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This article is original by Translational Medicine.
Please indicate the source for reprinting.
Author: Catalina Introduction: Since its discovery in the 1960s, autophagy has been considered to be related to diseases such as aging, cancer, and immunity
.
Recently, a study published in "Cell Reports" confirmed that enhancing autophagy in adipose tissue can increase insulin sensitivity and is expected to assist in the treatment of diabetes
.
Autophagy is an evolutionarily very conservative lysosome-mediated biodegradation process.
It is the recycling and reuse of the cell’s own waste and has an important regulatory effect on cell homeostasis.
Therefore, autophagy disorders are often involved in the pathogenesis of many metabolic diseases, such as: diabetes
.
However, the mechanism by which autophagy regulates body metabolism is currently unclear
.
Recently, researchers from Northwestern University in the United States published a paper entitled "The autophagy protein Becn1 improves insulin sensitivity by promoting adiponectin secretion via exocyst binding" in Cell Reports
.
They said that the autophagy protein Beclin 1 promotes the secretion of adiponectin through extracapsular binding and can improve insulin sensitivity
.
Autophagy plays a key role in many processes: remove long-lived and misfolded proteins, clean up damaged organelles, and regulate cell growth and metabolism
.
The main regulator of autophagy is a special protein, Beclin 1/Becn1
.
Beclin 1 makes cells sensitive to insulin by participating in the pathway of the hormone adiponectin.
Although some aspects of this process need further research, this mechanism can be used to treat insulin resistance in diabetic patients
.
In normal organisms, Beclin 1 is only activated under certain stress conditions, such as lack of nutrients or oxygen
.
The activation of Beclin 1 triggers autophagy, recirculating dysfunctional cell structures, and is expected to improve the stress factors that triggered this process in the first place
.
In a previous study, researchers used Beclin 1 gene mutations to modify mice to enhance their functions
.
They found that in addition to delaying the aging of the heart and kidneys, these mice also lived longer; at the same time, these mice became intolerant to glucose but more sensitive to insulin
.
In the current study, the researchers measured Beclin 1 to enhance blood-related parameters in mice and found high levels of adiponectin
.
Adiponectin is an insulin-sensitizing hormone (An Insulin-sensitizing Hormone) that helps activate AMPK metabolic pathways and is a general regulator of metabolism
.
Beclin 1 regulates adiponectin secretion and knocking out the adiponectin receptor prevents the activation of AMPK and subsequent sensitization of insulin response, so the researchers tried to examine the precise mechanism of action
.
They found that Beclin 1 is the culprit: In normal mice, Beclin 1 mainly binds to other inhibitory molecules and is only released when activated
.
In mutant mice with enhanced autophagy, there is more "free" Beclin 1 protein, resulting in a larger protein pool for transfer to adiponectin vesicles, promoting their secretion into the blood, and increasing insulin sensitivity Sex
.
Beclin 1 improves insulin sensitivity and glucose tolerance.
They said that excessive activation of Beclin 1 in insulin-secreting B cells may be harmful
.
Because it reduces the body's insulin storage, but activating the secretion of Beclin 1 and adiponectin in fat cells can make diabetic patients sensitive to insulin
.
This is achieved through a small molecule agonist to specifically activate the adiponectin pathway, or through Beclin 1 to promote autophagy intermittently, or through another autophagy inducer (such as fasting and physical exercise)
.
The author said: "Compared with B cells that store insulin, fat and other metabolic tissues are more sensitive to autophagy, so if you exercise or exercise intermittently quickly, it can activate fat autophagy earlier than other parts of the body.
Metabolism is beneficial
.
"Reference: https:// %2FS2211124721005295%3Fshowall%3Dtrue Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital
.
Please indicate the source for reprinting.
Author: Catalina Introduction: Since its discovery in the 1960s, autophagy has been considered to be related to diseases such as aging, cancer, and immunity
.
Recently, a study published in "Cell Reports" confirmed that enhancing autophagy in adipose tissue can increase insulin sensitivity and is expected to assist in the treatment of diabetes
.
Autophagy is an evolutionarily very conservative lysosome-mediated biodegradation process.
It is the recycling and reuse of the cell’s own waste and has an important regulatory effect on cell homeostasis.
Therefore, autophagy disorders are often involved in the pathogenesis of many metabolic diseases, such as: diabetes
.
However, the mechanism by which autophagy regulates body metabolism is currently unclear
.
Recently, researchers from Northwestern University in the United States published a paper entitled "The autophagy protein Becn1 improves insulin sensitivity by promoting adiponectin secretion via exocyst binding" in Cell Reports
.
They said that the autophagy protein Beclin 1 promotes the secretion of adiponectin through extracapsular binding and can improve insulin sensitivity
.
Autophagy plays a key role in many processes: remove long-lived and misfolded proteins, clean up damaged organelles, and regulate cell growth and metabolism
.
The main regulator of autophagy is a special protein, Beclin 1/Becn1
.
Beclin 1 makes cells sensitive to insulin by participating in the pathway of the hormone adiponectin.
Although some aspects of this process need further research, this mechanism can be used to treat insulin resistance in diabetic patients
.
In normal organisms, Beclin 1 is only activated under certain stress conditions, such as lack of nutrients or oxygen
.
The activation of Beclin 1 triggers autophagy, recirculating dysfunctional cell structures, and is expected to improve the stress factors that triggered this process in the first place
.
In a previous study, researchers used Beclin 1 gene mutations to modify mice to enhance their functions
.
They found that in addition to delaying the aging of the heart and kidneys, these mice also lived longer; at the same time, these mice became intolerant to glucose but more sensitive to insulin
.
In the current study, the researchers measured Beclin 1 to enhance blood-related parameters in mice and found high levels of adiponectin
.
Adiponectin is an insulin-sensitizing hormone (An Insulin-sensitizing Hormone) that helps activate AMPK metabolic pathways and is a general regulator of metabolism
.
Beclin 1 regulates adiponectin secretion and knocking out the adiponectin receptor prevents the activation of AMPK and subsequent sensitization of insulin response, so the researchers tried to examine the precise mechanism of action
.
They found that Beclin 1 is the culprit: In normal mice, Beclin 1 mainly binds to other inhibitory molecules and is only released when activated
.
In mutant mice with enhanced autophagy, there is more "free" Beclin 1 protein, resulting in a larger protein pool for transfer to adiponectin vesicles, promoting their secretion into the blood, and increasing insulin sensitivity Sex
.
Beclin 1 improves insulin sensitivity and glucose tolerance.
They said that excessive activation of Beclin 1 in insulin-secreting B cells may be harmful
.
Because it reduces the body's insulin storage, but activating the secretion of Beclin 1 and adiponectin in fat cells can make diabetic patients sensitive to insulin
.
This is achieved through a small molecule agonist to specifically activate the adiponectin pathway, or through Beclin 1 to promote autophagy intermittently, or through another autophagy inducer (such as fasting and physical exercise)
.
The author said: "Compared with B cells that store insulin, fat and other metabolic tissues are more sensitive to autophagy, so if you exercise or exercise intermittently quickly, it can activate fat autophagy earlier than other parts of the body.
Metabolism is beneficial
.
"Reference: https:// %2FS2211124721005295%3Fshowall%3Dtrue Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital
.
