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.

This study investigated the effects of lemon verbena extract (LVE) on sleep regulation using both a pentobarbital-induced sleep model and an EEG-based sleep assessment model in mice. To elucidate its potential mechanisms, mice were randomly assigned to five groups: control, positive control (diazepam, 2 mg/kg b.w.), and three LVE-treated groups receiving 40, 80, or 160 mg/kg b.w. via oral administration. In the pentobarbital-induced sleep model, mice underwent a two-week oral administration of LVE, followed by intraperitoneal pentobarbital injections. The results demonstrated that LVE significantly shortened sleep latency and prolonged sleep duration compared to the control group. Notably, adenosine A1 receptor expression, both at the mRNA and protein levels, was markedly upregulated in the brains of LVE-treated mice. Furthermore, LVE’s administration led to a significant increase in the mRNA expression of gamma-aminobutyric acid type A (GABA_A) receptor subunits (α2 and β2) in brain tissue. In the electroencephalography (EEG)/electromyogram (EMG)-based sleep model, mice underwent surgical implantation of EEG and EMG electrodes, followed by one week of LVE administration. Quantitative EEG analysis revealed that LVE treatment reduced wakefulness while significantly enhancing REM and NREM sleep’s duration, indicating its potential sleep-promoting effects. These findings suggest that LVE may serve as a promising natural sleep aid, improving both the quality and duration of sleep through the modulation of adenosine and GABAergic signaling pathways.

Background/Objectives: Kaempferia parviflora (KP), also known as black ginger, has been reported to exert metabolic regulatory effects, yet its influence on skeletal muscle glucose handling remains unclear. Because impaired glucose uptake in skeletal muscle is a major contributor to insulin resistance and type 2 diabetes mellitus (T2DM), this study investigated the effects of KP on glucose uptake and the GLUT4 signaling pathway both in vitro and in vivo. Methods: The effects of KP extract on glucose uptake and GLUT4-related signaling proteins were evaluated in differentiated C2C12 myotubes. In parallel, C57BL/6J and db/db mice were orally administered KP extract at varying doses for six weeks to evaluate its metabolic effects in vivo. Results: KP significantly increased glucose uptake in C2C12 myotubes, accompanied by increased GLUT4 expression and upregulation of GLUT4-related signaling proteins. In diabetic mice, KP administration improved fasting glucose, glucose tolerance and GLP-1 level while lowering insulin and HbA1c levels. Skeletal muscle tissues exhibited increased GLUT4 expression and modulation of downstream regulators involved in glucose homeostasis. Conclusions: These findings indicate that KP improves skeletal muscle glucose metabolism primarily through activation of the GLUT4 pathway. Taken together, KP may serve as a potential functional ingredient for regulating muscle glucose utilization and mitigating metabolic disturbances associated with T2DM.