Soluble Receptor For Advanced Glycation End Products Are Decreased But Not The Levels Of Advanced Glycation End Product Ne-(Carboxymethyl)Lysine In Chronic Obstructive Pulmonary Disease

BackgroundAdvanced glycation end-products (AGEs) have been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). However, the association between AGE accumulation in the skin measured by skin autofluorescence (SAF) and lung function in healthy subjects has not been explored in detail. We use a population-based study of 50–64-year-olds to assess spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) and impulse oscillometry (IOS) in relation to SAF.MethodsParticipants with information on SAF, lung function and potential confounding variables were included from the Swedish Cardiopulmonary Bioimage Study (SCAPIS) cohort (spirometry, n=4111; DLCO, n=3889; IOS, n=3970). Linear regression was used to assess changes in lung function (as measured by spirometry (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC), DLCO and IOS (resistance measured at 5 (R5) and 20 Hz (R20), R5−R20, area of reactance, reactance measured at 5 Hz (X5), and resonant frequency)) by a 1-sd increase in SAF.ResultsFEV1, FVC and DLCO were significantly and inversely associated with SAF after adjustment for potential confounding factors (per 1-sd increase in SAF: FEV1 −0.03 L (95% CI −0.04– −0.02 L), p<0.001; FVC −0.03 L (95% CI −0.05– −0.02 L), p<0.001; DLCO −0.07 mmol·min−1·kPa−1 (95% CI −0.11– −0.03 mmol·min−1·kPa−1), p<0.001). This association was also found in nonsmokers and in non-COPD subjects. Pulmonary reactance (X5) but not pulmonary resistance (R5, R20 and R5−R20) was significantly associated with SAF (per 1-sd increase in SAF: X5 −0.001 kPa·L−1·s (95% CI −0.003–0.00 kPa·L−1·s), p=0.042), which was mirrored in non-COPD patients but not in current nonsmokers.ConclusionsAGE accumulation, as measured by SAF, is significantly associated with lung function decrements indicative of changes in the lung parenchyma

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Plasma Levels of Pentosidine, Carboxymethyl-Lysine, Soluble Receptor for Advanced Glycation End Products, and Metabolic Syndrome: The Metformin Effect

Disease Markers ◽

10.1155/2016/6248264 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 19

Author(s):

Mohamed Haddad ◽

Ines Knani ◽

Hsan Bouzidi ◽

Olfa Berriche ◽

Mohamed Hammami ◽

...

Keyword(s):

Metabolic Syndrome ◽

Advanced Glycation End Products ◽

Plasma Levels ◽

Enzyme Linked Immunosorbent Assay ◽

Soluble Receptor ◽

Advanced Glycation ◽

Control Subjects ◽

Glycation End Products ◽

End Products ◽

Carboxymethyl Lysine

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<0.001andP=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.

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