Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2020, vol. 29, nr 3, March, p. 275–284

doi: 10.17219/acem/112611

Publication type: original article

Language: English

License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)

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Advanced glycation end products derived from serum albumin modification by glucose (AGE-1) reflect clustering of lipid-associated metabolic abnormalities and are decreased in patients treated with acarbose: A cross-sectional study

Agnieszka Bronowicka-Szydełko1,A,D, Małgorzata Krzystek-Korpacka1,C,D, Aleksandra Kuzan1,C, Kinga Gostomska-Pampuch1,C, Małgorzata Gacka2,B, Urszula Jakobsche-Policht2,B, Rajmund Adamiec2,D,E, Andrzej Gamian1,3,E,F

1 Department of Medical Biochemistry, Wroclaw Medical University, Poland

2 Department of Angiology, Diabetes and Hypertension, Wroclaw Medical University, Poland

3 Laboratory of Medical Microbiology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland


Background. Advanced glycation end products (AGEs) are formed during protein modification by a reduction of sugars or reactive aldehydes. Depending on the pathology, various AGEs may be formed. They are stable compounds and are considered as potential diseases markers.
Objectives. The objective of this study was to assess glucose-mediated albumin modification that yields non-standard epitopes of AGEs (AGE-1) in diabetes and in associated metabolic abnormalities.
Material and Methods. The AGE-1, expressed as median AGE-1 level and AGE-1 positivity, was determined in 246 individuals (198 with prediabetes/diabetes) using a new slot-dot-blot method (allowing for detection of barely traceable analytes) and related to the presence of diabetes-associated metabolic abnormalities and complications, and treatment.
Results. The AGE-1 level was higher in patients with prediabetes/diabetes than in controls. Its elevation was associated with metabolic syndrome (MetS), obesity, hyperlipidemia, and non-alcoholic fatty liver disease (NAFLD) but not with diabetic control or microand macroangiopathy, except for atherosclerotic plaques formation in carotid arteries. The AGE-1-positive patients had higher triglycerides and lower high-density lipoprotein (HDL)-cholesterol. In patients untreated with aspirin, AGE-1 positivity was associated with higher C-reactive protein (CRP) level. Treatment with aspirin, sulfonylureas and gliptins was associated with higher AGE-1 level and with dyslipidemia medications with higher AGE-1 positivity. In patients with abnormal glucose metabolism, acarbose treatment was associated with lower AGE-1 positivity. Multivariate analysis showed MetS, carotid artery plaques, NAFLD, and treatment with aspirin and acarbose to be independently associated with AGE-1 positivity.
Conclusion. Unlike standard AGEs, AGE-1 is more tightly associated with abnormalities in lipid than glucose metabolism, and lower in patients treated with acarbose but not with other antidiabetics.

Key words

metabolic syndrome, diabetes, atherosclerosis, acarbose, advanced glycation end products

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