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Singularity Cake feels that now everyone is paying more and more attention to healthy diet, and more and more aware of the harmful effects of sugar, and even some "talk about sugar color".
This is also very understandable.
After all, the more you read the paper, the more you realize that sugar, especially fructose, has many hidden dangers that we did not understand before.
What readers know best is the obesity epidemic brought about by the substantial increase in fructose use, and the simultaneous increase is the increase in various non-communicable diseases, such as type 2 diabetes, non-alcoholic fatty liver disease and other diseases.
The metabolism of fructose is different from glucose.
Our previous article also mentioned that fructose is 30% more efficient than glucose in terms of fat synthesis.
In contrast, the effect of fructose on immunity is less concerned.
In fact, in many pathophysiological conditions, such as a variety of hematological tumors, there is a phenomenon of extremely high fructose concentration in the peripheral blood/bone marrow microenvironment of patients; and some normal tissues and organs also have a metabolic preference for fructose-thus born The question is whether the immune cells exposed to the high fructose environment will produce some abnormal changes? Recently, the British scientific research team published a paper in the journal Nature Communications [1].
Researchers found that fructose can weaken the metabolic flexibility of monocytes, increase the secretion of monocyte pro-inflammatory cytokines, and induce inflammatory phenotypes.
Although this has not yet been associated with specific disease manifestations, it is still worthy of our attention.
Source | There are many sources of energy for the pixabay cells.
You can "eat" glucose, or "eat" fructose or other nutrients.
Under the conditions of different nutrient substrates, cells will also choose appropriate metabolic methods, or glycolysis or oxidative phosphorylation to produce energy.
This is what we call "metabolic flexibility".
But what is interesting is that when trying to treat human monocytes cultured with different carbohydrates with drugs that inhibit oxidative phosphorylation, the researchers found that monocytes cultured with glucose and galactose can all complement the human monocytes by increasing glycolysis.
Inhibited oxidative phosphorylation, but monocytes cultured with fructose failed to show this "compensation", and the levels of oxidative phosphorylation and glycolysis were reduced.
Obviously, monocytes after fructose culture become less "flexible".
"Eating" sugar metabolism to engage in production is a big deal.
Will the function of monocytes that are not "flexible" be affected? The researchers then measured the levels of cytokines produced by lipopolysaccharide (LPS) stimulated monocytes and found that monocytes cultured with fructose produced more IL-1β, IL-6, IL-8, IL-10 and TNF- α, there is not a small gap with glucose-cultured monocytes.
Monocytes cultured with fructose produced more pro-inflammatory cytokines.
However, although the secreted cytokines increased, there was no difference in the level of activation-related surface markers on the two groups of monocytes.
The RNA sequencing results also suggested transcription.
The level has not changed.
The researchers observed that the activation of downstream proteins of mTORC1 is consistent with the results previously found that fructose can activate mTORC1, indicating that mTORC1-mediated translation may increase the production of pro-inflammatory cytokines.
Through isotope labeling and chromatography-mass spectrometry (GC-MS) analysis, the researchers found that fructose can significantly increase the tricarboxylic acid (TCA) cycle, so carbon sources such as glutamine are also more needed as raw materials for the TCA cycle.
These are all cell experiments.
Are there any similar findings in vivo? The researchers first determined that the phenotype of bone marrow-derived macrophages (BMDMs) in mice is similar to that of human monocytes, and that they can also exhibit consistent metabolic changes and increased expression of pro-inflammatory cytokines under fructose culture.
The researchers provided two groups of mice with a 10% glucose solution and a 10% glucose/fructose mixed solution for two weeks of continuous feeding.
At this time, the mice will not develop metabolic-related diseases.
The experimental results showed that serum IL-1β levels of mice exposed to fructose increased significantly, and IL-6 and TNF-α also observed corresponding increases.
Mice that ate fructose had higher levels of pro-inflammatory cytokines.
Fortunately, the "bad" effects of fructose seemed to be limited to monocytes and macrophages.
Observations of cD4+/CD8+ T cells did not reveal any phenotypic changes.
This is the first time that fructose can enhance inflammation independently of metabolic diseases.
Based on the results of this study, it is not yet possible to explain whether fructose-mediated inflammation can lead to pathological manifestations.
For example, other studies have proposed the relationship between chronic fructose exposure to exacerbate infection inflammation, lead to non-alcoholic steatohepatitis, or carcinogenesis.
, This part still needs follow-up research to confirm.
Under the action of fructose, the metabolic flexibility of monocytes is weakened, which indicates that monocytes may not be able to perform normal immune functions in some environments with strict metabolic conditions, such as bacterial infections or tumor microenvironments.
Singularity is hiring everyone! Everybody Hi~! We need fresh blood to inject new energy into the singularity.
Come on, become the singularity cake and do a new job with us! These are the little friends we are currently looking for~ If you want to create and innovate with the singularity cakes, come join us.
Please send your resume and work (if any) to: hr@geekheal.
com or you can directly add to the WeChat (geekheal-xintan) of Geekheal-xintan for communication.
When adding friends, please note: recruitment + position + professional field.
