Ever heard of a fruitarian diet? It is one of the most restrictive diet choices available, which consists of 55% to 75% of raw fruit, with almost no evidence of health benefits. But fruit is good, you might argue. And you are right if fruit is eaten in moderate amounts. Fruits provide us with fructose, a simple sugar, like glucose. Although these simple sugars are structurally similar to each other, our body processes them in a different ways.
A recent study explained how fructose acts in our body. According to the study, the most of the fructose is absorbed by cells lining the intestine. Protein transporters called GLUT5 and GLUT2, expressed by intestinal cells, facilitate this absorption, with GLUT5 showing the highest affinity to fructose. Interestingly, these receptors are regulated in response to fructose levels. That is why GLUT5 deficiency can result in fructose malabsorption and intestinal dysfunction (think of bloating or fluid accumulation).
When fructose enters circulation, its levels in the blood (albeit much lower than glucose) are kept by the kidney and liver. In these organs, fructose is redirected for glucose production, via a process called “gluconeogenesis”. However, this reaction requires the breakdown of a molecule called “ATP” (the main source of energy in cells). Therefore, an excessive intake of fructose can lead to ATP depletion in cells, which activates another pathway involved in uric acid metabolism—leading to an accumulation of uric acid in the blood and joints and increasing the risk of developing a condition causing severe joint pain (“gout”). The researchers further explain that fructose consumption can also trigger an increase in cholesterol levels and abdominal fat, increasing the risk of heart illnesses. Moreover, excess of fructose can cause fat buildup in the liver, leading to insulin resistance in the liver and non-alcoholic fatty liver disease.
In addition, our genes are also involved in regulation of fructose metabolism. A protein called ChREBP is a crucial regulator of genes involved in the absorption, transport, and degradation of sugars. Animal studies in ChREBP-deficient mice suggest that ChREBP is essential for fructose absorption and clearance. How exactly ChREBP can be activated in response to fructose stimulation, is a question for further investigation.
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