Malondialdehyde Concentration, a Circulating Marker of Lipid Peroxidation, Increases Markedly after the Ingestion of Glucose but Not after Oral Intake of Lipids or Proteins
Presentation Number: SUN 581
Date of Presentation: April 2nd, 2017
Rafael Montes-Nieto, María Insenser, Mora Murri, M. Ángeles Martínez-García, Miriam Ojeda-Ojeda, Elena Fernández-Durán, Manuel Luque-Ramírez and Hector Francisco Escobar-Morreale*
Diabetes, Obesity and Human Reproduction Research Group. Instituto Ramón y Cajal de Investigación Sanitaria IRYCIS, CIBER Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Spanish Ministry of Science, Madrid, Spain
Oxidative stress (OS) consists of an imbalance between oxidant and antioxidants in favor of the former that may lead to cellular and tissue damage. A consumption of meals rich in lipids and/or carbohydrates could lead to a so-called postprandial oxidative stress (POS) status in the organism. We aimed not only to quantify the influence that each of the three main macronutrients –sugars, fats and proteins- can exert upon the POS intensity but also if these influences had links with obesity and sex. For this purpose, we conducted on alternate days three isocaloric oral loads of 300 kcal in the form of glucose, lipids and proteins on 19 men and 17 women that were classified into non-obese (BMI < 30 kg/m2) or obese (BMI ≥ 30 kg/m2) subgroups. Malondialdehyde (MDA) –a widely used circulating marker of lipid peroxidation and thus of OS- was determined in plasma samples obtained from blood drawn at fasting and during the postprandial phase. We calculated the areas under the curve (AUC) of MDA after each load as indexes of postprandial oxidative stress. MDA levels in plasma were increased in obese men compared with non-obese men in fasting state (1.67±0.06 vs. 2.12±0.08 μmol/l), whereas such increase was not observed in women (1.79±0.07 vs. 1.82±0.09 μmol/l), (P = 0.005 for the interaction). Plasma MDA concentrations increased markedly after the ingestion of glucose (AUC: 0.331±0.06 μmol/l/min), in parallel to the increase in plasma glucose, and not after the ingestion of lipids (AUC: -0.045±0.04 μmol/l/min) and proteins (AUC: -0.050±0.07 μmol/l/min), (P <0.005 for the differences). Sex and obesity did not influence postprandial plasma MDA concentrations. Our results pointed the glucose intake –and its following circulating glucose rising- to be the main trigger of MDA increasing during postprandial state irrespective of sex and obesity. Hence, in contrast with previous studies we did not find any connection between MDA and hypertriglyceridemia. On the other hand, we also determined that obesity in men can lead to increase MDA in fasting state in our subjects.
Nothing to Disclose: RM, MI, MM, MÁM, MO, EF, ML, HFE