Obesity (Silver Spring, Md.) · 2026
Adipose Tissue-Derived Small Extracellular Vesicles in Plasma Reveal Molecular Circuitries Underlying Glucose Intolerance.
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Mishra Shalini, Su Yixin, Kumar Ashish, Singh Sangeeta, Finlin Brian S, Hsu Fang-Chi, Lee Jingyun, Furdui Cristina M, Kern Philip A, Das Swapan K, Deep Gagan
Аннотация
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 (sEVAT) change in response to glucose availability and differ by GT status.
METHODS: sEVAT 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). sEVAT were characterized for size, concentration, surface expression of insulin receptor-α (INSRα), proteome, and insulin signaling-related miRNAs. C2C12 myotubes were treated with sEVAT for 48 h, followed by quantification of 84 insulin signaling-related genes.
RESULT: The size and concentration of sEVAT did not differ between groups. At fasting, INSRα expression on sEVAT was comparable; however, groups exhibited opposite directional changes at 1-h OGTT. LC-MS/MS identified significant proteomic differences between NGT and IGT sEVAT. miR-27a-5p and miR-145a-5p levels in sEVAT also differed significantly by GT status. Notably, treatment with sEVAT (IGT-0 h) significantly downregulated insulin signaling-related genes in myotubes.
CONCLUSIONS: Distinct molecular signatures in sEVAT offer a unique insight into AT dysfunction during IGT and offer novel diagnostic and therapeutic targets.
METHODS: sEVAT 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). sEVAT were characterized for size, concentration, surface expression of insulin receptor-α (INSRα), proteome, and insulin signaling-related miRNAs. C2C12 myotubes were treated with sEVAT for 48 h, followed by quantification of 84 insulin signaling-related genes.
RESULT: The size and concentration of sEVAT did not differ between groups. At fasting, INSRα expression on sEVAT was comparable; however, groups exhibited opposite directional changes at 1-h OGTT. LC-MS/MS identified significant proteomic differences between NGT and IGT sEVAT. miR-27a-5p and miR-145a-5p levels in sEVAT also differed significantly by GT status. Notably, treatment with sEVAT (IGT-0 h) significantly downregulated insulin signaling-related genes in myotubes.
CONCLUSIONS: Distinct molecular signatures in sEVAT offer a unique insight into AT dysfunction during IGT and offer novel diagnostic and therapeutic targets.