Gymnaster Koraiensis Extract Alleviated Metabolic Syndrome Symptoms and Stimulated UCP1‐Independent Energy Consumption via AMPK Activation in White Adipose Tissue

Scope Metabolic syndrome and obesity are rising worldwide concerns that are accompanied by adverse health consequences. Here, it is hypothesized that the ethanol extract from Gymnaster koraiensis (GK), an edible Korean plant known for its anti‐cancer and hepatoprotective properties, could attenuate metabolic syndrome‐related symptoms in high‐fat dietary‐induced obese (DIO) mice. Methods and Results Administration of 100 mg kg−1 GK extract to DIO mice effectively reduces body and white adipose tissue (WAT) weight. It also reduces cardiovascular disease risk and improves insulin resistance by lowering the fasting blood glucose levels and mitigating oxidative stress and inflammation. Moreover, supplementation with GK causes elevated energy expenditure in WAT by increasing the mitochondrial oxidative capacity and lipid catabolism through upregulated adenosine monophosphate‐activated protein kinase (AMPK) signaling. Orlistat is used as a positive control drug due to its widespread use in previous studies. It is found that GK extract causes weight loss, similar to Orlistat, and it additionally shows unique functions, such as upregulation of energy consumption in WAT. Conclusion GK extract treatment prominently reduces obesity and its associated metabolic complications, such as hyperlipidemia, hyperglycemia, and insulin resistance. Hence, It can be used as a promising multi‐target functional food that can improve metabolic syndrome‐related symptoms. GK extract relieves metabolic syndrome symptoms and stimulate UCP1‐independent energy consumption by activated AMPK phosphorylation in WAT. The GK extract ameliorates obesity, insulin resistance, hyperlipidemia, and hyperglycemia related to diabetes and CVD through activated AMPK phosphorylation. Moreover, GK extract increases energy expenditure by stimulating mitochondrial biogenesis, oxidative capacity, and lipid catabolism in WAT.