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A large number of clinical studies have shown that obese patients often suffer from mental illnesses such as depression and anxiety at the same time.
On March 26, 2021, the Wu Qi team of Baylor College of Medicine in the United States and collaborators published a paper Reciprocal control of obesity and anxiety–depressive disorder via a GABA and serotonin neural circuit in Molecular Psychiatry, providing new breakthrough insights for this association , They successfully discovered and explained a new neural circuit mechanism and targeted combination drug regimen for bidirectional regulation of feeding behavior and mental state.
It is reported that approximately 43% of adults with depression also suffer from obesity, and adults with mental illness are more likely to be obese than adults with mental health.
Similar to human patients, mice that have long-term intake of high-fat foods become not only obese, but also have obvious symptoms of anxiety and depression.
The Wu Qi group proposed for the first time that this highly co-occurring pathological phenomenon is caused by the dysfunction of a specific brain circuit.
After correcting the functional defects caused by the high-fat diet in the loop through a series of genetic or pharmacological methods, the group of researchers first found that the anxiety and depression symptoms completely disappeared, and then surprisingly found that the animal's food intake was strongly suppressed , And eventually lead to obesity symptoms are almost completely eliminated.
More interestingly, the weight loss produced here is not due to loss of appetite, but because the animals actively reduce their preference for high-fat foods.
Similar to humans, rodents, including mice, generally have a high preference for high-fat foods.
However, after intervention in this neural circuit, the food preferences of the mice actively turned to a healthy diet with a lower fat content and rich in protein and carbohydrates.
This discovery explains for the first time the co-occurrence mechanism of obesity and mental illness and reveals the possibility of targeted drug therapy for it.
In order to explore the neural circuits that can regulate weight gain and depression or anxiety in both directions, the research team provided mice with a high-fat diet, and the mice not only developed the expected symptoms of obesity, but also developed anxiety and depression at the same time.
In a series of studies conducted on this obese mouse model, Professor Wu’s team discovered a new type of neural circuit composed of two groups of neurons located in different brain regions, including the dorsal stria terminalis nucleus (dBNST) Melanocortin receptor 4 (MC4R) neurons and agouti peptide-related protein (AgRP) neurons located in the arcuate nucleus (ARC) of the hypothalamus.
Conducive to real-time neuroimaging and multi-channel electrophysiology and other technical means, researchers found that this neural circuit has different degrees of functional disorder in obese and depression mouse models.
Using targeted transgenes and optogenetics, a group of specific genes that participate in and mediate the loss of neural circuit function have been identified in mouse models of obesity and depression.
More importantly, the researchers found that after correcting the defects in the neural circuit to a normal state, the anxiety and depression caused by the high-fat diet can be effectively eliminated, and then the food intake and weight can be significantly reduced.
Surprisingly, the weight loss is not because the animal completely loses its appetite, but after the mental state is adjusted through genetic or pharmacological methods, the dietary preference is effectively corrected, that is, the original preference for high-fat food is actively changed to Healthier low-fat foods.
Considering the transformational potential and application prospects of this important discovery in clinical medicine, researchers used genomics and pharmacological methods to extensively screen and explore the possibility of combined drug therapy to correct the functional defect of this neural circuit.
Finally, it was discovered that a targeted combination drug therapy consisting of Zonisamide and Granisetron produced a synergistic effect by acting on two different signaling pathways in the newly discovered neural circuit, completely eliminating anxiety And depression symptoms, which in turn made animals tend to eat healthier, low-fat foods, and eventually significantly corrected the symptoms of obesity and overweight.
The results of these trials reveal the high feasibility of cocktail therapy consisting of Zonisamide and Granisetron or its derivatives in the treatment of obesity and comorbid mental illness, and is a useful tool for further development of pathological pharmacology.
Research and large-scale clinical medical trials provide strong support in molecular and neurophysiological mechanisms and translational medicine.
The corresponding author of this article is Professor Wu Qi from Baylor College of Medicine and the Child Nutrition Research Center of the United States Department of Agriculture.
He has won honorary titles such as Pew PEW Biomedical Scholar and Kavli Foundation Scholar.
The co-first authors of the paper are postdoctoral researcher Dr.
Xia Guobin and postdoctoral researcher Dr.
Han Yong.
Original link: Platemaker: Notice for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, and it is prohibited without permission Reprinted, the author has all legal rights, offenders must be investigated.
