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The antimicrobial peptide alpha defensin correlates to type 2 diabetes via the advanced glycation end products pathway

Background: Diabetes is a serious health problem that results in high mortality rates worldwide. α-defensins are antimicrobial peptides of the innate immune system that contribute to inflammation. However, data on serum levels of α-defensin in patients suffering from type 2 diabetes are limited. Obj...

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Bibliographic Details
Published in:African health sciences 2022-03, Vol.22 (1), p.303-11
Main Authors: El-Mowafy, Mohammed, Elgaml, Abdelaziz, Abass, Naglaa, A Mousa, Amany, N Amin, Mohamed
Format: Article
Language:English
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Summary:Background: Diabetes is a serious health problem that results in high mortality rates worldwide. α-defensins are antimicrobial peptides of the innate immune system that contribute to inflammation. However, data on serum levels of α-defensin in patients suffering from type 2 diabetes are limited. Objectives: This study aimed to assess the possible changes in α-defensin serum levels in patients suffering from type 2 diabetes and to investigate its correlation with relevant biomarkers. Methodology: Analysis of serum α-defensin levels in 47 type 2 diabetics with diabetic neuropathy, 19 type 2 diabetics with no complications and 19 healthy control subjects by enzyme-linked immunosorbent assay was established. Furthermore, measurement of advanced glycation end products (AGEs) and fasting blood glucose (FBG) serum levels was performed, together with the lipid profile analysis. Results: The serum levels of α-defensin were higher in patients with and without diabetic neuropathy in comparison to control subjects. In addition, there was a significant correlation between α-defensin serum levels and AGEs and FBG serum levels as well as with the body mass index. Conclusions: α-defensins are significantly elevated in serum of type II diabetics, and correlate with AGEs serum levels indicating a crosstalk that may aggravate inflammation in type 2 diabetes. Keywords: Alpha defensing; Advanced glycation end products; Hyperglycemia; Inflammation; Innate immunity; Type 2 diabetes.
ISSN:1680-6905
1680-6905
1729-0503
DOI:10.4314/ahs.v22i1.37