脂肪性肝炎
内科学
脂肪肝
肥胖
脂肪变性
脂质代谢
内分泌学
医学
体质指数
新陈代谢
背景(考古学)
胃肠病学
疾病
生物
古生物学
作者
María Á. Núñez-Sánchez,María Antonia Martínez‐Sánchez,José Ignacio Martínez‐Montoro,Andrés Balaguer‐Román,Elena Murcia-García,Virginia E. Fernández‐Ruiz,Mercedes Ferrer‐Gómez,Carlos Martínez,Tomasz Śledziński,María Dolores Frutos,Juan José Hernández Morante,José Carlos Fernández‐García,María Isabel Queipo‐Ortuño,Antonio J. Ruiz‐Alcaraz,Adriana Mika,Bruno Ramos‐Molina
标识
DOI:10.1210/clinem/dgae028
摘要
Abstract Context Metabolic dysfunction–associated steatotic liver disease (MASLD) is characterized by the intracellular lipid accumulation in hepatocytes. Excess caloric intake and high-fat diets are considered to significantly contribute to MASLD development. Objective To evaluate the hepatic and serum fatty acid (FA) composition in patients with different stages of MASLD, and their relationship with FA dietary intake and MASLD-related risk factors. Methods This was a case–control study in patients with obesity undergoing bariatric surgery at a university hospital between January 2020 and December 2021. Participants were distributed in 3 groups: no MASLD (n = 26), steatotic liver disease (n = 33), and metabolic dysfunction–associated steatohepatitis (n = 32). Hepatic and serum FA levels were determined by gas chromatography-mass spectrometry. Nutritional status was evaluated using validated food frequency questionnaires. The hepatic expression of genes involved in FA metabolism was analyzed by reverse transcription quantitative polymerase chain reaction. Results The hepatic, but not serum, FA profiles were significantly altered in patients with MASLD compared with those without MASLD. No differences were observed in FA intake between the groups. Levels of C16:0, C18:1, and the C18:1/C18:0 ratio were higher, while C18:0 levels and C18:0/C16:0 ratio were lower in patients with MASLD, being significantly different between the 3 groups. Hepatic FA levels and ratios correlated with histopathological diagnosis and other MASLD-related parameters. The expression of genes involved in the FA metabolism was upregulated in patients with MASLD. Conclusion Alterations in hepatic FA levels in MASLD patients were due to enhancement of de novo lipogenesis in the liver.
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