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Expression of liver alpha-amylase in obese mouse hepatocytes

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. Hepa...

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Autores principales: Afsartala, Zohreh, Savabkar, Sanaz, Nazemalhosseini Mojarad, Ehsan, Assadollahi, Vahideh, Tanha, Shima, Bijangi, Khosro, Gholami, Mohammadreza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5118852/
https://www.ncbi.nlm.nih.gov/pubmed/27895853
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author Afsartala, Zohreh
Savabkar, Sanaz
Nazemalhosseini Mojarad, Ehsan
Assadollahi, Vahideh
Tanha, Shima
Bijangi, Khosro
Gholami, Mohammadreza
author_facet Afsartala, Zohreh
Savabkar, Sanaz
Nazemalhosseini Mojarad, Ehsan
Assadollahi, Vahideh
Tanha, Shima
Bijangi, Khosro
Gholami, Mohammadreza
author_sort Afsartala, Zohreh
collection PubMed
description 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.
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spelling pubmed-51188522016-11-28 Expression of liver alpha-amylase in obese mouse hepatocytes Afsartala, Zohreh Savabkar, Sanaz Nazemalhosseini Mojarad, Ehsan Assadollahi, Vahideh Tanha, Shima Bijangi, Khosro Gholami, Mohammadreza Gastroenterol Hepatol Bed Bench Original Article 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. Shaheed Beheshti University of Medical Sciences 2016 /pmc/articles/PMC5118852/ /pubmed/27895853 Text en ©2016 RIGLD, Research Institute for Gastroenterology and Liver Diseases This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Afsartala, Zohreh
Savabkar, Sanaz
Nazemalhosseini Mojarad, Ehsan
Assadollahi, Vahideh
Tanha, Shima
Bijangi, Khosro
Gholami, Mohammadreza
Expression of liver alpha-amylase in obese mouse hepatocytes
title Expression of liver alpha-amylase in obese mouse hepatocytes
title_full Expression of liver alpha-amylase in obese mouse hepatocytes
title_fullStr Expression of liver alpha-amylase in obese mouse hepatocytes
title_full_unstemmed Expression of liver alpha-amylase in obese mouse hepatocytes
title_short Expression of liver alpha-amylase in obese mouse hepatocytes
title_sort expression of liver alpha-amylase in obese mouse hepatocytes
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5118852/
https://www.ncbi.nlm.nih.gov/pubmed/27895853
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