This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
Zhijun Luo
Nanchang University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
According to epidemiologic studies, it was found that people living in high altitude areas have a lower prevalence of obesity and diabetes, and the main environmental differences between high altitude areas and plain areas are temperature and oxygen concentration. In this study, we investigated the effect of chronic transient hypoxia on obesity and fatty liver caused by high-fat diet in mice.
Methods
Put the mice under 10% oxygen concentration for 1 hour every day, this method is different from high altitude hypoxia and will not cause a series of acute altitude sicknesses. Intraperitoneal injection of epinephrine or propranolol was employed to examine the effect of chronic transient hypoxia on HFD-induced obesity, hyperglycemia and hepatic lipid accumulation.
Results
It showed that chronic transient hypoxia environment reduces the weight of mice and improve glucose tolerance, reduce the fat content of mice and alleviate fatty liver, reduces liver fat synthesis, promotes the expression M2 phenotype of macrophage genes in liver and thermogenic genes in brown fat. Furthermore, we showed that blocking the rise of epinephrine will compromise the chronic transient hypoxia environment beneficial ability to obesity and fatty liver, diminished expression of the liver AMPK phosphorylation and CD206.
Conclusions
These results suggest that chronic transient hypoxia activation of AMPK, induction of M2 type macrophage marker CD206 expression in the liver leads to significant weight loss and remission the severity of fatty liver through the adrenergic system.
Keywords
Chronic transient hypoxia, obesity, fatty liver, epinephrine, inflammation.
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
Zhijun Luo
Nanchang University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 12 Mar, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Translational Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
According to epidemiologic studies, it was found that people living in high altitude areas have a lower prevalence of obesity and diabetes, and the main environmental differences between high altitude areas and plain areas are temperature and oxygen concentration. In this study, we investigated the effect of chronic transient hypoxia on obesity and fatty liver caused by high-fat diet in mice.
Methods
Put the mice under 10% oxygen concentration for 1 hour every day, this method is different from high altitude hypoxia and will not cause a series of acute altitude sicknesses. Intraperitoneal injection of epinephrine or propranolol was employed to examine the effect of chronic transient hypoxia on HFD-induced obesity, hyperglycemia and hepatic lipid accumulation.
Results
It showed that chronic transient hypoxia environment reduces the weight of mice and improve glucose tolerance, reduce the fat content of mice and alleviate fatty liver, reduces liver fat synthesis, promotes the expression M2 phenotype of macrophage genes in liver and thermogenic genes in brown fat. Furthermore, we showed that blocking the rise of epinephrine will compromise the chronic transient hypoxia environment beneficial ability to obesity and fatty liver, diminished expression of the liver AMPK phosphorylation and CD206.
Conclusions
These results suggest that chronic transient hypoxia activation of AMPK, induction of M2 type macrophage marker CD206 expression in the liver leads to significant weight loss and remission the severity of fatty liver through the adrenergic system.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
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