ABSTRACT
Aim: The aim of this study is to demonstrate the relation between the expression of liver alpha-amylase and obesity
Background: 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
Material and methods: 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
Results: 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
Conclusion: 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
ABSTRACT
This study aimed to determine the association between PD-1.5C/T [rs2227981, +7785] and the risk of gastric cancer [GC] in an Iranian population. Gastric cancer is the fourth most common cancer in the world. The programmed death 1 [PD-1] is a member of the CD28 super family. PD-1 is a negative regulator of T-cell effector mechanisms which decrease immune responses against cancer. we conducted case- control study to investigate the association of PD-1.5 C/T polymorphism in 122 GC patients and 166 control individuals. DNA was extracted from blood specimens. Genotypes were analyzed using polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP] assay. The frequency of CC, CT and TT genotypes was 53.6%, 42.2% and 4.2% in control group and 41%, 54.1% and 4.9% in gastric cancer patients respectively. CC genotype was more frequent in control individuals than in patients but we found no statically significant association. The frequencies of PD-1.5CT genotypes were significantly higher in GC patient compared with control individuals [OR= 1.77, 95% CI= 1.077-2.931; P=0.026]. Allele distribution was similar in patients and healthy individuals [p=0.061].Frequency of C and T alleles was 74.7%, 25.3% in control individuals and 68.03% and 31.97% in gastric cancer patients respectively. These results suggest that PD-1.5 C/T polymorphism may affect the GC risk and prognosis in an Iranian population