PTG‐Dependent Glycogen Metabolic Dysfunction Drives Impaired Adipose Browning: A Novel Mechanism Linking PM <sub>2.5</sub> to Metabolic Disorders

Fine particulate matter (PM<sub>2.5</sub>) contributes to metabolic dysfunction, but its effects on adipose tissue browning remain unclear. Here, we showed that PM<sub>2.5</sub> exposure inhibited inguinal white adipose tissue (iWAT) browning by downregulating protein targeting to glycogen (PTG), disrupting glycogen homeostasis. PTG overexpression in iWAT restored glycogen metabolism, thermogenesis, and mitochondrial function, reversing PM<sub>2.5</sub>-induced impairment in iWAT browning and metabolic disorders. Mechanistically, PTG negatively regulated vascular endothelial growth factor B (VEGFB), and VEGFB knockdown rescued browning. Activation of β3-adrenergic receptor (ADRB3) mitigated PM<sub>2.5</sub>'s effects by restoring PTG and normalizing VEGFB, defining the ADRB3-PTG-VEGFB axis as central to PM<sub>2.5</sub>-induced metabolic dysfunction. Our findings identify adipose glycogen metabolism as a target for countering environmental metabolic disruption.

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Publication Details

Journal
Advanced Science
Published
2026-01-09
DOI
https://doi.org/10.1002/advs.202512589
Primary Topic
Adipose Tissue and Metabolism
Type
article
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article

PTG‐Dependent Glycogen Metabolic Dysfunction Drives Impaired Adipose Browning: A Novel Mechanism Linking PM 2.5 to Metabolic Disorders

Xiaoli Hou, Qinghua Sun, Ping He, Li Qin et al.
Advanced Science
Adipose Tissue and Metabolism
article

PTG‐Dependent Glycogen Metabolic Dysfunction Drives Impaired Adipose Browning: A Novel Mechanism Linking PM 2.5 to Metabolic Disorders

Xiaoli Hou, Qinghua Sun, Ping He, Li Qin, Yanxi Chai, Wenbin Zhao, Liu Zhao, Renjie Hu, Sanduo Li, Limin Wang, Lu Zhang, Ran Li, Cuiqing Liu
article en

Abstract

Fine particulate matter (PM<sub>2.5</sub>) contributes to metabolic dysfunction, but its effects on adipose tissue browning remain unclear. Here, we showed that PM<sub>2.5</sub> exposure inhibited inguinal white adipose tissue (iWAT) browning by downregulating protein targeting to glycogen (PTG), disrupting glycogen homeostasis. PTG overexpression in iWAT restored glycogen metabolism, thermogenesis, and mitochondrial function, reversing PM<sub>2.5</sub>-induced impairment in iWAT browning and metabolic disorders. Mechanistically, PTG negatively regulated vascular endothelial growth factor B (VEGFB), and VEGFB knockdown rescued browning. Activation of β3-adrenergic receptor (ADRB3) mitigated PM<sub>2.5</sub>'s effects by restoring PTG and normalizing VEGFB, defining the ADRB3-PTG-VEGFB axis as central to PM<sub>2.5</sub>-induced metabolic dysfunction. Our findings identify adipose glycogen metabolism as a target for countering environmental metabolic disruption.

Advanced ScienceVol. 13(16)
Zhejiang International Studies University (CN), Zhejiang Chinese Medical University (CN)
Openalex Percentile: Top 93%
Adipose Tissue and Metabolism
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PTG‐Dependent Glycogen Metabolic Dysfunction Drives Impaired Adipose Browning: A Novel Mechanism Linking PM <sub>2.5</sub> to Metabolic Disorders — Xiaoli Hou, Qinghua Sun, et al. · Advanced Science (2026) | TGRS Research Map | TGRS