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Vascular dysfunction is considered to be the main factor causing the increase in obesity-related mortality and disability
.
Obesity usually causes damage to large blood vessels in the form of atherosclerosis and arterial hypertension, while microvessels undergo structural remodeling under pathological conditions
.
Microvascular remodeling is not limited to peripheral tissues, but can also occur in the brain
.
In animal model experiments and human studies, it has been found that eating a high-calorie diet can cause the remodeling of the hypothalamic microvascular system
.
Astrocytes regulate the blood-brain barrier in two ways: directly participating in the formation of the blood-brain barrier; indirectly affecting the function of the blood-brain barrier through the released factors
.
Astrocytes are also involved in the process of vascular remodeling
.
On June 1, 2021, the research team of Cristina Garcı´a-Ca´ceres at the Helmholtz Munich Center of the German Environmental Health Research Center revealed that hyperleptinemia is promoted by the HIF1a-VEGF signaling cascade in hypothalamic astrocytes Obesity-induced hypertension
.
Obesity-induced hypothalamic vascular remodeling.
They found that after 20 weeks of high-fat and high-sugar diet (HFHS) in mice, the blood pressure also increased significantly; the microvessel density in the hypothalamus area increased significantly, and the weight of the microvessels was significantly increased.
The row only occurs in this area
.
In addition, the blood-brain barrier in this brain area is obstructed, and serum proteins are highly extravasated
.
The electron microscope also observed a decrease in the thickness of the capillaries in this brain area
.
This indicates that obesity can cause a series of vascular structural diseases such as hypertension, hypothalamic microvascular remodeling, and damage to the blood-brain barrier structure
.
From the moment of weight gain, hypothalamic blood vessels are reconstructed.
Researchers have found that the increase in hypothalamic blood vessels caused by a long-term high-fat diet appears in the period of significant weight gain, which is the period of beginning to gain weight.
During this period, the serum leptin level rises.
High, the expression of vascular endothelial factor also increases
.
What's even more amazing is that these obese mice lost weight after 5 weeks of normal diet.
At the same time, the dense capillaries in the hypothalamus gradually decreased and returned to normal levels
.
It's really a fat ruin everything, nothing thin! Leptin knockout mice received a high-fat and high-sugar diet and did not cause an excessive increase in hypothalamic blood vessels, but after exogenous injection of leptin, leptin knockout mice showed increased hypothalamic blood vessels
.
The promotion of leptin expression in normal mice can cause a significant increase in hypothalamic endothelial cells
.
This exogenous increase in leptin promotes the expression of vascular endothelial factor is much stronger than feeding high-fat and high-sugar feed alone for 2 weeks
.
This indicates that leptin plays a key role in causing changes in cerebral blood vessels
.
A high-fat diet causes astrocytes to secrete more vascular endothelial factors.
Where do these vascular endothelial factors come from? Immunofluorescence experiments found that there is a high degree of overlap between vascular endothelial factor and astrocytes in obese mice
.
After knocking out astrocytes, the expression of vascular endothelial factor in the hypothalamus decreased significantly
.
Astrocytes, which promote the expression of vascular endothelial factor, depend on leptin receptors
.
Using viral vector tools to specifically knock down the expression of vascular endothelial factor in astrocytes, a high-fat and high-sugar diet will not cause an increase in blood vessel density in the hypothalamus.
After re-promoting the expression of vascular endothelial factor through a dual virus strategy Obese mice will still have hypervascularity similar to the previous hypothalamic brain area
.
The expression of hypoxia-inducible factor-1α (HIF1α), which directly regulates vascular endothelial factor (VEGF), is increased in the hypothalamus of obese mice.
Acute exogenous administration of leptin can also promote its expression
.
After specifically knocking out HIF1α on astrocytes, the high-fat and high-sugar diet did not cause the mice to increase blood pressure, nor did it promote the increase of vascular endothelial factor expression in the hypothalamus, nor did it promote the increase of blood vessel density.
This indicates that leptin promotes angiogenesis through the HIF1α-VEGF signaling pathway acting on astrocytes
.
In summary, this article found that in the obese state, blood vessels and astrocytes in the hypothalamic area have undergone structural remodeling that other brain areas have not experienced.
The HIF1α-VEGF signal in this area activates the downstream leptin signaling pathway.
Increased blood pressure
.
[References] 1.
https://doi.
org/10.
1016/j.
celrep.
2021.
109191, the pictures in the text are all from the reference original download link: Baidu Netdisk https://pan.
baidu.
com/s/1noBe3RJbm7XnNdFU-uLbAQ Extraction code: hhuu
Vascular dysfunction is considered to be the main factor causing the increase in obesity-related mortality and disability
.
