Diabetes, Acidity And Digestion: How Can They Be Linked?
One aspect of digestive issues that diabetics face can come about from the concept of glycation.
One of the common blood tests that diabetics undertake regularly is to measure the levels of HbA1c in their blood. HbA1c is what we would know as glycated haemoglobin, or how much haemoglobin proteins in the blood have reacted with the free glucose in the blood?
The idea being that this HbA1c sugar-protein conjugate isn’t as great at moving molecular oxygen through the body. When the haemoglobin protein has been glycated, or, in other words, reacted with glucose, it cannot be counted upon to transport oxygen to the cells and tissues in our body.
For a more severe diabetes case, we’d be looking at a higher level of HbA1c in the blood, and a greater problem at transporting oxygen to those tissues. As the oxygen transfer efficiency is reduced, the diabetic would face issues such as:
- A reduced energy generation efficiency, which can lead to the problem of an earlier fatigue onset or a lack of stamina.
- A reduced ability for the immune system to heal the body from the injuries that it may experience, which is also why the severely diabetic ought to be extremely careful about not cutting their feet, as that can potentially lead into gangrene, necrosis and amputations.
It is a fallacious assumption to think that diabetes is just a case of having too much glucose in the blood — because these glucose molecules are chemically reactive and can potentially react with any biomolecules or cells within our body.
We just don’t think about glucose in that manner, do we?
How does that link to our digestive system?
We have to understand that the hydrochloric acid being produced for digesting foods in our stomach is also based on enzymatic activity.
The acids in the stomach are produced based on the activity of the carbonic anhydrase (CA) enzyme. CA is an enzyme “that assists rapid inter-conversion of carbon dioxide and water into carbonic acid, protons and bicarbonate ions”.
In our digestive system, CA is responsible for the production of gastric acid by the parietal cells:
HCl is produced by the parietal cells of the stomach. To begin with, water (H2O) and carbon dioxide (CO2) combine within the parietal cell cytoplasm to produce carbonic acid (H2CO3), catalysed by carbonic anhydrase. Carbonic acid then spontaneously dissociates into a hydrogen ion (H+) and a bicarbonate ion (HCO3–).
The hydrogen ion that was formed is transported into the stomach lumen via the H+– K+ ATPase. This channel uses ATP energy to exchange potassium ions in the stomach with hydrogen ions in the parietal cell.
The bicarbonate ion is transported out of the cell into the blood via a transporter protein called anion exchanger which transports the bicarbonate ion out the cell in exchange for a chloride ion (Cl–). This chloride ion is then transported into the stomach lumen via a chloride channel.
This results in both hydrogen and chloride ions being present within the stomach lumen. Their opposing charges leads to them associating with each other to form hydrochloric acid (HCl).
Similarly, CA in the kidneys is thought to maintain the acid/base equilibrium in our blood based on controlling bicarbonate resorption from our urine before excretion, with the mechanism outlined here:
In the proximal convoluted tubule (PCT) cell, carbonic anhydrase (not shown) generates bicarbonate and hydrogen from water and carbon dioxide. Sodium in filtered urine is resorbed in exchange (with a sodium/hydrogen cotransporter) for the hydrogen produced from carbonic anhydrase. The excreted hydrogen then combines with filtered bicarbonate. This forms the weak acid, carbonic acid, which then disassociates to produce water and carbon dioxide in the urine (tubular lumen). The bicarbonate created by carbonic anhydrase is transported, with the resorbed sodium, into the blood via a basolateral (blood side) sodium/bicarbonate cotransporter. Thus, through carbonic anhydrase and sodium absorption, the proximal tubules “reclaim” the filtered bicarbonate (or, in reality, generate new bicarbonate which replaces that lost in the urine, so there is no net gain of bicarbonate).
When the acidity in our body is compromised
In our kidneys and our stomach, the CA enzyme is extremely important for maintaining the appropriate levels of acidity, which would have a significant bearing on our digestive functions otherwise.
So the problem that a diabetic would face, therefore, would be related to the potential glycation of the CA enzymes in the stomach and in the kidneys, because CA is a protein as haemoglobin is. If haemoglobin can be glycated and lose its functionality in one’s body, it wouldn’t be surprising to see that CA can be affected in the same way via glycation.
If the CA enzyme is damaged via glycation, it cannot do its work in maintaining stomach acidity or blood/urine pH control. These symptoms would manifest themselves in a reduced food digestion ability or blood acidosis over time. They’re just symptoms of excess glucose in the blood.
It’s amazing how the little cells in our body contain the genes encoded within our DNA to produce small minuscule enzymes that can affect the body’s functions at the macro level, isn’t it?
For the readers out there who know people living through chronic diabetes: how informed are these diabetic patients about what diabetes can do to their digestive systems in the long run?
Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 5 ebooks (available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should.
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