Department of Biochemistry, Amala Cancer Research Center (Recognized Centre of the University of Calicut), Thrissur, Kerala, India.
Department of Biotechnology, University of Calicut, Thenhipalam, Kerala, India.
J Basic Clin Physiol Pharmacol. 2024 Jul 19;35(4-5):273-284. doi: 10.1515/jbcpp-2024-0042. eCollection 2024 Jul 1.
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.
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.
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.
Overall, the results indicate that alcohol consumption in T2DM conditions is more deleterious than pre diabetic conditions in progressing to hepatic fibrosis.
2 型糖尿病（T2DM）和酗酒被认为是与生活方式相关的独立风险因素，可导致脂肪性肝病（FLD）相关的肝硬化和肝细胞癌（HCC）。这两种情况的联合作用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详细机制。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。
在这项实验研究中，将 12 只 Wistar 大鼠（180-220g）随机分为三组：正常组（喂食正常大鼠饲料）、酒精组（20%酒精喂食糖尿病组（HFD+STZ）和糖尿病前期组（单独 HFD）。在实验期两个月后，通过生化和组织学方法收集血液和肝脏组织，以确定脂质代谢改变、肝损伤和纤维化。采用单因素方差分析和 Dunnett 事后检验进行数据分析。
酒精摄入后，糖尿病和糖尿病前期大鼠的肝脏组织出现明显的血脂异常。糖尿病动物的脂质过氧化状态和肝标志物酶活性显著增加（p<0.0001）（p<0.05）。肝组织苏木精和伊红染色的结果与这些观察结果一致，显示出窦状扩张以及严重受损的肝细胞和炎症细胞浸润。此外，肝组织羟脯氨酸含量显著增加（p<0.001），以及 Picrosirius 红染色的胶原面积延长，表明酒精喂养的糖尿病大鼠开始发生纤维化。
总的来说，结果表明，在进展为肝纤维化方面，T2DM 情况下的酒精摄入比糖尿病前期更为有害。
