Acta cirurgica brasileira Pub Date : 2025-03-14 eCollection Date: 2025-01-01 DOI:10.1590/acb402325
Silvio Pires Gomes, Gabriela Salim de Castro, Vinicius Pedro Silva de Oliveira, Bruno Cogliati, Andressa Galvão da Silva Iacopino, Ivanir Santana de Oliveira Pires, Bruno Cesar Schimming, Fernanda Gosuen Gonçalves Dias, José Roberto Kfoury Junior, Tais Harumi de Castro Sasahara
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摘要

目的:从组织学和立体学角度分析肥胖 Zucker 大鼠(胖,n = 6,瘦素受体 - Leprfa 突变)和对照 Zucker 大鼠(瘦,n = 6)肝脏脂肪变性的特征,分析宏观和微观差异,以了解肥胖对肝脏病理学的影响:方法:用标准饲料喂养扎克大鼠 90 天。方法:用标准饲料喂养 Zucker 大鼠 90 天,采用宏观、定性和组织定量(立体学)方法,包括体重和肝脏重量测量、形态学分析以及代谢功能障碍相关脂肪性肝病的组织病理学分类:结果:与扎克瘦大鼠相比,扎克肥大鼠的体重(p = 0.0022)、肝脏重量(p = 0.0022)、血清总胆固醇(p = 0.0022)和三酰甘油(p = 0.0022)均较高。立体学分析表明,与瘦鼠相比,Zucker 肥鼠的肝细胞体积密度(p = 0.0022)和肝细胞总体积(p = 0.0001)较低,脂肪变性的体积密度(p = 0.002)和总体积(p = 0.002)较高:结论:研究结果表明,肥胖会引起 Zucker 大鼠肝脏形态的显著改变,肥胖动物的肝细胞体积较小。这项研究加强了肥胖 Zucker 大鼠模型在研究肥胖对肝脏健康影响方面的实用性,并表明肝脂肪变性需要以调节这些参数为重点的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hepatic stereological analysis in obese Zucker rats (Leprfa) with dyslipidemia.

Purpose: To characterize histologically and stereologically the hepatic steatosis in obese Zucker (fat, n = 6, with a mutation in the leptin receptor - Leprfa) and control Zucker (lean, n = 6) rats, analyzing macroscopic and microscopic differences to understand the influence of obesity on hepatic pathology.

Methods: Zucker rats were fed standard chow for 90 days. Macroscopic, qualitative, and histoquantitative (stereological) approaches were used, involving body and liver weight measurement, morphological analysis, and histopathological classification of metabolic dysfunction-associated steatotic liver disease.

Results: Zucker fat rats had higher body weight (p = 0.0022), liver weight (p = 0.0022), serum total cholesterol (p = 0.0022), and triacylglycerol (p = 0.0022) compared to Zucker lean rats. Stereological analysis showed that hepatocyte volume density (p = 0.0022) and total hepatocyte volume (p = 0.0001) were lower, and the volume density (p = 0.002) and total volume of steatosis (p = 0.002) were higher in Zucker fat rats compared to lean rats.

Conclusion: The findings indicated that obesity induces significant alterations in the hepatic morphology of Zucker rats, showing that hepatocyte volume is lower in obese animals. This study reinforces the utility of the obese Zucker rat model to investigate the effects of obesity on liver health and suggests hepatic steatosis requires therapeutic strategies focused on modulating these parameters.

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