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Fructose is a sweetener naturally found in fruits and honey.
Fructose is a sweetener naturally found in fruits and honey.
It is also a component of high fructose corn syrup and is used to sweeten foods and beverages
.
Fructose is contained in fruit drinks, milk tea, baked goods, and sweetened yogurt
.
The more milk tea shops opened, the drinks became more and more delicious .
We are now consuming more fructose than at any time in history, but the price of increased fructose consumption is the increased incidence of obesity and cancer .
Fructose metabolism begins in the epithelium of the small intestine, where fructose is transported by the type 5 glucose transporter (GLUT5; encoded by SLC2A5) and is phosphorylated by kethexaol to form fructose 1-phosphate, which can accumulate to a high level in the cell Level .
Although this pathway is related to the promotion of obesity and tumors, the exact mechanism is still unclear .
Recently, a study published in the journal Nature found that eating fructose can increase the survival rate of intestinal epithelial cells, thereby increasing the length of intestinal villi and enabling them to absorb more nutrients .
Studies have shown that the main metabolite of fructose promotes the elongation of villi .
The villi of mice fed a fructose diet were 25% to 40% longer than mice that were not fed fructose, which caused the mice to gain weight .
DOI: 10.
1038/s41586-021-03827-2 Villus (villus) is a slender hair-like structure arranged inside the small intestine .
Fluff to expand the surface area of the intestine to help the body in food through digestion time channel to absorb nutrients from food, including fat .
Therefore, the increase in villi length is related to the nutrient absorption, weight gain and fat accumulation of animals .
Digestion
Interestingly, the result of fructose's increase in villi was unexpectedly discovered
.
At first, the research team did not intend to study the small intestinal villi
.
A previous study published by the team in 2019 found that dietary fructose can increase tumor size in mouse models of colorectal cancer , and blocking fructose metabolism can prevent this from happening .
Considering that fructose may also promote the proliferation or accelerated growth of the small intestine, the researchers examined the tissue structure of mice treated with fructose or a control diet under a microscope .
Colorectal cancer studies have observed that in mice on a high fructose diet, the length of the villi of the mice increased significantly .
When the researcher discovered this unexpected result, the research team immediately began to study the villi, trying to determine whether the function of the villi would be different as the length of these hairs increased .
Therefore, they divided the mice into 3 groups: a control diet without fructose, a standard high-fat diet with glucose and no fructose (45% of calories come from fat), and an isocaloric high-fat diet (glucose is replaced by sucrose, sucrose In half glucose, half fructose) .
The study found that although the energy consumed by each group of mice was the same , the mice fed with fructose in the form of sucrose had a significant increase in body weight and fat compared with mice in the high-fat diet without fructose, and the intestinal villi were longer .
Mice fed with fructose had higher body weight and longer villi.
In addition, mice fed with fructose in the form of sucrose had higher serum triglyceride levels after oral fat intake compared with control mice without sucrose .
These data indicate that the fructose in the diet can increase the length of the intestinal villi and the absorption of nutrients .
Then, the researchers carefully studied the metabolic changes in the fructose group of mice and found that a specific metabolite of fructose, called fructose 1-phosphate, accumulates at high levels in the cells .
In hypoxic intestinal cells, fructose 1-phosphate increases the survival rate of intestinal epithelial cells by inhibiting the M2 isoform of pyruvate kinase (PK), thereby increasing the length of intestinal villi .
In addition, previous animal studies have shown that this fructose metabolite also contributes to tumors
Fructose metabolism enhances the viability of hypoxic cells and reduces the activity of pyruvate kinase.
Then the research team activated pyruvate kinase through TEPP-46, thereby preventing the increase in intestinal villi length and eliminating the weight caused by high-fructose-fed mice Increase and tumor growth .
The activation of PK weakens the effect of fructose on hypoxic survival.
The study author Taylor said that from an evolutionary point of view, it is reasonable that high fructose intake increases fat synthesis .
"Among mammals, especially those hibernating in temperate climates, it is very convenient to obtain fructose in the autumn months when the fruits are ripe .
Eating large amounts of fructose may help these animals absorb more nutrients and convert them into fat.
, So that they can survive the winter safely .
Dr.
Goncalves added that humans have not yet evolved to eat what we eat every day .
Before, fructose was not freely available throughout the year, but only in limited seasons.
You can enjoy it .
However, nowadays, fructose is almost everywhere, whether it comes from milk tea, beverages, biscuits, or natural foods such as fruits, we can get and enjoy them at any time .
"Although fructose itself is not harmful, fructose has been ingested.
More is harmful .
Our bodies are not designed to eat so much fructose .
"He said .
"This study found that there is an opportunity to be transformed into humans .
There are already some clinical trial drugs for other purposes that can target the enzyme responsible for the production of fructose-1-phosphate.
Dr.
Goncalves said that we hope to find a way to use them to shorten villi, thereby reducing fat absorption and possibly slowing tumors.
Grow .
" Not only for a healthy body, but also to reduce the risk of cancer, don't overtake fructose .
