Plasma Levels of Pentosidine, Carboxymethyl-Lysine, Soluble Receptor for Advanced Glycation End Products, and Metabolic Syndrome: The Metformin Effect.
Metabolic syndrome (MetS) is considered one of the most important public health problems. Several and controversial studies showed that the role of advanced glycation end products (AGEs) and their receptor in the development of metabolic syndrome and therapeutic pathways is still unsolved. We have investigated whether plasma pentosidine, carboxymethyl-lysine (CML), and soluble receptor for advanced glycation end products (sRAGE) levels were increased in patients with MetS and the effect of metformin in plasma levels of pentosidine, CML, and sRAGE. 80 control subjects and 86 patients were included in this study. Pentosidine, CML, and sRAGE were measured in plasma by enzyme-linked immunosorbent assay (ELISA). Plasma pentosidine, CML, and sRAGE levels were significantly increased in patients compared to control subjects (P< 0.001,P< 0.001, andP= 0.014, resp.). Plasma levels of pentosidine were significantly decreased in patients who received metformin compared to untreated patients (P= 0.01). However, there was no significant difference between patients treated with metformin and untreated patients in plasma CML levels. Plasma levels of sRAGE were significantly increased in patients who received metformin and ACE inhibitors (P< 0.001 andP= 0.002, resp.). However, in a multiple stepwise regression analysis, pentosidine, sRAGE, and drugs treatments were not independently associated. Patients with metabolic syndrome showed increased levels of AGEs such as pentosidine and CML. Metformin treatment showed a decreased level of pentosidine but not of CML. Therapeutic pathways of AGEs development should be taken into account and further experimental andin vitrostudies merit for advanced research.
Laboratory of Biochemistry (LR12ES05) "Nutrition-Aliment Fonctionnel et Santé vasculaire", Faculty of Medicine, University of Monastir, Monastir, Tunisia.
Mohamed
M
Haddad
Laboratory of Biochemistry (LR12ES05) "Nutrition-Aliment Fonctionnel et Santé vasculaire", Faculty of Medicine, University of Monastir, Monastir, Tunisia.
Ines
I
Knani
Laboratory of Biochemistry, CHU Thar Sfar, Mahdia, Tunisia.
Hsan
H
Bouzidi
Laboratory of Endocrinology, CHU Thar Sfar, Mahdia, Tunisia.
Olfa
O
Berriche
Laboratory of Biochemistry (LR12ES05) "Nutrition-Aliment Fonctionnel et Santé vasculaire", Faculty of Medicine, University of Monastir, Monastir, Tunisia.
Mohamed
M
Hammami
Laboratory of Biochemistry (LR12ES05) "Nutrition-Aliment Fonctionnel et Santé vasculaire", Faculty of Medicine, University of Monastir, Monastir, Tunisia.
Mohsen
0000-0001-5594-7451
M
Kerkeni
D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D015415:Biomarkers; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008239:Lysine / Q000031:analogs & derivatives* / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis* / Q000188:drug therapy / Q000378:metabolism; D008687:Metformin / Q000627:therapeutic use*; D008875:Middle Aged; D011379:Prognosis; D000067759:Receptor for Advanced Glycation End Products / Q000097:blood*
D001120:Arginine; D015415:Biomarkers; D007004:Hypoglycemic Agents; D008239:Lysine; D008687:Metformin; D000067759:Receptor for Advanced Glycation End Products; C048496:N(6)-carboxymethyllysine; C062187:pentosidine; C000593871:AGER protein, human