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Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes
Before this study, there had been no research evaluating the relationship between a lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin- (STZ-) induced type 1 diabetes. In our work, rats were divided into 4 groups of 8 animals each: control grou...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5804338/ https://www.ncbi.nlm.nih.gov/pubmed/29464184 http://dx.doi.org/10.1155/2017/9850398 |
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author | Maciejczyk, Mateusz Kossakowska, Agnieszka Szulimowska, Julita Klimiuk, Anna Knaś, Małgorzata Car, Halina Niklińska, Wiesława Ładny, Jerzy Robert Chabowski, Adrian Zalewska, Anna |
author_facet | Maciejczyk, Mateusz Kossakowska, Agnieszka Szulimowska, Julita Klimiuk, Anna Knaś, Małgorzata Car, Halina Niklińska, Wiesława Ładny, Jerzy Robert Chabowski, Adrian Zalewska, Anna |
author_sort | Maciejczyk, Mateusz |
collection | PubMed |
description | Before this study, there had been no research evaluating the relationship between a lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin- (STZ-) induced type 1 diabetes. In our work, rats were divided into 4 groups of 8 animals each: control groups (C2, C4) and diabetic groups (STZ2, STZ4). The secretory function of salivary glands—nonstimulated and stimulated salivary flow, α-amylase, total protein—and salivary exoglycosidase activities—N-acetyl-β-hexosaminidase (HEX, HEX A, and HEX B), β-glucuronidase, α-fucosidase, β-galactosidase, and α-mannosidase—was estimated both in the parotid and submandibular glands of STZ-diabetic and control rats. The study has demonstrated that the activity of most salivary exoglycosidases is significantly higher in the parotid and submandibular glands of STZ-diabetic rats as compared to the healthy controls and that it increases as the disease progresses. Reduced secretory function of diabetic salivary glands was also observed. A significant inverse correlation between HEX B, α-amylase activity, and stimulated salivary flow in diabetic parotid gland has also been shown. Summarizing, STZ-induced diabetes leads to a change in the lysosomal exoglycosidase profile and reduced function of the salivary glands. |
format | Online Article Text |
id | pubmed-5804338 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-58043382018-02-20 Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes Maciejczyk, Mateusz Kossakowska, Agnieszka Szulimowska, Julita Klimiuk, Anna Knaś, Małgorzata Car, Halina Niklińska, Wiesława Ładny, Jerzy Robert Chabowski, Adrian Zalewska, Anna J Diabetes Res Research Article Before this study, there had been no research evaluating the relationship between a lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin- (STZ-) induced type 1 diabetes. In our work, rats were divided into 4 groups of 8 animals each: control groups (C2, C4) and diabetic groups (STZ2, STZ4). The secretory function of salivary glands—nonstimulated and stimulated salivary flow, α-amylase, total protein—and salivary exoglycosidase activities—N-acetyl-β-hexosaminidase (HEX, HEX A, and HEX B), β-glucuronidase, α-fucosidase, β-galactosidase, and α-mannosidase—was estimated both in the parotid and submandibular glands of STZ-diabetic and control rats. The study has demonstrated that the activity of most salivary exoglycosidases is significantly higher in the parotid and submandibular glands of STZ-diabetic rats as compared to the healthy controls and that it increases as the disease progresses. Reduced secretory function of diabetic salivary glands was also observed. A significant inverse correlation between HEX B, α-amylase activity, and stimulated salivary flow in diabetic parotid gland has also been shown. Summarizing, STZ-induced diabetes leads to a change in the lysosomal exoglycosidase profile and reduced function of the salivary glands. Hindawi 2017 2017-12-31 /pmc/articles/PMC5804338/ /pubmed/29464184 http://dx.doi.org/10.1155/2017/9850398 Text en Copyright © 2017 Mateusz Maciejczyk et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Maciejczyk, Mateusz Kossakowska, Agnieszka Szulimowska, Julita Klimiuk, Anna Knaś, Małgorzata Car, Halina Niklińska, Wiesława Ładny, Jerzy Robert Chabowski, Adrian Zalewska, Anna Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title | Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title_full | Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title_fullStr | Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title_full_unstemmed | Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title_short | Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes |
title_sort | lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin-induced diabetes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5804338/ https://www.ncbi.nlm.nih.gov/pubmed/29464184 http://dx.doi.org/10.1155/2017/9850398 |
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