-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
High comorbidities between iNature obesity and mental illnesses (such as depression and anxiety) usually significantly exacerbate metabolic and neurological symptoms.
However, the neural mechanisms that collectively control eating and mental state are largely elusive.
On March 26, 2021, the Wu Qi team and collaborators of Baylor College of Medicine in the United States published an online publication titled "Reciprocal control of obesity and anxiety–depressive disorder via a GABA and serotonin neural circuit" in Molecular Psychiatry (IF=12.
38) Research paper, the study successfully discovered and explained a new neural circuit mechanism and targeted combination medication regimen for bidirectional regulation of feeding behavior and mental state.
In short, the results of this study revealed the neural mechanism of mutual control of appetite and mental state, and finally formed a new zonisamide (enhance GABAAR-α5 signal transduction)-granisetron (selective 5-HT3R antagonist) cocktail therapy, which has potential Solve psychiatric-obesity comorbidities.
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.
The article pattern (picture from Molecular Psychiatry) is conducive to real-time neuroimaging and multi-channel electrophysiology.
The study found that this neural circuit has different degrees of functional disorder in obese and depression mouse models.
Using targeted transgenes and optogenetics, the study identified a set of specific genes involved in and mediating the loss of neural circuit function in mouse models of obesity and depression.
More importantly, the study found that after correcting the defects in the neural circuit to a normal state, the anxiety and depression caused by a 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 foods is actively changed to healthier Low-fat food.
Taking into account the potential and application prospects of this important discovery in clinical medicine, the study extensively screened and explored the possibility of combined drug therapy to correct the functional defects of this neural circuit through genomics and pharmacological methods.
The study finally found 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.
Eliminates symptoms of anxiety and depression, which in turn makes animals tend to eat healthier, low-fat foods, and ultimately significantly corrects 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 and researcher of 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.
Reference message:
However, the neural mechanisms that collectively control eating and mental state are largely elusive.
On March 26, 2021, the Wu Qi team and collaborators of Baylor College of Medicine in the United States published an online publication titled "Reciprocal control of obesity and anxiety–depressive disorder via a GABA and serotonin neural circuit" in Molecular Psychiatry (IF=12.
38) Research paper, the study successfully discovered and explained a new neural circuit mechanism and targeted combination medication regimen for bidirectional regulation of feeding behavior and mental state.
In short, the results of this study revealed the neural mechanism of mutual control of appetite and mental state, and finally formed a new zonisamide (enhance GABAAR-α5 signal transduction)-granisetron (selective 5-HT3R antagonist) cocktail therapy, which has potential Solve psychiatric-obesity comorbidities.
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.
The article pattern (picture from Molecular Psychiatry) is conducive to real-time neuroimaging and multi-channel electrophysiology.
The study found that this neural circuit has different degrees of functional disorder in obese and depression mouse models.
Using targeted transgenes and optogenetics, the study identified a set of specific genes involved in and mediating the loss of neural circuit function in mouse models of obesity and depression.
More importantly, the study found that after correcting the defects in the neural circuit to a normal state, the anxiety and depression caused by a 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 foods is actively changed to healthier Low-fat food.
Taking into account the potential and application prospects of this important discovery in clinical medicine, the study extensively screened and explored the possibility of combined drug therapy to correct the functional defects of this neural circuit through genomics and pharmacological methods.
The study finally found 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.
Eliminates symptoms of anxiety and depression, which in turn makes animals tend to eat healthier, low-fat foods, and ultimately significantly corrects 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 and researcher of 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.
Reference message:
