Surreal illustration of a desert transforming into an oasis, symbolizing the shift from dehydration to hydration.

Thirsty Camel? What Long-Term Dehydration Does to Your Gut

Theo Raines in Health & Wellness November 2025 • 4 min read.

"New research explores the surprising effects of dehydration on the gastric mucosa, revealing how your body adapts to survive water scarcity."

We all know that drinking water is essential for survival. But what happens when dehydration becomes a long-term issue? While short-term dehydration can cause headaches and fatigue, chronic dehydration can lead to more serious health problems. A recent study published in Molecular and Cellular Biochemistry has shed light on the effects of long-term dehydration on the gastric mucosa, the lining of the stomach, using the one-humped dromedary camel as a model.

Camels are renowned for their ability to survive in harsh, arid environments with limited access to water. This makes them an ideal subject for understanding how the body adapts to prolonged dehydration. The study investigated various parameters, including oxidative stress, apoptosis (cell death), gastric epithelial histology, and levels of gastric neuropeptides and their receptors.

The research involved dividing camels into three groups: a control group with unrestricted access to water, a dehydrated group deprived of water for 20 days, and a rehydrated group that was dehydrated for 20 days and then allowed free access to water for 72 hours. The researchers then analyzed the gastric mucosa of these camels to identify the specific changes caused by dehydration and subsequent rehydration.

Dehydration's Impact: How Does It Affect Your Stomach Lining?

Surreal illustration of a desert transforming into an oasis, symbolizing the shift from dehydration to hydration.

The study's findings revealed significant changes in the gastric mucosa of dehydrated camels. One of the key observations was an increase in oxidative stress, indicated by higher levels of malondialdehyde (MDA), glutathione, nitric oxide, and catalase. Oxidative stress occurs when there's an imbalance between the production of free radicals and the body's ability to neutralize them, leading to cell damage.

Further analysis revealed that dehydration caused structural changes in the gastric mucosa, including cellular vacuoles of varying sizes and focal necrosis, which is the premature death of cells in living tissue. These changes suggest that dehydration inflicts damage to the stomach lining at a cellular level.

Oxidative Stress: Increased levels of MDA, glutathione, nitric oxide, and catalase.
Cellular Damage: Formation of cellular vacuoles and focal necrosis in the gastric mucosa.
Apoptosis: Significant increase in apoptotic markers like tumor necrosis factor α, caspases 8 and 3, BcL-x1, and TGFβ.
Neuropeptide Changes: Increased prostaglandin E2 receptors and somatostatin, decreased cholecystokinin-8 receptors.
Enzyme Activity: Significant decrease in hydrogen potassium ATPase enzyme activity.

The researchers also examined the effects of rehydration on the gastric mucosa. While rehydration for 72 hours improved some parameters, it wasn't sufficient to completely reverse the effects of dehydration. The study noted a significant increase in apoptotic markers, indicating that dehydration triggers programmed cell death. Specifically, the levels of tumor necrosis factor α, caspases 8 and 3, BcL-x1, and TGFβ were elevated in dehydrated camels.

Adapting to Survive: What It Means for Humans?

This study provides valuable insights into how the body adapts to survive dehydration. The researchers concluded that long-term dehydration induces oxidative stress and apoptosis in the camel's gastric mucosa and that camels adjust gastric functions during dehydration towards water economy. More than 72 hours are needed before all the effects of dehydration are reversed by rehydration. While camels have unique adaptations, these findings highlight the importance of staying hydrated for overall health and well-being. Understanding the specific impacts of dehydration on the gastric mucosa can inform strategies for preventing and managing dehydration-related health issues in humans.

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This article is based on research published under:

DOI-LINK: 10.1007/s11010-018-3474-x, Alternate LINK

Title: Effects Of Long-Term Dehydration On Oxidative Stress, Apoptotic Markers And Neuropeptides In The Gastric Mucosa Of The Dromedary Camel

Subject: Cell Biology

Journal: Molecular and Cellular Biochemistry

Publisher: Springer Science and Business Media LLC

Authors: Mahmoud A. Ali, Hassan Abu Damir, Naheed Amir, E. A. Adeghate, Salim Bastaki, David Murphy, Abdu Adem

Published: 2018-11-26

Everything You Need To Know

What specific changes occur in the gastric mucosa as a result of long-term dehydration?

Long-term dehydration impacts the gastric mucosa by increasing oxidative stress, leading to higher levels of malondialdehyde (MDA), glutathione, nitric oxide, and catalase. It also causes structural changes like cellular vacuoles and focal necrosis, indicating damage at the cellular level. Furthermore, dehydration triggers apoptosis, with elevated levels of tumor necrosis factor α, caspases 8 and 3, BcL-x1, and TGFβ.

Can the effects of dehydration on the gastric mucosa be fully reversed by rehydration? If not, what are the limitations?

The study found that rehydration for 72 hours improved some parameters in the gastric mucosa but was not sufficient to completely reverse the effects of dehydration. Specifically, there was still a significant increase in apoptotic markers, suggesting that more time is needed to fully recover from the damage caused by prolonged water deprivation. The enzyme hydrogen potassium ATPase activity also requires more than 72 hours to recover.

How do camels adapt their gastric functions to survive long-term dehydration, and what specific neuropeptide changes are involved?

Camels adapt to long-term dehydration by adjusting gastric functions towards water economy, as evidenced by the changes in neuropeptide levels in the gastric mucosa. This includes increased prostaglandin E2 receptors and somatostatin, along with decreased cholecystokinin-8 receptors, helping the animal conserve water and maintain gut health under arid conditions. The changes observed allow the one-humped dromedary camel to survive water scarcity.

What impact does dehydration have on the activity of the hydrogen potassium ATPase enzyme in the gastric mucosa, and what are the potential implications?

The study on camels revealed a significant decrease in hydrogen potassium ATPase enzyme activity in the gastric mucosa due to dehydration. This enzyme is crucial for acid production in the stomach, and its reduced activity could impact digestion and nutrient absorption during periods of water scarcity. Further research could explore the long-term effects of this reduced activity and how it affects overall gastric function and the gastric acid secretion.

Why does apoptosis increase in the gastric mucosa due to dehydration, and what role do tumor necrosis factor α, caspases 8 and 3, BcL-x1, and TGFβ play in this process?

Apoptosis, or programmed cell death, is significantly increased in the gastric mucosa during dehydration, as indicated by elevated levels of tumor necrosis factor α, caspases 8 and 3, BcL-x1, and TGFβ. This process allows the gastric mucosa to remove damaged cells and prevent further harm during times of water scarcity, but prolonged apoptosis can lead to tissue damage and impaired function. Understanding how to modulate apoptosis could provide insights into managing dehydration-related gut issues.