Cold Stress-Induced Adipose Tissue Remodeling in Min pigs: Involvement of the ADRB3-ERK Axis, Autophagy, and Inflammatory Pathways
- 1Key Laboratory of Combining Farming and Animal Husbandry of Ministry of Agriculture and Rural Affairs, Heilongjiang Academy of Agricultural Sciences, Harbin 150086, China
- 2College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China
Abstract
Cold stress induces adaptive remodeling of adipose tissue, yet the coordinated molecular network, particularly the interplay between upstream signaling pathways and downstream cellular responses, remains incompletely understood. This study investigated whether cold stress regulates adipose tissue beiging, apoptosis, and systemic metabolic remodeling through autophagy and inflammation mediated by the β3-adrenergic receptor (ADRB3)-extracellular signal-regulated kinase (ERK) signaling axis. The results demonstrated that cold stress significantly increased energy expenditure and markedly improved glucose tolerance and insulin sensitivity in Min pigs. In subcutaneous adipose tissue, cold stress induced pronounced beiging, as evidenced by reduced adipocyte size, the presence of multilocular lipid droplets, and upregulation of beige adipocyte marker genes, accompanied by increased preadipocyte apoptosis. Transcriptomic analysis revealed significant enrichment of pathways related to autophagy and lipolysis, with inflammation (notably the TNF signaling pathway) also identified as a potential contributing process. Mechanistically, cold stress activated the ADRB3-ERK signaling axis, leading to enhanced autophagic activity, and inflammation-related genes were also upregulated, suggesting that inflammation may serve as a candidate process cooperating with autophagy. In conclusion, this study reveals a novel molecular mechanism whereby cold stress activates the ADRB3-ERK signaling axis to stimulate autophagy, with inflammation potentially cooperating as a candidate process, thereby driving adipose tissue beiging, apoptosis, and systemic metabolic remodeling.
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BibTeX
@article{yang2026cold,
title = {{Cold Stress-Induced Adipose Tissue Remodeling in Min pigs: Involvement of the ADRB3-ERK Axis, Autophagy, and Inflammatory Pathways}},
author = {Shuo Yang and Heshu Chen and Dongjie Zhang and Xinmiao He and Hong Ma and Zhenhua Guo and Liang Wang and Bo Fu and Wentao Wang and Di Liu},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16101464},
url = {https://www.mdpi.com/2218-273X/16/10/1464},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Cold Stress-Induced Adipose Tissue Remodeling in Min pigs: Involvement of the ADRB3-ERK Axis, Autophagy, and Inflammatory Pathways
AU - Shuo Yang
AU - Heshu Chen
AU - Dongjie Zhang
AU - Xinmiao He
AU - Hong Ma
AU - Zhenhua Guo
AU - Liang Wang
AU - Bo Fu
AU - Wentao Wang
AU - Di Liu
PY - 2026
DA - 2026/10/01
JO - Biomolecules
DO - 10.3390/biom16101464
UR - https://www.mdpi.com/2218-273X/16/10/1464
AB - Cold stress induces adaptive remodeling of adipose tissue, yet the coordinated molecular network, particularly the interplay between upstream signaling pathways and downstream cellular responses, remains incompletely understood. This study investigated whether cold stress regulates adipose tissue beiging, apoptosis, and systemic metabolic remodeling through autophagy and inflammation mediated by the β3-adrenergic receptor (ADRB3)-extracellular signal-regulated kinase (ERK) signaling axis. The results demonstrated that cold stress significantly increased energy expenditure and markedly improved glucose tolerance and insulin sensitivity in Min pigs. In subcutaneous adipose tissue, cold stress induced pronounced beiging, as evidenced by reduced adipocyte size, the presence of multilocular lipid droplets, and upregulation of beige adipocyte marker genes, accompanied by increased preadipocyte apoptosis. Transcriptomic analysis revealed significant enrichment of pathways related to autophagy and lipolysis, with inflammation (notably the TNF signaling pathway) also identified as a potential contributing process. Mechanistically, cold stress activated the ADRB3-ERK signaling axis, leading to enhanced autophagic activity, and inflammation-related genes were also upregulated, suggesting that inflammation may serve as a candidate process cooperating with autophagy. In conclusion, this study reveals a novel molecular mechanism whereby cold stress activates the ADRB3-ERK signaling axis to stimulate autophagy, with inflammation potentially cooperating as a candidate process, thereby driving adipose tissue beiging, apoptosis, and systemic metabolic remodeling.
SN - 2218-273X
ER -