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The Sugar Shift: How Starchy Foods Turn into Fructose in Our Body

In the realm of nutrition, the sweet siblings - glucose and fructose - have captured our attention. They’re not twins, but they’re often mistakenly treated as such. Understanding the differences between them and how our body processes them is vital for our health.

Glucose and fructose are simple sugars or monosaccharides. Glucose is the primary energy source for our body, and its levels in our bloodstream are tightly regulated. Fructose, often found in fruits and honey, is not an essential nutrient and can pose problems when consumed in excess, particularly as it’s metabolized mainly in the liver, potentially leading to liver overload, insulin resistance, and obesity [1].

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An often overlooked fact is that our body can convert glucose into fructose via a process called the polyol pathway. This process primarily takes place in the liver, kidneys, and potentially to a lesser extent in other organs [2].


The polyol pathway is an alternative metabolic pathway for glucose that becomes more active when blood glucose levels are high. It involves the reduction of glucose to sorbitol, a sugar alcohol, by the enzyme aldose reductase. Sorbitol is then further metabolized to fructose by another enzyme, sorbitol dehydrogenase.

Various factors can influence the extend of this conversion. High blood glucose levels, low insulin levels or insulin resistance, high levels of the enzymes involved in the conversion process, and the availability of necessary cofactors can enhance this conversion [2]. Certain disease states like diabetes, metabolic syndrome, or obesity can also drive this process [3].


Foods and drinks with a high glycemic index, such as sugary and starchy foods, can contribute to rapid increases in blood glucose levels and potentially trigger this conversion process. Consuming these foods, especially in excess, can lead to an overproduction of endogenous fructose.


Aging can also bring changes in glucose metabolism, insulin sensitivity, and enzyme function, which might impact the glucose-fructose conversion process, but individual responses vary, necessitating more research in this area.


So, what are the implications for health and disease?


An overproduction of endogenous fructose can trigger health issues similar to those caused by high dietary fructose intake, including insulin resistance, fatty liver disease, and obesity [4].


Chronic hyperglycemia and over-activation of the polyol pathway can lead to various complications, particularly in tissues where glucose uptake is independent of insulin, such as the lenses of the eyes, nerves, and kidneys. This can result in osmotic stress, as well as oxidative stress, contributing to diabetic complications [5].


Re-think Starchy Foods!

Despite increasing awareness of the harmful metabolic effects of sugar, especially fructose, high-glucose foods like starchy carbs are still often considered healthy. However, the high glucose load of these foods, when rapidly absorbed, can contribute to metabolic disturbances, including the transformation of glucose into fructose. It's vital to reconsider our understanding of "healthy" carbohydrates in light of these effects!

 

[1] Tappy, L., & Lê, K. A. (2010). Metabolic effects of fructose and the worldwide increase in obesity. Physiological reviews, 90(1), 23-46. https://doi.org/10.1152/physrev.00019.2009


[2] Lanaspa, M. A., Ishimoto, T., Li, N., Cicerchi, C., Orlicky, D. J., Ruzycki, P., ... & Roncal-Jimenez, C. (2013). Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nature Communications, 4(1), 1-10. https://doi.org/10.1038/ncomms3434

[3] Giacco, F., & Brownlee, M. (2010). Oxidative stress and diabetic complications. Circulation research, 107(9), 1058-1070. https://doi.org/10.1161/CIRCRESAHA.110.223545


[4] Softic, S., Cohen, D. E., & Kahn, C. R. (2016). Role of dietary fructose and hepatic de novo lipogenesis in fatty liver disease. Digestive diseases and sciences, 61(5), 1282-1293. https://doi.org/10.1007/s10620-016-4054-0


[5] Brownlee, M. Biochemistry and molecular cell biology of diabetic complications. Nature 414, 813–820 (2001). https://doi.org/10.1038/414813a

 

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