We are waiting for you at Singularity.
Reference materials: [1] The author of this articleDai Siyu
This is also very understandable.
After all, the more you read the paper, the more you realize that sugar, especially fructose, has many hidden dangers that we did not understand before.
What readers know best is the obesity epidemic brought about by the substantial increase in fructose use, and the simultaneous increase is the increase in various non-communicable diseases, such as type 2 diabetes, non-alcoholic fatty liver disease and other diseases.
The metabolism of fructose is different from glucose.
Our previous article also mentioned that fructose is 30% more efficient than glucose in terms of fat synthesis.
In contrast, the effect of fructose on immunity is less concerned.
In fact, in many pathophysiological conditions, such as a variety of hematological tumors, there is a phenomenon of extremely high fructose concentration in the peripheral blood/bone marrow microenvironment of patients; and some normal tissues and organs also have a metabolic preference for fructose-thus born The question is whether the immune cells exposed to the high fructose environment will produce some abnormal changes? Recently, the British scientific research team published a paper in the journal Nature Communications [1].
Researchers found that fructose can weaken the metabolic flexibility of monocytes, increase the secretion of monocyte pro-inflammatory cytokines, and induce inflammatory phenotypes.
Although this has not yet been associated with specific disease manifestations, it is still worthy of our attention.
Source | There are many sources of energy for the pixabay cells.
You can "eat" glucose, or "eat" fructose or other nutrients.
Under the conditions of different nutrient substrates, cells will also choose appropriate metabolic methods, or glycolysis or oxidative phosphorylation to produce energy.
This is what we call "metabolic flexibility".
But what is interesting is that when trying to treat human monocytes cultured with different carbohydrates with drugs that inhibit oxidative phosphorylation, the researchers found that monocytes cultured with glucose and galactose can all complement the human monocytes by increasing glycolysis.
Inhibited oxidative phosphorylation, but monocytes cultured with fructose failed to show this "compensation", and the levels of oxidative phosphorylation and glycolysis were reduced.
Obviously, monocytes after fructose culture become less "flexible".
"Eating" sugar metabolism to engage in production is a big deal.
Will the function of monocytes that are not "flexible" be affected? The researchers then measured the levels of cytokines produced by lipopolysaccharide (LPS) stimulated monocytes and found that monocytes cultured with fructose produced more IL-1β, IL-6, IL-8, IL-10 and TNF- α, there is not a small gap with glucose-cultured monocytes.
Monocytes cultured with fructose produced more pro-inflammatory cytokines.
However, although the secreted cytokines increased, there was no difference in the level of activation-related surface markers on the two groups of monocytes.
The RNA sequencing results also suggested transcription.
The level has not changed.
The researchers observed that the activation of downstream proteins of mTORC1 is consistent with the results previously found that fructose can activate mTORC1, indicating that mTORC1-mediated translation may increase the production of pro-inflammatory cytokines.
Through isotope labeling and chromatography-mass spectrometry (GC-MS) analysis, the researchers found that fructose can significantly increase the tricarboxylic acid (TCA) cycle, so carbon sources such as glutamine are also more needed as raw materials for the TCA cycle.
These are all cell experiments.
Are there any similar findings in vivo? The researchers first determined that the phenotype of bone marrow-derived macrophages (BMDMs) in mice is similar to that of human monocytes, and that they can also exhibit consistent metabolic changes and increased expression of pro-inflammatory cytokines under fructose culture.
The researchers provided two groups of mice with a 10% glucose solution and a 10% glucose/fructose mixed solution for two weeks of continuous feeding.
At this time, the mice will not develop metabolic-related diseases.
The experimental results showed that serum IL-1β levels of mice exposed to fructose increased significantly, and IL-6 and TNF-α also observed corresponding increases.
Mice that ate fructose had higher levels of pro-inflammatory cytokines.
Fortunately, the "bad" effects of fructose seemed to be limited to monocytes and macrophages.
Observations of cD4+/CD8+ T cells did not reveal any phenotypic changes.
This is the first time that fructose can enhance inflammation independently of metabolic diseases.
Based on the results of this study, it is not yet possible to explain whether fructose-mediated inflammation can lead to pathological manifestations.
For example, other studies have proposed the relationship between chronic fructose exposure to exacerbate infection inflammation, lead to non-alcoholic steatohepatitis, or carcinogenesis.
, This part still needs follow-up research to confirm.
Under the action of fructose, the metabolic flexibility of monocytes is weakened, which indicates that monocytes may not be able to perform normal immune functions in some environments with strict metabolic conditions, such as bacterial infections or tumor microenvironments.
Singularity is hiring everyone! Everybody Hi~! We need fresh blood to inject new energy into the singularity.
Come on, become the singularity cake and do a new job with us! These are the little friends we are currently looking for~ If you want to create and innovate with the singularity cakes, come join us.
Please send your resume and work (if any) to: hr@geekheal.
com or you can directly add to the WeChat (geekheal-xintan) of Geekheal-xintan for communication.
When adding friends, please note: recruitment + position + professional field.
We are waiting for you at Singularity.
Reference materials: [1] The author of this articleDai Siyu
