Alcohol promotes liver fibrosis in high fat diet induced diabetic rats.

Q3 Pharmacology, Toxicology and Pharmaceutics Journal of Basic and Clinical Physiology and Pharmacology Pub Date : 2024-07-19 eCollection Date: 2024-07-01 DOI:10.1515/jbcpp-2024-0042
Veena Gopinath, Aleena Mariya Davis, Thara K Menon, Achuthan C Raghavamenon
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Abstract

Objectives: Type 2 diabetes (T2DM) and alcoholism are considered to be lifestyle-associated independent risk factors in fatty liver diseases (FLD) mediated cirrhosis and hepatocellular carcinoma (HCC). A combined effect of both these conditions may exacerbate the pathological changes and a pre-clinical exploration of this is expected to provide a mechanical detail of the pathophysiology. The present study aims to understand the effect of alcohol on pre- diabetic and type 2 diabetic female Wistar rats.

Methods: In this experimental study, 12 Wistar rats (180-220 g) were randomly assigned into three groups: Normal (fed normal rat chow), alcohol (20 %) fed diabetic (HFD + STZ), and pre-diabetic rats (HFD alone). After, two months of the experimental period, blood and liver tissues were collected lipid metabolic alteration, liver injury, and fibrosis were determined following biochemical and histological methods. Data were analyzed using one-way ANOVA and Dunnett's Post Hoc test.

Results: Significant dyslipidemia was observed in the liver tissues of diabetic and pre-diabetic rats following alcohol ingestion. A significant (p<0.05) increase in lipid peroxidation status, and hepatic marker enzyme activities (p<0.0001) were observed in diabetic animals. In corroborating with these observations, hematoxylin and eosin staining of hepatic tissue revealed the presence of sinusoidal dilation along with heavily damaged hepatocytes and inflammatory cell infiltration. Further, significantly (p<0.001) increased hepatic hydroxyproline content and extended picrosirius red stained areas of collagen in liver tissue indicated initiation of fibrosis in alcohol-fed diabetic rats.

Conclusions: Overall, the results indicate that alcohol consumption in T2DM conditions is more deleterious than pre diabetic conditions in progressing to hepatic fibrosis.

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酒精会促进高脂饮食诱导的糖尿病大鼠肝纤维化。
目的:2型糖尿病(T2DM)和酗酒被认为是与生活方式相关的脂肪肝(FLD)介导的肝硬化和肝细胞癌(HCC)的独立危险因素。这两种病症的综合效应可能会加剧病理变化,对其进行临床前探索有望提供病理生理学的机械细节。本研究旨在了解酒精对糖尿病前期和 2 型糖尿病雌性 Wistar 大鼠的影响:在本实验研究中,12 只 Wistar 大鼠(180-220 克)被随机分为三组:正常组(喂食正常大鼠饲料)、酒精(20%)喂养糖尿病大鼠组(HFD + STZ)和糖尿病前期大鼠组(仅喂食 HFD)。实验两个月后,收集血液和肝组织,采用生化和组织学方法测定脂质代谢改变、肝损伤和肝纤维化。数据采用单因素方差分析和 Dunnett 后验法进行分析:结果:糖尿病大鼠和糖尿病前期大鼠摄入酒精后,其肝脏组织出现了明显的血脂异常。结论总之,研究结果表明,在 T2DM 条件下饮酒比在糖尿病前期条件下饮酒更容易导致肝纤维化。
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来源期刊
Journal of Basic and Clinical Physiology and Pharmacology
Journal of Basic and Clinical Physiology and Pharmacology Pharmacology, Toxicology and Pharmaceutics-Pharmacology
CiteScore
3.90
自引率
0.00%
发文量
53
期刊介绍: The Journal of Basic and Clinical Physiology and Pharmacology (JBCPP) is a peer-reviewed bi-monthly published journal in experimental medicine. JBCPP publishes novel research in the physiological and pharmacological sciences, including brain research; cardiovascular-pulmonary interactions; exercise; thermal control; haematology; immune response; inflammation; metabolism; oxidative stress; and phytotherapy. As the borders between physiology, pharmacology and biochemistry become increasingly blurred, we also welcome papers using cutting-edge techniques in cellular and/or molecular biology to link descriptive or behavioral studies with cellular and molecular mechanisms underlying the integrative processes. Topics: Behavior and Neuroprotection, Reproduction, Genotoxicity and Cytotoxicity, Vascular Conditions, Cardiovascular Function, Cardiovascular-Pulmonary Interactions, Oxidative Stress, Metabolism, Immune Response, Hematological Profile, Inflammation, Infection, Phytotherapy.
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