High fat diet enhances catalase loading into adipose tissue derived extracellular vesicles with limited effect on oxidative stress
Abstract Obesity is closely related to liver disease. However, few studies have focused on the impact of adipose tissue-derived extracellular vesicles (EVs) in obesity on liver disease. Therefore, we aimed to investigate the effect of adipose tissue-derived EVs from high-fat diet (HFD)-fed obese mic...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2025-08-01
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| Series: | Scientific Reports |
| Subjects: | |
| Online Access: | https://doi.org/10.1038/s41598-025-15594-5 |
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| Summary: | Abstract Obesity is closely related to liver disease. However, few studies have focused on the impact of adipose tissue-derived extracellular vesicles (EVs) in obesity on liver disease. Therefore, we aimed to investigate the effect of adipose tissue-derived EVs from high-fat diet (HFD)-fed obese mice (EV-HFD) on liver damage induced by oxidative stress. We investigated alterations in the expression of antioxidant enzymes in adipose tissue, and the loading of those enzymes into adipose tissue-derived EVs. Furthermore, we treated alpha mouse liver 12 (AML12) cells with adipose tissue-derived EVs and induced oxidative stress. We observed that the HFD did not exert an effect on the protein expressions of antioxidant enzymes in adipose tissue. Intriguingly, the EV-HFD exhibited an upregulation in the loading of catalase (CAT) when compared to the adipose tissue-derived EVs from normal chow-fed mice (EV-NC). Notably, both types of EVs exhibited a similar capacity to mitigate cell damage when exposed to oxidative stress. Our findings indicate that obesity-induced loading of more CAT into adipose tissue-derived EVs cannot improve their antioxidant capacity in AML12 cells. We suggest that adipose tissue-derived EVs can serve as a tool to maintain homeostasis and defend against oxidative stress, thereby supporting normal physiological functions. |
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| ISSN: | 2045-2322 |