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Serum chitotriosidase enzyme activity is closely related to HbA1c levels and the complications in patients with diabetes mellitus type 2

Abstract Aims Chitotriosidase, is a macrophage sourced enzyme which shows high activity during the course of various storage disorders such as Gaucher's Disease. The aforementioned macrophage sourced enzyme, which has a role in basic immune response, is also high in patients with diabetes. This...

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Bibliographic Details
Published in:Diabetes & metabolic syndrome clinical research & reviews 2017-11, Vol.11, p.S503-S506
Main Authors: Turan, Emre, Sozmen, Bulent, Eltutan, Mine, Sozmen, Eser Y
Format: Article
Language:English
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Summary:Abstract Aims Chitotriosidase, is a macrophage sourced enzyme which shows high activity during the course of various storage disorders such as Gaucher's Disease. The aforementioned macrophage sourced enzyme, which has a role in basic immune response, is also high in patients with diabetes. This study was designed to determine the chitotriosidase activities in patients with diabetes and the relationship between the complication of diabetes and chitotriosidase activity. Materials methods This study included 76 patients with type2 diabetes mellitus and 76 healthy subjects. The chitotriosidase activity of all serum samples were determined by fluorometric method. Results and conclusion The chitotriosidase activity of patients having complications (neuropathy or nephropathy) were statistically significantly higher (p < 0.05) than those of the controls. When the chitotriosidase activity of patients was evaluated regarding their glycosylated hemoglobin (HbA1c) levels, a progressive increase in chitotriosidase activity was observed in patients. The chitotriosidase activity of patients having higher HbA1c > 10% levels was statistically significant higher than those of the control group's (p < 0.05). It is shown that chitotriosidase activity might be a marker for some complications and is closely related to HbA1c levels.
ISSN:1871-4021
1878-0334
DOI:10.1016/j.dsx.2017.03.044