The impact of a short-term high-fat diet on coagulation function in a mouse model and its role in exacerbating concanavalin A-induced liver injury.

Autor: Nanizawa E; Department of Anatomy, Aichi Medical University, 1-1, Yazakokarimata, Nagakute City, Aichi, 480-1195, Japan. nanizawa.e@aichi-med-u.ac.jp., Tamaki Y; Department of Anatomy, Aichi Medical University, 1-1, Yazakokarimata, Nagakute City, Aichi, 480-1195, Japan., Yakura T; Department of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-Ku, Tokyo, 160-8402, Japan., Otsuka S; Department of Anatomy, Aichi Medical University, 1-1, Yazakokarimata, Nagakute City, Aichi, 480-1195, Japan., Hatayama N; Department of Anatomy, Aichi Medical University, 1-1, Yazakokarimata, Nagakute City, Aichi, 480-1195, Japan., Naito M; Department of Anatomy, Aichi Medical University, 1-1, Yazakokarimata, Nagakute City, Aichi, 480-1195, Japan.
Jazyk: angličtina
Zdroj: BMC nutrition [BMC Nutr] 2024 Dec 18; Vol. 10 (1), pp. 158. Date of Electronic Publication: 2024 Dec 18.
DOI: 10.1186/s40795-024-00966-3
Abstrakt: Background: Recently, the number of patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and its more advanced condition, metabolic dysfunction-associated steatohepatitis (MASH), has been increasing. These patients are at a higher risk of cardiovascular events and thromboembolism. However, the direct impact of high-fat diet (HFD), a cause of MASLD, on liver coagulation function is not well understood. Previously, we demonstrated that a short-term, 4-day intake of a HFD exacerbates concanavalin A (Con A)-induced acute liver injury in mice by promoting coagulation and inflammation. This model demonstrates that the liver exposed to a short-term HFD is vulnerable even before disease onset. In this study, using this model, we elucidated the detailed mechanisms by which short-term HFD intake promotes coagulation, considering primary and secondary hemostasis.
Methods: C57BL/6 mice normally fed a normal diet (ND) were subjected to a HFD for 4 days. Liver tissue and blood samples were collected before and 4 and 24 h after Con A administration. Histological analysis, flow cytometry for platelet analysis, and blood coagulation tests related to secondary hemostasis were performed.
Results: Even with short-term consumption of a HFD alone, platelet and fibrinogen levels increased in the peripheral blood and liver. Additionally, when Con A was administered to mice on a short-term HFD, an increase in P-selectin expression was observed in the liver, with no upregulation in peripheral blood platelets. Furthermore, in mice subjected to a short-term HFD and treated with Con A, prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT) were observed.
Conclusions: Consuming a HFD in short-term can enhance primary and secondary hemostasis, thereby increasing the risk of thrombosis. These conditions are presumed to be a risk factor that exacerbates Con A-induced liver injury. The findings provide insight into early intervention strategies for chronic liver diseases, such as MASLD and MASH.
Competing Interests: Declarations. Ethics approval and consent to participate: All procedures involving animals in this study were conducted in accordance with protocols approved by the Aichi Medical University Animal Care and Use Committee (approval number 2023–53). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.
(© 2024. The Author(s).)
Databáze: MEDLINE
Externí odkaz: