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Updated: Jul 16, 2026
07:24
Assessment of Human Adipose Tissue Microvascular Function Using Videomicroscopy
Published on: September 29, 2017
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GSK3β Deficiency Expands Obese Adipose Vasculature to Mitigate Metabolic Disorders
Li Wang1,2,3, Jiajia Li1, Ping Tang1
1Department of Biomedical Sciences, Faculty of Health Sciences (L.W., J.L., P.T., D.Z., L.T., Y.W., L.D.), University of Macau, China.
Circulation Research
|December 4, 2024
Summary
Deleting GSK3β in fat cells improves vascularization and reduces metabolic issues in obesity. This research highlights GSK3β
Area of Science:
- Metabolic disorders
- Obesity research
- Adipose tissue biology
- Vascular biology
Background:
- A healthy vascular system is crucial for adipose tissue (AT) expansion to prevent metabolic complications.
- Glycogen synthase kinase-3 beta (GSK3β) has known cellular roles, but its function in AT and body homeostasis is unclear.
Purpose of the Study:
- To investigate the role of GSK3β in adipose tissue (AT) and its impact on metabolic homeostasis.
- To determine if GSK3β in adipocytes influences vascularization and obesity-related metabolic disorders.
Main Methods:
- Generated adipocyte-specific knockout mice for GSK3β (GSK3βADKO) and GSK3α (GSK3αADKO).
- Conducted whole-body metabolism analysis, RNA sequencing, vessel perfusion studies, and in vitro assays on obese GSK3βADKO mice and cultured cells.
Main Results:
- Adipocyte-specific knockout of GSK3β expanded AT vascularization and mitigated obesity-related metabolic disorders.
- GSK3β deficiency in adipocytes activated the AMPK/HIF-2α/VEGF/VEGFR2 axis, promoting angiogenesis and improving AT microenvironment.
- This led to increased adiponectin, reduced fibrosis, reactive oxygen species, and ER stress in obese AT.
Conclusions:
- Deletion of GSK3β in adipocytes promotes vasculature expansion in obese AT via the AMPK/HIF-2α/VEGF/VEGFR2 pathway.
- This vascularization improves the local AT microenvironment, reducing inflammation and ameliorating obesity-associated metabolic disorders.
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