Background. Obesity and pregnancy increase levels of maternal oxidative stress (OS). However, little is known about the maternal, placental, and neonatal OS status. Objective. To analyze the relation between prepregnancy obesity and the expression of OS markers and antioxidant capacity in the fetomaternal unit and their association with dietary intake. Methods. This cross-sectional study included 33 women with singleton, noncomplicated pregnancies. Two groups were formed: women with prepregnancy body mass index (pBMI) within normal range (18.5-24.9 kg/m², n = 18) and women with pBMI ≥ 30 kg/m², suggestive of obesity (n = 15). Dietary and clinical information was obtained by questionnaire and from clinical records. Total antioxidant capacity (TAC) and malondialdehyde (MDA) concentration were measured on maternal and cord serum by colorimetric techniques, and placental expression of glutathione peroxidase 4 (GPx4) was measured by immunohistochemistry. Results. Placental GPx4 expression was lower in the group with pBMI suggestive of obesity than in the normal weight group (ß = -0.08, p = 0.03, adjusted for gestational age and magnesium intake). Concentrations of TAC and MDA in maternal and cord blood were not statistically different between groups (p>0.05). Cord MDA concentration was related to maternal MDA concentration (ß = 0.40, p < 0.01), vitamin A intake (tertile 2: ß = -0.04, p = 0.40, tertile 3: ß = 0.13, p = 0.03, vs tertile 1), and placental GPx4 expression (ß = -0.09, p = 0.02). Conclusion. Prepregnancy obesity is associated with a decrease in GPx4 expression in the placenta, which is related to OS in the newborn. The influence of micronutrient intake on OS biomarkers highlights the importance of nutritional assessment during pregnancy and adequate prenatal care.

Objective: To evaluate the morphology of the placenta in patients with pregestational overweight (OW), pregestational obesity (PGOB), or normal weight. Methods: A cross-sectional study including women (n = 114) ≥20 years of age with a singleton pregnancy was carried out. The groups were integrated according to pregestational body mass index (BMI): 51 patients had a normal BMI (18.5–24.99 kg/m²), 30 were overweight (25–29.99 kg/m²), and 33 women were obese (≥30.0 kg/m²). A morphometric study of the placenta was performed and the placental maturity index (PMI) was calculated according to the formula: PMI = number of vasculo-syncytial membranes (VSM) in 1 mm²/VSM thickness. In the histopathological study, the presence of infarcts, calcifications, hemorrhage, thrombosis, fibrosis, cysts, and edema was determined. Results: The weight and length of newborns at birth were greater in the group with PGOB (p < .01). We observed a lower number of VSM (29 ± 9 versus 39 ± 13 and 34 ± 11) and a greater thickness (1.05 ± 0.24 versus 0.95 ± 0.08 and 0.89 ± 0.09) and, therefore, a lower PMI (29.75 ± 12.63 versus 40.88 ± 15.25 and 39.28 ± 14.4) in the group of women with PGOB compared with the group of women with OW or normal weight (p < .01). The histopathological analyses showed a greater frequency of edema and cysts in the PGOB group. Conclusion: PGOB is associated with a higher placental weight and newborn weight, a lower PMI, and the presence of histopathological alterations. The preceding points highlight the importance of promoting an appropriate pregestational weight in women of reproductive age.

Peroxisome proliferator-activated receptors (PPARs) play roles in glucose and lipid metabolism regulation. Pro12Ala PPAR-γ2 and +294T/C PPAR-δ have been associated with dyslipidemia, hyperglycemia and high body mass index (BMI). We compared metabolic traits and determined associations with Pro12Ala PPAR-γ2 or +294T/C PPAR-δ polymorphism among teenagers from different ethnicity. Four hundred and twelve samples with previous biochemical and biometric measurements were used. Genomic DNA from peripheral blood was extracted and analyzed by end-point PCR for Pro12Ala PPAR-γ2. The +294T/C PPAR-δ PCR product was also digested with Bsl I. Two genotype groups were formed: major allele homozygous and minor allele carriers. Pro12Ala PPAR-γ2 G minor allele frequencies were: 10% in Mestizo-1, 19% in Mestizo-2, 23% in Tarahumara, 12% in Mennonite, and 17% in the total studied population. The +294T/C PPAR-δ C minor allele frequencies were: 18% in Mestizo-1, 20% in Mestizo-2, 6% in Tarahumara, 13% in Mennonite, and 12% in the total studied population. Teenagers with PPAR-γ2 G allele showed a greater risk for either high waist/height ratio or low high-density lipoprotein; and, also had lower total cholesterol. Whereas, PPAR-γ2 G allele showed lower overweight/obesity phenotype (BMI Z-score) frequency, PPAR-δ C allele was a risk factor for it. Metabolic traits were associated with both PPAR polymorphisms.

