Research
Hormonal
Adipose tissue macrophage (ATM)-derived EVs containing miR-155 contribute to glucose intolerance and insulin resistance by suppressing adipogenic transcription factors PPARγ and CEBPβ.
Immune cells in your fat tissue send out tiny vesicles that can affect how your body handles sugar. In obesity, these vesicles may carry specific RNA molecules that worsen insulin resistance. Losing weight can change the content of these vesicles, potentially improving your metabolic health.
GoodSupportsHIGH confidence
In obese mice, ATMs secrete miRNA-containing exosomes, which cause glucose intolerance and insulin resistance when administered to lean mice. Conversely, ATM exosomes obtained from lean mice improve glucose tolerance and insulin sensitivity when administered to obese recipients. miR-155, one of the miRNAs overexpressed in exosomes derived from obese ATMs, was shown to regulate adipose tissue homeostasis through direct suppression of its targets, the adipogenic transcription factors peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein β (CEBPβ) [48].
Why this rating
Supported by specific studies cited in the review, demonstrating causal effects in mouse models.
Source
Extracellular vesicles in metabolic disease
Naveed Akbar et al. · Diabetologia · 2019
DOI 10.1007/s00125-019-05014-5
narrative_reviewCited 182×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Obesity and metabolic dysfunction are associated with significantly elevated circulating levels of extracellular vesicles (EVs), particularly those derived from platelets, endothelial cells, and adipocytes, which serve as biomarkers for metabolic stress and insulin resistance.Good
- Adipose tissue-derived extracellular vesicles (EVs) mediate communication between adipose tissue and other organs (like the liver), contributing to insulin resistance and systemic metabolic dysfunction in obesity.Good
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