Entity

Time filter

Source Type


Enriquez J.,National Institute of Medical science and Nutrition Salvador Zubiran | Larrea F.,National Institute of Medical science and Nutrition Salvador Zubiran | Santillan R.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Hernandez A.,Metropolitan Autonomous University | And 5 more authors.
Hormone Molecular Biology and Clinical Investigation | Year: 2013

Testosterone (T) restores bone mass loss in postmenopausal women and osteoporotic men mainly through its bioconversion to estradiol (E2 ). In target tissues, T is also biotransformed to the A-ring-reduced metabolites 3α,5α -androstanediol (3α,5α -diol) and 3β ,5α -androstanediol (3β ,5α -diol), which are potent estrogen receptor (ER) agonists; however, their biological role in bone has not been completely elucidated. To assess if osteoblasts bioconvert T to 3α,5α -diol and to 3β ,5α -diol, we studied in cultured neonatal rat osteoblasts the metabolism of [14C]-labeled T. In addition, the intrinsic estrogenic potency of diols on cell proliferation and differentiation in neonatal calvarial rat osteoblasts was also investigated. Osteoblast function was assessed by determining cell DNA, cell-associated osteocalcin, and calcium content, as well as alkaline phosphatase activity and Alp1 gene expression. The results demonstrated that diols were the major bioconversion products of T, with dihydrotestosterone being an obligatory intermediary, thus demonstrating in the rat osteoblasts the activities of 5α -steroid reductase and 3α - and 3β -hydroxysteroid dehydrogenases. The most important finding was that 3β ,5α - and 3α,5α -diols induced osteoblast proliferation and differentiation, mimicking the effect of E2. The observation that osteoblast differentiation induced by diols was abolished by the presence of the antiestrogen ICI 182,780, but not by the antiandrogen 2-hydroxyflutamide, suggests that diols effects are mediated through an ER mechanism. The osteoblast capability to bioconvert T into diols with intrinsic estrogen-like potency offers new insights to understand the mechanism of action of T on bone cells and provides new avenues for hormone replacement therapy to maintain bone mass density. Source


Lopez-Alarcon M.,Mexican Institute of Social Security | Perichart-Perera O.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Flores-Huerta S.,Infantile Hospital of Mexico Federico Gomez | Inda-Icaza P.,Anahuac University of North Mexico | And 4 more authors.
Mediators of Inflammation | Year: 2014

Background. Low-grade inflammation is the link between obesity and insulin resistance. Because physiologic insulin resistance occurs at puberty, obese pubertal children are at higher risk for insulin resistance. Excessive diets in refined carbohydrates and saturated fats are risk factors for insulin resistance, but calcium, magnesium, vitamin-D, and the omega-3 fatty acids likely protect against inflammation and insulin resistance. Objective. To analyze interactions among dietary saturated fat, refined carbohydrates, calcium, magnesium, vitamin D, and omega-3 fatty acids on the risk of inflammation and insulin resistance in a sample of prepubertal and pubertal children. Methods. A sample of 229 children from Mexico City was analyzed in a cross-sectional design. Anthropometric measurements, 24 h recall questionnaires, and blood samples were obtained. Serum insulin, glucose, calcium, magnesium, 25-OHD3, C-reactive protein, leptin, adiponectin, and erythrocytes fatty acids were measured. Parametric and nonparametric statistics were used for analysis. Results. While mean macronutrients intake was excessive, micronutrients intake was deficient (P<0.01). Inflammation determinants were central obesity and magnesium-deficient diets. Determinants of insulin resistance were carbohydrates intake and circulating magnesium and adiponectin. Conclusions. Magnesium-deficient diets are determinants of inflammation, while high intake of refined carbohydrates is a risk factor for insulin resistance, independently of central adiposity. © 2014 Mardia López-Alarcón et al. Source


Osorio-Caballero M.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Perdigon-Palacio C.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Garcia-Lopez G.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Flores-Herrera O.,National Autonomous University of Mexico | And 8 more authors.
Placenta | Year: 2015

Introduction Escherichia coli is recognized as an etiological bacteria associated with chorioamnionitis and the preterm premature rupture of fetal membranes. This pathological condition induces pro-inflammatory cytokines and degradative metalloproteinases, which are considered biological markers secreted in an acute stage of infection. Heat-shock proteins (HSPs) are an important component of the innate immunity response and are found in different pathological conditions. They have not been previously measured in human fetal membranes in response to infectious conditions. We hypothesized that the choriodecidual tissue and amniotic epithelium secreted temporal and differential Hsp-60, Hsp-70, and interleukin (IL)-1β mediated by E. coli infection. Methods Fetal membranes were mounted in a two-compartment culture system and infected with two passes of live E. coli at different doses (102, 104, 105, and 106 colony-forming units (CFU)/mL) and intervals of incubation (3, 6, and 24 h). The culture medium was collected, and Hsp-60, Hsp-70, and IL-1β were assessed using the enzyme-linked immunosorbent assay (ELISA) method. Results After 3 and 6 h of infection, E. coli induced an increase in Hsp-70 secretion in the choriodecidual tissue. However, after 24 h of incubation, Hsp-70 was downregulated and we observed an increase in IL-1β secretion. By contrast, E. coli induced a lower Hsp-60 secretion in the amnion compared to Hsp-70. Discussion Human fetal membranes responded actively to E. coli infection, with an increase in Hsp-70 during the first hours of infection. After 24 h, there was an increase in the liberation of IL-1β. © 2014 Elsevier Ltd. All rights reserved. Source


Flores-Herrera H.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Garcia-Lopez G.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Diaz N.F.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | Molina-Hernandez A.,National Institute Of Perinatology Isidro Espinosa Of Los Reyes | And 3 more authors.
Placenta | Year: 2012

Overall, 1-4% of all births in the US are complicated by choriamnionitis. Choriamnionitis is a polymicrobial infection most often due to ascending genital microbes which, in over 65% of positive amniotic fluid cultures, involves two or more organisms. In this study, we determine the cytokines expression (IL-1β, TNFα) and prometalloproteinase activation (proMMP-2 and proMMP-9) after double o single infection an in vitro model of human fetal membranes. Fetal membranes at term were mounted in the Transwell culture system and after 24 h of infection, choriodecidual, and amnion media was collected. IL-1β and TNFα were evaluated by ELISA, whereas proMMP-9 and proMMP-2 were determined by substrate gel zymography. The choriodecidual and amnion compartments actively respond to the infectious process, which induced the secretion of IL-1β, TNFα, and proMMP-9 after either mixed or single infection. The proMMP-2 secretion profile was the same after all experimental conditions. There was no synergy between Streptococcus agalactiae and Escherichia coli for inducing the secretion of inflammatory factors or degradative metalloproteinase. In conclusion, these two bacteria could initiate different pathways to induce chorioamnioitis. © 2012 Elsevier Ltd. All rights reserved. Source

Discover hidden collaborations