Effect of Semaglutide on High-Fat-Diet-Induced Liver Cancer in Obese Mice.
J Proteome Res · 2024
Last updated 2026-05-28In a study of 16 obese mice fed a high-fat diet, half were given semaglutide while the other half were not. Researchers found that semaglutide slowed the progression of liver cancer by increasing levels of four specific proteins in the mice's fat tissue, which are linked to cancer development pathways.
AI summary of the abstract below.
| Journal | J Proteome Res, 2024 |
|---|---|
| Citations | 7 |
| Relative citation ratio | 1.57 |
| NIH percentile | 66 |
| Molecules | semaglutide |
| Conditions studied | Obesity, Mash |
Abstract
This study aims to investigate the impact of semaglutide on the expression of liver cancer proteins in obese mice induced by a high-fat diet. Sixteen obese mice were randomly divided into two groups: the high-fat diet group and the semaglutide group, each consisting of eight mice. Additionally, eight normal male mice were included as the control group. Serum samples were collected, and a differential expression analysis of total proteins in adipose tissue was performed using quantitative tandem mass spectrometry (TMT) in combination with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Significant differential proteins were identified and subjected to a bioinformatics analysis. The findings revealed that these differential proteins, namely, integrin αV (ITGAV), laminin γ1 (LAMC1), fatty acid-binding protein 5 (FABP5), and lipoprotein lipase (LPL), regulate the occurrence and development of liver cancer by participating in the extracellular matrix (ECM) signaling pathway and the peroxisome proliferator-activated receptor (PPAR) signaling pathway. Notably, semaglutide can decelerate the progression of liver cancer by inducing the expression of ITGAV, LAMC1, FABP5, and LPL in the adipose tissue of obese mice.
Verbatim abstract via PubMed 38227547 ↗
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