Afsartala Zohreh, Savabkar Sanaz, Nazemalhosseini Mojarad Ehsan, Assadollahi Vahideh, Tanha Shima, Bijangi Khosro, Gholami Mohammadreza
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroenterol Hepatol Bed Bench. 2016 Fall;9(4):278-285.
The aim of this study is to demonstrate the relation between the expression of liver alpha-amylase and obesity.
Alpha-amylase catalyses the hydrolysis of 1, 4-alpha-glucosidic linkages in polysaccharides and has three main subtypes, including: salivary, pancreatic, and hepatic. Hepatic alpha-amylase is involved in glycogen metabolism, and has a role in obesity and its management. In this study, we aimed to analyze the expression of liver alpha-amylase in overweight and obese mouse.
In this study, NMRI male mice were randomly divided into two groups. The sample group (obese) took a high-fat and carbohydrate diet, while the control group (normal) took a laboratory pellet chow for eight weeks. During this period, their weight was measured. After eight weeks, liver hepatocytes were isolated using an enzymatic digestion method. Immunocytochemistry (ICC) and flow cytometry analysis were performed to measure alpha amylase protein expression in mouse liver hepatocyte cells.
A significant difference in the body weight was observed between the two groups (p<0.05). The qualitative protein expression of liver alpha-amylase was found to be higher in the obese group in both tests (immunocytochemistry and flow cytometry). Animals from the test group presented higher alpha-amylase expression, which suggests that this hepatic protein may constitute a potential indicator of susceptibility for fat tissue accumulation and obesity. The present data demonstrates an increased expression of liver amylase in obese mice.
These results suggest that liver amylase secretion might be useful for predicting susceptibility to obesity induced by consumption of a high-fat and carbohydrate diet.
本研究旨在阐明肝脏α-淀粉酶表达与肥胖之间的关系。
α-淀粉酶催化多糖中1,4-α-糖苷键的水解，有三种主要亚型，包括：唾液型、胰腺型和肝脏型。肝脏α-淀粉酶参与糖原代谢，在肥胖及其管理中发挥作用。在本研究中，我们旨在分析超重和肥胖小鼠肝脏α-淀粉酶的表达情况。
本研究中，将NMRI雄性小鼠随机分为两组。样本组（肥胖组）给予高脂高碳水化合物饮食，而对照组（正常组）给予实验室颗粒饲料，持续八周。在此期间，测量它们的体重。八周后，采用酶消化法分离肝脏肝细胞。进行免疫细胞化学（ICC）和流式细胞术分析，以测量小鼠肝脏肝细胞中α-淀粉酶蛋白的表达。
两组之间观察到体重有显著差异（p<0.05）。在两项测试（免疫细胞化学和流式细胞术）中，均发现肥胖组肝脏α-淀粉酶的定性蛋白表达较高。测试组的动物呈现出更高的α-淀粉酶表达，这表明这种肝脏蛋白可能构成脂肪组织积累和肥胖易感性的潜在指标。目前的数据表明肥胖小鼠肝脏淀粉酶表达增加。
这些结果表明肝脏淀粉酶分泌可能有助于预测由高脂高碳水化合物饮食引起的肥胖易感性。
