The Extract of Camellia Seed Cake Alleviates Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Mice by Promoting Coenzyme Q Synthesis.

Journal: Nutrients
Published:
Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder. Camellia seed cake, a byproduct of oil extraction, contains a variety of bioactive compounds. This study investigated the regulatory effects and underlying mechanisms of camellia seed cake extract (CSCE) using a high-fat diet (HFD)-induced MASLD mouse model.

Methods: Mice were divided into four groups: normal control (N, standard diet), HFD model (M), HFD-fed mice treated with low-dose CSCE (L), and HFD-fed mice treated with high-dose CSCE (H). CSCE was administered via oral gavage for eight weeks. Body weight, blood lipid levels, liver weight, hepatic lipid accumulation, oxidative stress markers, ATP levels, and the NADH/NAD+ ratio were measured. Transcriptomic and lipidomic analyses were performed to identify potential regulatory pathways, and qPCR analysis was conducted to confirm the expression levels of essential genes.

Results: CSCE significantly reduced HFD-induced increases in body and liver weights, improved blood lipid profiles and hepatic lipid accumulation, alleviated oxidative stress, increased ATP levels, and reduced the NADH/NAD+ ratio. Transcriptomic analysis demonstrated notable enrichment of genes associated with oxidative phosphorylation, mitochondrial function, and lipid metabolism after treatment. The lipidomic analysis demonstrated that the hepatic lipid profile of the H group approached that of the N group, with Coenzyme Q9 (CoQ9) and Coenzyme Q10 (CoQ10) levels significantly increased by 173.32% and 202.73%, respectively, compared to the M group. qPCR validation confirmed that CoQ synthesis-related genes (Coq2-10, Pdss1, Pdss2, and Hmgcr) were significantly upregulated in the treatment groups.

Conclusions: CSCE enhances mitochondrial function by promoting CoQ synthesis, alleviates metabolic dysfunction, and could represent a potential natural intervention for MASLD.

Authors
Xinzhi Chen, Bolin Chen, Zhigang Li, Li Ma, Qinhe Zhu, Changwei Liu, Haixiang He, Zhixu Zhang, Chuyi Zhou, Guanying Liu, Yuqiao Zhou, Senwen Deng, Shiyin Guo, Yongzhong Chen