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The neuroprotective effect of virgin olive oil (VOO) polyphenols has been related to their antioxidant effect. The main objective was to analyze how tyrosol and hydroxytyrosol contribute to the antioxidant and neuroprotective effects of VOO in a model of hypoxia-reoxygenation in rat brain slices. Rats were treated per os (po) (10 or 20 mg/kg/day) with hydroxytyrosol ethyl ether (HTEE), tyrosol ethyl ether (TEE), or 3,4-di-o-methylidene-hydroxytyrosol ethyl ether (MHTEE), used as a negative control for antioxidant effects. Lipid peroxidation was inhibited with HTEE, TEE, and MHTEE (from 5.0 ± 1.5 to 2.6 ± 1.5, 4.5 ± 1.5, and 4.8 ± 1.5 nmol/mg protein, respectively). However, all three compounds had similar neuroprotective effects: from 2.8 ± 0.07 to 1.8 ± 0.02 arbitrary units for HTEE, 1.4 ± 0.09 arbitrary units for TEE, and 1.3 ± 0.2 arbitrary units for MHTEE. All three compounds inhibited 3-nitrotyrosine production (from 3.7 ± 0.3 to 1.2 ± 0.03 nmol/0.1 g tissue for HTEE, 1.0 ± 0.2 nmol/0.1 g tissue for TEE, and 1.3 ± 0.1 nmol/0.1 g tissue for MHTEE), prostaglandin E2 production (from 55.7 ± 2.2 to 46.4 ± 1.9 pg/0.1 g tissue for HTEE, 24.7 ± 1.3 pg/0.1 g tissue for TEE, and 27.6 ± 2.6 pg/0.1 g tissue for MHTEE), whereas only HTEE inhibited IL1β production (from 35.7 ± 1.5 to 21.6 ± 0.8 pg/0.1 g tissue). Pearson correlation coefficients related neuroprotective effect with an antioxidant effect for HTEE (R = 0.72, p < 0.001), and inhibition of nitrosative stress (R = 0.78, 0.67, and 0.66 for HTEE, TEE, and MHTEE, respectively, p < 0.001) and inflammatory mediators (R = 0.72, 0.79, and 0.64 for HTEE, TEE, and MHTEE, respectively, p < 0.001) with all three compounds.

Aim: Arteriosclerotic cardiovascular disease, one of the world’s leading causes of death, first manifests itself at an early age. The identification of children who may have increased cardiovascular risk in the future could be an important prevention strategy. Our aim was to assess the clinical, analytical, and dietary variables associated with arterial stiffness (AS), measured by carotid-femoral pulse wave velocity (cfPWV) in a prepubescent population with metabolically healthy obesity (MHO). Subjects and Methods: A cross-sectional study in prepubescent subjects with obesity who had ≤1 metabolic syndrome criteria (abdominal perimeter and blood pressure ≥90th percentile, triglycerides >150 mg/dL, HDL-cholesterol <40 mg/dL, fasting plasma glucose ≥100 mg/dL) was conducted. Adherence to Mediterranean Diet, blood pressure, BMI, waist/height ratio (WHtR), glycemic status, lipid profile, and cfPWV were analyzed. 75 MHO children (boys: 43; girls: 32; p = 0.20) (age = 10.05 ± 1.29 years; BMI = 25.29 ± 3.5 kg/m2) were included. Results: We found a positive correlation between cfPWV and weight (r = 0.51; p < 0.0001), BMI (r = 0.44; p < 0.0001), WHtR (r = 0.26; p = 0.02), fasting insulin levels (r = 0.28; p = 0.02), and insulin resistance (Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index) (r = 0.25; p = 0.04). Multiple linear regression analysis identified BMI and HOMA-IR as independent parameters associated with cfPWV. Conclusions: Prepubescent children with obesity who were shown to be metabolically healthy presented with arterial stiffness, which is closely related to BMI and the state of insulin resistance.

Background Metabolically healthy obesity (MHO) is a considerably controversial concept as it is considered a transitory condition towards the development of different pathologies (type 2 diabetes, insulin resistance, or cardiovascular disease). MHO is closely related to lifestyle and environmental factors. Epigenetics has become an essential biological tool to analyze the link between obesity and metabolic status. The aim of this study was to determine whether MHO status is conditioned by the DNA methylation (DNAm) of several genes related to lipid metabolism (lipoprotein lipase, retinoid X receptor alpha, liver X receptor, stearoyl-CoA desaturase, sterol regulatory element binding factor 1), and inflammation (LEP) in peripheral blood mononuclear cells (PBMCs) from 131 prepubertal subjects with MHO phenotype after lifestyle modifications with personalized Mediterranean diet (MedDiet) combined with a physical activity (PA) program. Results The DNAm of all studied genes were significantly modified in the population after 12 months of lifestyle modifications (MedDiet and PA). In addition, associations were found between the DNAm studies and BMI, homeostatic model assessment of insulin resistance, monounsaturated fatty acid and polyunsaturated fatty acid, moderate-vigorous PA, fat mass, and adherence to MedDiet. Conclusions It was found that DNAm of genes related to lipid metabolism and inflammation are also present in childhood and that this methylation profile can be modified by interventions based on MedDiet and PA.