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Updated: Feb 24, 2026

Characterization of Adipocyte-Derived Extracellular Vesicle Secretion Using a CD63-GFP Reporter Mouse Model In Vivo and In Vitro

Characterization of Adipocyte-Derived Extracellular Vesicle Secretion Using a CD63-GFP Reporter Mouse Model In Vivo and In Vitro

Published on: December 5, 2025

脂肪組織由来の小型エクソソームは、糖不耐症の根底にある分子回路を明らかにする

Shalini Mishra¹, Yixin Su¹, Ashish Kumar¹

¹Section of Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.

Obesity (Silver Spring, Md.)

|February 23, 2026

要旨

Objective:

Glucose tolerance (GT) is a major effector for adipose tissue (AT) remodeling in obesity, yet its molecular mechanisms remain incompletely defined. We hypothesized that the biophysical and molecular profiles of AT-derived small extracellular vesicles (sEV^AT) change in response to glucose availability and differ by GT status.

Methods:

sEV^AT were isolated from plasma of individuals with normal GT (NGT) and impaired GT (IGT) (n = 5/group) at fasting (0 h) and 1 h post glucose challenge during oral glucose tolerance test (OGTT). sEV^AT were characterized for size, concentration, surface expression of insulin receptor-α (INSRα), proteome, and insulin signaling-related miRNAs. C2C12 myotubes were treated with sEV^AT for 48 h, followed by quantification of 84 insulin signaling-related genes.

Result:

The size and concentration of sEV^AT did not differ between groups. At fasting, INSRα expression on sEV^AT was comparable; however, groups exhibited opposite directional changes at 1-h OGTT. LC-MS/MS identified significant proteomic differences between NGT and IGT sEV^AT. miR-27a-5p and miR-145a-5p levels in sEV^AT also differed significantly by GT status. Notably, treatment with sEV^AT (IGT-0 h) significantly downregulated insulin signaling-related genes in myotubes.

Conclusions:

Distinct molecular signatures in sEV^AT offer a unique insight into AT dysfunction during IGT and offer novel diagnostic and therapeutic targets.

キーワード:

脂肪組織エクソソーム糖不耐症代謝性疾患バイオマーカー

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