Obesity usually causes damage to large blood vessels in the form of atherosclerosis and arterial hypertension, while microvessels undergo structural remodeling under pathological conditions
.
Microvascular remodeling is not limited to peripheral tissues, but can also occur in the brain
.
In animal model experiments and human studies, it has been found that eating a high-calorie diet can cause the remodeling of the hypothalamic microvascular system
.
Astrocytes regulate the blood-brain barrier in two ways: directly participating in the formation of the blood-brain barrier; indirectly affecting the function of the blood-brain barrier through the released factors
.
Astrocytes are also involved in the process of vascular remodeling
.
On June 1, 2021, the research team of Cristina Garcı´a-Ca´ceres at the Helmholtz Munich Center of the German Environmental Health Research Center revealed that hyperleptinemia is promoted by the HIF1a-VEGF signaling cascade in hypothalamic astrocytes Obesity-induced hypertension
.
Obesity-induced hypothalamic vascular remodeling.
They found that after 20 weeks of high-fat and high-sugar diet (HFHS) in mice, the blood pressure also increased significantly; the microvessel density in the hypothalamus area increased significantly, and the weight of the microvessels was significantly increased.
The row only occurs in this area
.
In addition, the blood-brain barrier in this brain area is obstructed, and serum proteins are highly extravasated
.
The electron microscope also observed a decrease in the thickness of the capillaries in this brain area
.
This indicates that obesity can cause a series of vascular structural diseases such as hypertension, hypothalamic microvascular remodeling, and damage to the blood-brain barrier structure
.
From the moment of weight gain, hypothalamic blood vessels are reconstructed.
Researchers have found that the increase in hypothalamic blood vessels caused by a long-term high-fat diet appears in the period of significant weight gain, which is the period of beginning to gain weight.
During this period, the serum leptin level rises.
High, the expression of vascular endothelial factor also increases
.
What's even more amazing is that these obese mice lost weight after 5 weeks of normal diet.
At the same time, the dense capillaries in the hypothalamus gradually decreased and returned to normal levels
.
It's really a fat ruin everything, nothing thin! Leptin knockout mice received a high-fat and high-sugar diet and did not cause an excessive increase in hypothalamic blood vessels, but after exogenous injection of leptin, leptin knockout mice showed increased hypothalamic blood vessels
.
The promotion of leptin expression in normal mice can cause a significant increase in hypothalamic endothelial cells
.
This exogenous increase in leptin promotes the expression of vascular endothelial factor is much stronger than feeding high-fat and high-sugar feed alone for 2 weeks
.
This indicates that leptin plays a key role in causing changes in cerebral blood vessels
.
A high-fat diet causes astrocytes to secrete more vascular endothelial factors.
Where do these vascular endothelial factors come from? Immunofluorescence experiments found that there is a high degree of overlap between vascular endothelial factor and astrocytes in obese mice
.
After knocking out astrocytes, the expression of vascular endothelial factor in the hypothalamus decreased significantly
.
Astrocytes, which promote the expression of vascular endothelial factor, depend on leptin receptors
.
Using viral vector tools to specifically knock down the expression of vascular endothelial factor in astrocytes, a high-fat and high-sugar diet will not cause an increase in blood vessel density in the hypothalamus.
After re-promoting the expression of vascular endothelial factor through a dual virus strategy Obese mice will still have hypervascularity similar to the previous hypothalamic brain area
.
The expression of hypoxia-inducible factor-1α (HIF1α), which directly regulates vascular endothelial factor (VEGF), is increased in the hypothalamus of obese mice.
Acute exogenous administration of leptin can also promote its expression
.
After specifically knocking out HIF1α on astrocytes, the high-fat and high-sugar diet did not cause the mice to increase blood pressure, nor did it promote the increase of vascular endothelial factor expression in the hypothalamus, nor did it promote the increase of blood vessel density.
This indicates that leptin promotes angiogenesis through the HIF1α-VEGF signaling pathway acting on astrocytes
.
In summary, this article found that in the obese state, blood vessels and astrocytes in the hypothalamic area have undergone structural remodeling that other brain areas have not experienced.
The HIF1α-VEGF signal in this area activates the downstream leptin signaling pathway.
Increased blood pressure
.
[References] 1.
https://doi.
org/10.
1016/j.
celrep.
2021.
109191, the pictures in the text are all from the reference original download link: Baidu Netdisk https://pan.
baidu.
com/s/1noBe3RJbm7XnNdFU-uLbAQ Extraction code: hhuu
