidation step fails.
Which Animals Cannot Convert Glucose to Vitamin C?
The answer to the question, "Which one of the following cannot convert glucose to vitamin C?" is rooted in this genetic and evolutionary context. The animals that cannot perform this conversion lack the functional GULO enzyme. These include:
- Haplorrhini Primates: This suborder includes apes, monkeys, and humans. All humans, therefore, cannot convert glucose to vitamin C. Our primate ancestors lost this ability millions of years ago, likely when their diets were already rich in fruits, making the endogenous production unnecessary for survival.
- Guinea Pigs: These rodents are famously unable to produce their own vitamin C, which is why their diets must be supplemented. The guinea pig GULO gene is mutated differently than the primate GULO gene, indicating an independent evolutionary event.
- Fruit-eating Bats: Some species of fruit-eating bats also lack the functional GULO gene, relying on their fruit-heavy diets for their vitamin C needs.
- Teleost Fish: This diverse group of fish, which includes most modern fish species, also cannot synthesize vitamin C. The loss occurred in their lineage hundreds of millions of years ago.
- Select Birds: A few species of birds, particularly in the Passeriformes order, have also independently lost the ability to produce vitamin C.
Comparing Vitamin C Synthesis Across Species
| Feature | Mammals with GULO (e.g., Cats, Dogs, Rats) | Mammals without GULO (e.g., Humans, Guinea Pigs) |
|---|---|---|
| GULO Enzyme | Functional and active. | Non-functional due to genetic mutation (pseudogene). |
| Vitamin C Source | Synthesized internally from glucose. | Obtained externally through diet. |
| Dietary Requirement | Not an essential dietary vitamin. | An essential dietary vitamin. |
| Result of Deficiency | Unlikely under normal conditions. | Scurvy, a potentially fatal disease. |
| Storage | Biosynthesis is regulated based on the body's needs. | Cannot be stored significantly; must be consumed regularly. |
| Example Species | Dogs, cats, goats, rats, mice. | Humans, apes, monkeys, guinea pigs. |
The Health Implications of a Missing Gene
For humans, the non-functional GULO gene means that a consistent dietary intake of vitamin C is critical to prevent scurvy, a disease caused by severe deficiency. Our bodies cannot fall back on internal production, so without sufficient consumption of fruits and vegetables, collagen synthesis is impaired, leading to fatigue, bleeding gums, and other severe symptoms. This dependency explains why a lack of fresh produce was historically so devastating for sailors on long voyages.
The story of the GULO pseudogene serves as a powerful reminder of our evolutionary past and highlights the fragility of biological systems. It also underscores the importance of a balanced diet for maintaining optimal health, as the metabolic solution for our ancestors was simply a shift in diet to accommodate for the lost genetic function.
For more information on the biochemistry and evolution of vitamin C, the NCBI's PubMed Central offers numerous peer-reviewed studies, including those on the L-gulonolactone oxidase deficiency in various species.
Conclusion
The simple answer to "Which one of the following cannot convert glucose to vitamin C?" is any animal with a non-functional L-gulonolactone oxidase (GULO) gene. This genetic defect, present in humans, guinea pigs, and certain other animals, means they must rely entirely on dietary sources of vitamin C. This dependency, a result of millions of years of evolution, makes vitamin C a true vitamin for us, unlike for the vast majority of mammals that can synthesize it on their own. Understanding this biological distinction is key to appreciating our nutritional needs and the fascinating role of genetics in shaping our health.