On March 26, 2021, the Wu Qi team of Baylor College of Medicine in the United States and collaborators published a paper Reciprocal control of obesity and anxiety–depressive disorder via a GABA and serotonin neural circuit in Molecular Psychiatry, providing new breakthrough insights for this association , They successfully discovered and explained a new neural circuit mechanism and targeted combination drug regimen for bidirectional regulation of feeding behavior and mental state.
It is reported that approximately 43% of adults with depression also suffer from obesity, and adults with mental illness are more likely to be obese than adults with mental health.
Similar to human patients, mice that have long-term intake of high-fat foods become not only obese, but also have obvious symptoms of anxiety and depression.
The Wu Qi group proposed for the first time that this highly co-occurring pathological phenomenon is caused by the dysfunction of a specific brain circuit.
After correcting the functional defects caused by the high-fat diet in the loop through a series of genetic or pharmacological methods, the group of researchers first found that the anxiety and depression symptoms completely disappeared, and then surprisingly found that the animal's food intake was strongly suppressed , And eventually lead to obesity symptoms are almost completely eliminated.
More interestingly, the weight loss produced here is not due to loss of appetite, but because the animals actively reduce their preference for high-fat foods.
Similar to humans, rodents, including mice, generally have a high preference for high-fat foods.
However, after intervention in this neural circuit, the food preferences of the mice actively turned to a healthy diet with a lower fat content and rich in protein and carbohydrates.
This discovery explains for the first time the co-occurrence mechanism of obesity and mental illness and reveals the possibility of targeted drug therapy for it.
In order to explore the neural circuits that can regulate weight gain and depression or anxiety in both directions, the research team provided mice with a high-fat diet, and the mice not only developed the expected symptoms of obesity, but also developed anxiety and depression at the same time.
In a series of studies conducted on this obese mouse model, Professor Wu’s team discovered a new type of neural circuit composed of two groups of neurons located in different brain regions, including the dorsal stria terminalis nucleus (dBNST) Melanocortin receptor 4 (MC4R) neurons and agouti peptide-related protein (AgRP) neurons located in the arcuate nucleus (ARC) of the hypothalamus.
Conducive to real-time neuroimaging and multi-channel electrophysiology and other technical means, researchers found that this neural circuit has different degrees of functional disorder in obese and depression mouse models.
Using targeted transgenes and optogenetics, a group of specific genes that participate in and mediate the loss of neural circuit function have been identified in mouse models of obesity and depression.
More importantly, the researchers found that after correcting the defects in the neural circuit to a normal state, the anxiety and depression caused by the high-fat diet can be effectively eliminated, and then the food intake and weight can be significantly reduced.
Surprisingly, the weight loss is not because the animal completely loses its appetite, but after the mental state is adjusted through genetic or pharmacological methods, the dietary preference is effectively corrected, that is, the original preference for high-fat food is actively changed to Healthier low-fat foods.
Considering the transformational potential and application prospects of this important discovery in clinical medicine, researchers used genomics and pharmacological methods to extensively screen and explore the possibility of combined drug therapy to correct the functional defect of this neural circuit.
Finally, it was discovered that a targeted combination drug therapy consisting of Zonisamide and Granisetron produced a synergistic effect by acting on two different signaling pathways in the newly discovered neural circuit, completely eliminating anxiety And depression symptoms, which in turn made animals tend to eat healthier, low-fat foods, and eventually significantly corrected the symptoms of obesity and overweight.
The results of these trials reveal the high feasibility of cocktail therapy consisting of Zonisamide and Granisetron or its derivatives in the treatment of obesity and comorbid mental illness, and is a useful tool for further development of pathological pharmacology.
Research and large-scale clinical medical trials provide strong support in molecular and neurophysiological mechanisms and translational medicine.
The corresponding author of this article is Professor Wu Qi from Baylor College of Medicine and the Child Nutrition Research Center of the United States Department of Agriculture.
He has won honorary titles such as Pew PEW Biomedical Scholar and Kavli Foundation Scholar.
The co-first authors of the paper are postdoctoral researcher Dr.
Xia Guobin and postdoctoral researcher Dr.
Han Yong.
Original link: Platemaker: Notice for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, and it is prohibited without permission Reprinted, the author has all legal rights, offenders must be investigated.
