Advanced Glycation End Products Evolution after Pancreas-Kidney Transplantation: Plasmatic and Cutaneous Assessments. (5th January 2016)

• Record Type: Journal Article
• Authors: Martins, La Salete; Oliveira, José C.; Vizcaíno, José Ramón; Fonseca, Isabel; Gouveia, Carlos; Silva, Donzília; Henriques, António C.; Noronha, Irene L.; Rodrigues, Anabela
• Other Names: Pialoux Vincent Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2016(2016)
• Publication Date: 2016-01-05
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2016/2189582
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Diabetes mellitus leads to increased Advanced Glycation End Products (AGE) production, which has been associated with secondary diabetic complications. Type 1 diabetic patients undergoing pancreas-kidney transplantation (SPKT) can restore normoglycemia and renal function, eventually decreasing AGE accumulation. We aimed to prospectively study AGE evolution after SPKT. Circulating AGE were assessed in 20 patients, at time 0 (T0), 3 months (T3), 6 months (T6), and 12 months (T12) after successful SPKT. Global AGE and carboxymethyllysine (CML) were analyzed, as well as advanced oxidation protein products (AOPP). Skin biopsies were obtained at T0 and T12. Immunohistochemistry with anti-AGE antibody evaluated skin AGE deposition. AGE mean values were16.8 ± 6.4 μ g/mL at T0;17.1 ± 3.8 μ g/mL at T3;17.5 ± 5.6 μ g/mL at T6; and16.0 ± 5.2 μ g/mL at T12. CML mean values were0.94 ± 0.36 ng/mL at T0;1.11 ± 0.48 ng/mL at T3;0.99 ± 0.42 ng/mL at T6; and0.78 ± 0.38 ng/mL at T12. AOPP mean values were130.1 ± 76 . 8 μ Mol/L at T0;137.3 ± 110 . 6 μ Mol/L at T3;116.4 ± 51 . 2 μ Mol/L at T6; and106.4 ± 57 . 9 μ Mol/L at T12. CML variation was significant (P = 0.022 ); AOPP variation was nearly significant (P = 0.076 ). Skin biopsies evolved mostly from a cytoplasmic diffuse to a peripheral interkeratinocytic immunoreaction pattern; in 7 cases, a reduction in AGE immunoreaction intensity was evident at T12. In conclusion, glycoxidation markers decrease, plasmatic and on tissues, may start early after SPKT. Studies with prolonged follow-up may confirm these data.