Characterization of depot-specific adipokine release in diet-induced obese mice reveals a distinct secretion profile in paracardial adipose tissue
4 affiliations
- 1Department of Anatomy and Physiology, University of Melbourne, Melbourne, VIC 3010 Australia
- 2Department of Microbiology, Anatomy, Physiology & Pharmacology, La Trobe University, Melbourne, VIC 3086 Australia
- 3Centre for Cardiovascular Biology & Disease Research, La Trobe Institute of Molecular Sciences, La Trobe University, Melbourne, VIC 3086 Australia
- 4Department of Physiology, University of Otago | Ōtākou Whakaihu Waka, Dunedin, 9016 Otago New Zealand
Abstract
Obesity is characterized by excessive adipose tissue deposition across multiple depots, accompanied by profound alterations in systemic metabolism. Beyond their role in lipid storage, adipose tissues are active endocrine organs that secrete a range of bioactive proteins, i.e., adipokines, that regulate energy homeostasis, inflammation, and metabolic health. Alterations in adipokine secretion are increasingly recognized as key contributors to the development of obesity-related comorbidities. Here, we investigate depot-specific patterns of adipokine release from paracardial (PAT), inguinal (ING), and epididymal (EPI) adipose tissues in healthy lean mice and mice fed a high-fat diet. Using untargeted proteomics, we identify distinct secretory profiles across depots, revealing marked heterogeneity in the composition and magnitude of secreted proteins. In healthy lean mice, PAT exhibited the highest overall protein secretion rates, with enrichment in proteins linked to cellular and oxidative stress responses. High fat feeding induced extensive remodelling of the adipose secretome across all depots. EPI adipose tissue displayed increased secretion of proteins involved in cellular stress, injury and inflammation, whereas both ING and PAT depots demonstrated substantial suppression of protein release, including reductions in proteins associated with carbohydrate homeostasis and insulin signalling. These findings highlight that obesity drives depot-specific adaptations in adipokine secretion, potentially contributing to regional differences in metabolic risk. Together, this study provides an in-depth proteomic characterization of adipose tissue secretory remodeling in diet-induced obesity, offering new insights into how distinct fat depots influence systemic metabolic regulation.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-64158-8.
Related
- Distinct sFOLR1 and Cytokine Secretion Profiles Across Marker-Enriched OVCAR-3 Ovarian Cancer Cell Subpopulations: A Pilot Study
- β-cell NCK1 is reduced in type 2 diabetes, impairing the unfolded protein response and insulin secretion while revealing sex-specific adaptation
- Redefining the Gut-Brain Axis: A Specific Bidirectional System Distinct from General Interorgan Communication
- Multimodal Imaging of Fundus Abnormalities in Stickler Syndrome: Characterization of 15 Distinct Features Using Ultra-Widefield Swept-Source OCT Angiography
- Baseline adipokine profiles have limited predictive value for weight-loss outcomes after laparoscopic sleeve gastrectomy: a prospective longitudinal cohort study
BibTeX
@article{bell2026characterization,
title = {{Characterization of depot-specific adipokine release in diet-induced obese mice reveals a distinct secretion profile in paracardial adipose tissue}},
author = {James R Bell and Paula M Miotto and Helen MM Waddell and Lea MD Delbridge and Matthew J Watt and Magdalene K Montgomery},
journal = {Scientific Reports},
year = {2026},
month = aug,
doi = {10.1038/s41598-026-64158-8},
url = {https://doi.org/10.1038/s41598-026-64158-8},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Characterization of depot-specific adipokine release in diet-induced obese mice reveals a distinct secretion profile in paracardial adipose tissue
AU - James R Bell
AU - Paula M Miotto
AU - Helen MM Waddell
AU - Lea MD Delbridge
AU - Matthew J Watt
AU - Magdalene K Montgomery
PY - 2026
DA - 2026/08/07
JO - Scientific Reports
DO - 10.1038/s41598-026-64158-8
UR - https://doi.org/10.1038/s41598-026-64158-8
AB - Obesity is characterized by excessive adipose tissue deposition across multiple depots, accompanied by profound alterations in systemic metabolism. Beyond their role in lipid storage, adipose tissues are active endocrine organs that secrete a range of bioactive proteins, i.e., adipokines, that regulate energy homeostasis, inflammation, and metabolic health. Alterations in adipokine secretion are increasingly recognized as key contributors to the development of obesity-related comorbidities. Here, we investigate depot-specific patterns of adipokine release from paracardial (PAT), inguinal (ING), and epididymal (EPI) adipose tissues in healthy lean mice and mice fed a high-fat diet. Using untargeted proteomics, we identify distinct secretory profiles across depots, revealing marked heterogeneity in the composition and magnitude of secreted proteins. In healthy lean mice, PAT exhibited the highest overall protein secretion rates, with enrichment in proteins linked to cellular and oxidative stress responses. High fat feeding induced extensive remodelling of the adipose secretome across all depots. EPI adipose tissue displayed increased secretion of proteins involved in cellular stress, injury and inflammation, whereas both ING and PAT depots demonstrated substantial suppression of protein release, including reductions in proteins associated with carbohydrate homeostasis and insulin signalling. These findings highlight that obesity drives depot-specific adaptations in adipokine secretion, potentially contributing to regional differences in metabolic risk. Together, this study provides an in-depth proteomic characterization of adipose tissue secretory remodeling in diet-induced obesity, offering new insights into how distinct fat depots influence systemic metabolic regulation. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-64158-8.
SN - 2045-2322
ER -