Objectives: To compare maturity of placentas from women with hypertensive disorders with those from normotensive pregnancies and to determine the relationship between placental maturity (PM) and the diagnosis of small-for-gestational-age (SGA) in the newborns. Materials and methods: We examined placental stained specimens from women with normotensive pregnancies (n = 100), diagnosis of gestational hypertension (n = 38), mild (n = 10), or severe preeclampsia (n = 34) in an optical microscope. Placental Maturity Index (PMI) was calculated as the number of vasculo-syncytial membranes (VSM) in 1 mm² divided by VSM thickness (µm). Hypermaturity was defined as >90th percentile of the PMI from placentas of normotensive pregnancies. Newborns were classified as SGA, adequate-for-gestational-age (AGA) or large-for-gestational-age (90th percentile from weight for gestational age reference tables, respectively). Results: PMI in preeclamptic women (taking together mild and severe preeclampsia, PMI = 43.4 ± 1.6) was significantly higher than in normotensive women (PMI = 36 ± 2, p = 0.045). Hypermaturity was more frequent (p < 0.05) in placentas from women with preeclampsia than in those from normotensive women only in preterm pregnancies (<37 weeks), but not in those at term (p = 0.41). The frequency of hypermaturity in placentas from women with gestational hypertension was not statistically different than in normotensive women. Hypermaturity was also more frequent in placentas from SGA (OR = 2.63, p < 0.05) than in AGA newborns. Conclusion: The PMI was increased in preeclampsia, but not in gestational hypertension. Placental hypermaturity was also associated with the diagnosis of SGA in newborns. PM might have a role in the relationship between maternal factors and SGA.

Physical activity (PA) is a component of total energy expenditure. PA and PA energy expenditure (PAEE) can be estimated by objective techniques (OTs). However, the use of questionnaires is frequent in clinical settings and epidemiological studies. We conducted a search on PubMed, Scopus, and Google Scholar databases to perform a review of studies reporting the reliability and validity of PA questionnaires validated against OTs—doubly labeled water (DLW) or accelerometers—in free-living adults. We selected original articles published between 2009 and 2019 that reported validation studies of PA questionnaires. We identified 53 studies that fulfilled the eligibility criteria. Four PA questionnaires were validated against DLW and the remaining against accelerometers. Three questionnaires were compared with both DLW and accelerometer results. The correlation between questionnaire-estimated PAEE and DLW results ranged from r = .22 to r = .46, while that between questionnaire-estimated total PA (TPA) and accelerometer results ranged from r = .11 to r = .54 The intraclass correlation coefficients were between .56 and .84. Despite having good reliability, most of the questionnaires included in this review have shown limited validity for estimating TPA in adults. OTs should be considered as a first option, when possible. Further research is warranted on techniques to obtain more accurate PA and PAEE estimates.

Glucose and lipid metabolism regulation by the peroxisome proliferator-activated receptors (PPARs) has been extensively reported. However, the role of their polymorphisms remains unclear. Objective: To determine the relation between PPAR-γ2 rs1801282 (Pro12Ala) and PPAR-β/δ rs2016520 (+294T/C) polymorphisms and metabolic biomarkers in adults with type 2 diabetes (T2D). Materials and Methods: We included 314 patients with T2D. Information on anthropometric, fasting plasma glucose (FPG), HbA1c and lipid profile measurements was taken from clinical records. Genomic DNA was obtained from peripheral blood. End-point PCR was used for PPAR-γ2 rs1801282, while for PPAR-β/δ rs2016520 the PCR product was digested with Bsl-I enzyme. Data were compared with parametric or non-parametric tests. Multivariate models were used to adjust for covariates and interaction effects. Results: minor allele frequency was 12.42% for PPAR-γ2 rs1801282-G and 13.85% for PPAR-β/δ rs2016520-C. Both polymorphisms were related to waist circumference; they showed independent effects on HbA1c, while they interacted for FPG; carriers of both PPAR minor alleles had the highest values. Interactions between FPG and polymorphisms were identified in their relation to triglyceride level. Conclusions: PPAR-γ2 rs1801282 and PPAR-β/δ rs2016520 polymorphisms are associated with anthropometric, glucose, and lipid metabolism biomarkers in T2D patients. Further research is required on the molecular mechanisms involved.