Leave a message here
Fructose is a sweetener naturally found in fruits and honey.
It is also a component of high fructose corn syrup and is used to sweeten foods and beverages
.
Fructose is contained in fruit drinks, milk tea, baked goods, and sweetened yogurt
.
The more milk tea shops opened, the drinks became more and more delicious .
We are now consuming more fructose than at any time in history, but the price of increased fructose consumption is the increased incidence of obesity and cancer .
Fructose metabolism begins in the epithelium of the small intestine, where fructose is transported by the type 5 glucose transporter (GLUT5; encoded by SLC2A5) and is phosphorylated by kethexaol to form fructose 1-phosphate, which can accumulate to a high level in the cell Level .
Although this pathway is related to the promotion of obesity and tumors, the exact mechanism is still unclear .
Recently, a study published in the journal Nature found that eating fructose can increase the survival rate of intestinal epithelial cells, thereby increasing the length of intestinal villi and enabling them to absorb more nutrients .
Studies have shown that the main metabolite of fructose promotes the elongation of villi .
The villi of mice fed a fructose diet were 25% to 40% longer than mice that were not fed fructose, which caused the mice to gain weight .
DOI: 10.
1038/s41586-021-03827-2 Villus (villus) is a slender hair-like structure arranged inside the small intestine .
Fluff to expand the surface area of the intestine to help the body in food through digestion time channel to absorb nutrients from food, including fat .
Therefore, the increase in villi length is related to the nutrient absorption, weight gain and fat accumulation of animals .
Digestion
Interestingly, the result of fructose's increase in villi was unexpectedly discovered
.
At first, the research team did not intend to study the small intestinal villi
.
A previous study published by the team in 2019 found that dietary fructose can increase tumor size in mouse models of colorectal cancer , and blocking fructose metabolism can prevent this from happening .
Considering that fructose may also promote the proliferation or accelerated growth of the small intestine, the researchers examined the tissue structure of mice treated with fructose or a control diet under a microscope .
Colorectal cancer studies have observed that in mice on a high fructose diet, the length of the villi of the mice increased significantly .
When the researcher discovered this unexpected result, the research team immediately began to study the villi, trying to determine whether the function of the villi would be different as the length of these hairs increased .
Therefore, they divided the mice into 3 groups: a control diet without fructose, a standard high-fat diet with glucose and no fructose (45% of calories come from fat), and an isocaloric high-fat diet (glucose is replaced by sucrose, sucrose In half glucose, half fructose) .
The study found that although the energy consumed by each group of mice was the same , the mice fed with fructose in the form of sucrose had a significant increase in body weight and fat compared with mice in the high-fat diet without fructose, and the intestinal villi were longer .
Mice fed with fructose had higher body weight and longer villi.
In addition, mice fed with fructose in the form of sucrose had higher serum triglyceride levels after oral fat intake compared with control mice without sucrose .
These data indicate that the fructose in the diet can increase the length of the intestinal villi and the absorption of nutrients .
Then, the researchers carefully studied the metabolic changes in the fructose group of mice and found that a specific metabolite of fructose, called fructose 1-phosphate, accumulates at high levels in the cells .
In hypoxic intestinal cells, fructose 1-phosphate increases the survival rate of intestinal epithelial cells by inhibiting the M2 isoform of pyruvate kinase (PK), thereby increasing the length of intestinal villi .
In addition, previous animal studies have shown that this fructose metabolite also contributes to tumors
Fructose metabolism enhances the viability of hypoxic cells and reduces the activity of pyruvate kinase.
Then the research team activated pyruvate kinase through TEPP-46, thereby preventing the increase in intestinal villi length and eliminating the weight caused by high-fructose-fed mice Increase and tumor growth .
The activation of PK weakens the effect of fructose on hypoxic survival.
The study author Taylor said that from an evolutionary point of view, it is reasonable that high fructose intake increases fat synthesis .
"Among mammals, especially those hibernating in temperate climates, it is very convenient to obtain fructose in the autumn months when the fruits are ripe .
Eating large amounts of fructose may help these animals absorb more nutrients and convert them into fat.
, So that they can survive the winter safely .
Dr.
Goncalves added that humans have not yet evolved to eat what we eat every day .
Before, fructose was not freely available throughout the year, but only in limited seasons.
You can enjoy it .
However, nowadays, fructose is almost everywhere, whether it comes from milk tea, beverages, biscuits, or natural foods such as fruits, we can get and enjoy them at any time .
"Although fructose itself is not harmful, fructose has been ingested.
More is harmful .
Our bodies are not designed to eat so much fructose .
"He said .
"This study found that there is an opportunity to be transformed into humans .
There are already some clinical trial drugs for other purposes that can target the enzyme responsible for the production of fructose-1-phosphate.
Dr.
Goncalves said that we hope to find a way to use them to shorten villi, thereby reducing fat absorption and possibly slowing tumors.
Grow .
" Not only for a healthy body, but also to reduce the risk of cancer, don't overtake fructose .
Leave a message here
