Mojbafan Marzieh, Afsartala Zohreh, Amoli Mahsa M, Mahmoudi Mahdi, Yaghmaei Parichehreh, Larijani Bagher, Ebrahim-Habibi Azadeh
Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran; Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Pharmacol Rep. 2017 Apr;69(2):229-234. doi: 10.1016/j.pharep.2016.11.001. Epub 2016 Nov 5.
Obesity is a major health problem worldwide, for which preventive and therapeutic means are still needed. Alpha-amylase is a digestive enzyme whose inhibition has been targeted as a potential anti-obesity strategy. However, alpha-amylase gene expression has not been particularly attended to, and in contrast with pancreatic and salivary amylases, fewer studies have focused on liver alpha-amylase. The present study aimed at investigating the expression of alpha-amylase gene in obese and normal mice at RNA and protein level as well as acarbose effect on this gene expression in hepatocyte cell culture.
Control and case groups were fed by normal mouse pellet and high-fat diet respectively, during 8 weeks. After this period, serum biochemical parameters including glucose, cholesterol, triglycerides, AST, ALT and alpha-amylase were assayed. Liver alpha-amylase gene was analyzed by real time PCR, and liver enzyme was assayed with Bernfeld and ELISA methods Hepatocyte cell culture derived from both group were also treated by acarbose and alpha-amylase activity and gene expression was analyzed by above mentioned methods.
All biochemical factors showed an increase in obese mice, but the increase in ALT and AST were not statistically significant. Alpha-amylase levels were also increased in obese mice, both at RNA and protein level, while a decrease was seen in obese mice derived hepatocytes after acarbose treatment.
Elevated liver alpha-amylase levels may be indicative of initial stages of obesity and the use of acarbose could be considered as a treatment of obesity which could be potentially effective at multiple levels.
肥胖是全球主要的健康问题，仍需要预防和治疗手段。α-淀粉酶是一种消化酶，其抑制作用已被作为一种潜在的抗肥胖策略。然而，α-淀粉酶基因表达并未得到特别关注，与胰腺和唾液淀粉酶相比，关注肝脏α-淀粉酶的研究较少。本研究旨在调查肥胖和正常小鼠中α-淀粉酶基因在RNA和蛋白质水平的表达，以及阿卡波糖对肝细胞培养中该基因表达的影响。
对照组和病例组分别喂食正常小鼠颗粒饲料和高脂饮食，持续8周。在此期间后，检测血清生化参数，包括葡萄糖、胆固醇、甘油三酯、AST、ALT和α-淀粉酶。通过实时PCR分析肝脏α-淀粉酶基因，并用伯恩菲尔德法和ELISA法检测肝酶。来自两组的肝细胞培养物也用阿卡波糖处理，并用上述方法分析α-淀粉酶活性和基因表达。
所有生化因子在肥胖小鼠中均升高，但ALT和AST的升高无统计学意义。肥胖小鼠中α-淀粉酶水平在RNA和蛋白质水平均升高，而阿卡波糖处理后肥胖小鼠来源的肝细胞中α-淀粉酶水平下降。
肝脏α-淀粉酶水平升高可能指示肥胖的初始阶段，阿卡波糖的使用可被视为一种肥胖治疗方法，可能在多个层面上具有潜在疗效。
