Small Intestine Shields Liver from Fructose Toxicity
Many considered the liver to be the primary organ responsible for breaking down fructose, a sugar commonly present in fruit and other sweets. Although previous research identified metabolic pathways of fructose, the processing site remained a controversial issue in the science community. Contrary to the common belief that the liver metabolizes fructose, researchers have recently reported that the small intestine is the primary organ that clears fructose from the body. Further research also suggested that overdosing of fructose would overwhelm the small intestine, introducing excess fructose into the liver, increasing toxicity.
Fructose, along with glucose, is a hexose sugar that is responsible for the taste of sweetness in food. High fructose consumption is associated with metabolic disease, such as fatty liver disease. This creates a common misconception that the liver, an organ that is responsible for detoxifying the metabolites within the body, is responsible for the clearance of all consumed sugars. However, researchers found that the small intestine is the primary organ that is responsible for fructose clearance. In an effort to further understand how fructose is processed within the body, the researchers in the Jang Lab from Princeton University studied the fructose metabolism in mice. In this experiment, the researchers passed radioactive-isotope fructose through the digestive system in mice to visualize the fructose pathway upon consumption. To test their hypothesis, the researchers were able to disable the protein genetically in mice within the small intestine called KhK that is responsible for converting fructose to glucose and other metabolites that can be easily processed by the body.
What the researchers found was surprising. By tracking the radioactive fructose within the digestive system of mice, the researchers found that the small intestine clears more than 90% of the fructose in low doses. Yet, at higher doses of fructose, excess fructose is passed to the liver and the colon where microbacteria would breakdown the sugar. The excess fructose poured over to the liver is toxic as it exceeds the liver’s capacity to process fructose. This result is supported with the genetically modified mouse, in which the defective protein resulted in the inability to break down fructose, leaving excess fructose within the urine of the specimens. As a result, the small intestine was the major site of fructose metabolism to prevent excess fructose from poisoning the liver, a risk factor that may lead to major metabolic diseases such as diabetes or fatty liver disease.
Fructose, along with glucose, is a hexose sugar that is responsible for the taste of sweetness in food. High fructose consumption is associated with metabolic disease, such as fatty liver disease. This creates a common misconception that the liver, an organ that is responsible for detoxifying the metabolites within the body, is responsible for the clearance of all consumed sugars. However, researchers found that the small intestine is the primary organ that is responsible for fructose clearance. In an effort to further understand how fructose is processed within the body, the researchers in the Jang Lab from Princeton University studied the fructose metabolism in mice. In this experiment, the researchers passed radioactive-isotope fructose through the digestive system in mice to visualize the fructose pathway upon consumption. To test their hypothesis, the researchers were able to disable the protein genetically in mice within the small intestine called KhK that is responsible for converting fructose to glucose and other metabolites that can be easily processed by the body.
What the researchers found was surprising. By tracking the radioactive fructose within the digestive system of mice, the researchers found that the small intestine clears more than 90% of the fructose in low doses. Yet, at higher doses of fructose, excess fructose is passed to the liver and the colon where microbacteria would breakdown the sugar. The excess fructose poured over to the liver is toxic as it exceeds the liver’s capacity to process fructose. This result is supported with the genetically modified mouse, in which the defective protein resulted in the inability to break down fructose, leaving excess fructose within the urine of the specimens. As a result, the small intestine was the major site of fructose metabolism to prevent excess fructose from poisoning the liver, a risk factor that may lead to major metabolic diseases such as diabetes or fatty liver disease.
Image Source: bodymybody
This revised knowledge of the fructose metabolic process may be a crucial step in studying metabolism and its relation to common metabolic diseases. Further research is needed to elucidate the specific causes of these metabolic diseases that would help develop a method of cure and prevention to diseases such as diabetes and fatty liver disease.
Featured Image Source: Daria-Yakovleva
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