Objective: Increased C3 has been related to body mass index (BMI) and insulin resistance, although there are not sufficient studies in subjects with morbid obesity. The purpose of this study was to evaluate the levels of C3 as a function of the BMI in subjects of both sexes, with severe, morbid and extreme obesity, and their possible relationship to insulin resistance or associated diseases such as diabetes, hypertension and dyslipidemia. Subjects: The study included a total of 316 patients (110 men and 206 women) with severe obesity (17.1%), morbid obesity (54.4%) and extreme obesity (28.4%), with an average BMI of 46.7077.37 kg/m 2 . Measurements: The glucose and insulin levels were determined baseline, and 2 h after a 75 g of oral glucose load. The homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated. A lipid profile (total cholesterol, triglycerides, high-density lipoprotein cholesterol, apolipoprotein AI and apolipoprotein B100) was obtained and C3 levels determined by nephelometry. Results: When distributing the patients by quartiles of BMI, we found a progressive increase in the levels of C3, and no significant differences in the rest of analytical variables studied were found; the mean values of C3 were 127.78729.7 mg/dl. A significant correlation was found between C3 and the BMI (r ¼ 0.263, Po0.001), baseline insulin (r ¼ 0.237, P ¼ 0.001) and HOMA-IR (r ¼ 0.237, P ¼ 0.001). High blood pressure was found in 111 patients, type 2 diabetes in 74 patients and dyslipidemia in 139 cases. When distributing the levels of C3 according to the number of associated risk factors (hypertension, diabetes and dyslipidemia), we found significant differences between these patients and those who presented no associated diseases (Po0.01). Conclusion: A relationship between C3 and the progressive increase of BMI in subjects with severe, morbid or extreme obesity was established. This increase in C3 was closely related to insulin levels and the values for HOMA-IR. Furthermore, we also found an increase in C3 as more diseases related to insulin resistance, such as diabetes, hypertension and dyslipidemia, were associated with the obesity.

Objective: To study how temperature, serum, and gonadotropin supplementation affect the organotypic culture of human immature testicular tissue (ITT) in vitro. Design: Experimental basic science study. Setting: Reproductive biology laboratory. Patient(s): ITT from 4 boys with cancer that had testicular tissue cryopreserved as part of their fertility preservation treatment. Intervention(s): In vitro organotypic culture of ITT, exposed to different temperatures (37 C vs. 34 C), serum (fetal bovine serum [FBS] vs. Knockout Serum Replacement [KOS]), and gonadotropin supplementation (with and without FSH and LH). Main Outcome Measure(s): Characterization of the tissue was performed at days 0, 14, and 70 with the use of reverse-transcription quantitative polymerase chain reaction, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling, histologic analysis by means of hematoxylin-eosin staining, and immunohistochemical staining. Hormonal secretion was determined at days 3, 14, 28, and 70 by means of immunofluorescent assay. Result(s): The 37 C conditions showed an accelerated loss of tubular morphology and higher intratubular apoptosis. KOS supplementation triggered the up-regulation of STAR, SOX9, DAZL, DDX4, PLZF, and UTF1, the percentage of SOX9þ/androgen receptor (AR)-positive mature Sertoli cells at day 14, and testosterone secretion. Gonadotropin supplementation increased the numbers of both undifferentiated UTF1þ spermatogonia and premeiotic VASAþ/SYCP3þ spermatogonia at day 14, and the number of SOX9þ Sertoli cells at day 70. The low SOX9þ/ARþ colocalization, the disorganized pattern of ZO-1, and the progressive decrease of antim€ ullerian hormone secretion indicated inefficient Sertoli cell maturation in vitro. Conclusion(s):The 34 C condition in KOS showed the best results for the survival of both spermatogonia and Sertoli cells. FSH/LH supplementation also improved long-term survival of Sertoli cells and the maturation of spermatogonia up to meiotic initiation in short-term culture. (Fertil Steril Ò 2018;110:1045-57. Ó2018 by American Society for Reproductive Medicine.) El resumen está disponible en Español al final del artículo.

We conclude that, in subjects with a mean age of 44 years, metabolic syndrome increases VTE risk, although abdominal obesity is the pivotal factor.

OBJECTIVE:To analyse the relation between overweight, obesity and fat distribution with I/D polymorphism of the angiotensinconverting enzyme (ACE) gene and its association with coronary heart disease (CHD). DESIGN: Cross-sectional, case-control study. SUBJECTS: A total of 185 cases (141 males) who had suffered at least one episode of CHD and 182 controls (127 males). MEASUREMENTS: Body mass index, waist circumference, blood pressure, plasma total cholesterol, triglycerides, HDL cholestrol and fasting glucose were measured with standard methods, genotyping the I/D polymorphism of ACE gene. RESULTS: Obesity and abdominal fat deposit are associated with CHD in women, but not independently. We have found an association between obesity and abdominal fat deposit with the ACE gene I/D polymorphism in subjects with CHD. Subjects with CHD and DD or ID genotypes have significantly higher prevalence of obesity and abdominal fat deposit and higher values of weight and waist circumference. In addition, the DD and ID genotypes increased crude OR of obesity. The DD and ID genotypes of the ACE gene I/D polymorphism and BMI are independently associated with CHD. CONCLUSION: There is a relation between the type and grade of obesity with the genotypes of the ACE gene I/D polymorphism in subjects with CHD.

Phytosterols (PS) are recommended to reduce LDL-cholesterol. However, the influence of cholesterol and fat intake on the lipid-lowering effect of PS in mildly hypercholesterolaemia is unclear. Thus, the aim of the present study was to evaluate whether the efficacy of PS is related to the composition of saturated fat and dietary cholesterol intake. Additionally, serum carotenoid content was analysed to evaluate to what extent it was undermined by PS. This was a 3-month randomised, parallel trial with a three-arm design. Patients were divided into three groups: healthy diet (n 24), healthy diet þ PS (n 31) and free diet þ PS (n 29), receiving 2 g/d of PS. Healthy and free diets were characterised by a daily ingestion of 6·8 % of saturated fat and 194·4 mg of cholesterol and 12·7 % of saturated fat and 268·1 mg of cholesterol, respectively. After PS therapy, patients receiving the healthy diet þ PS or a free diet þ PS exhibited a similar reduction in total cholesterol (6·7 and 5·5 %), LDL-cholesterol (9·6 and 7·0 %), non-HDL-cholesterol (12·2 and 8·9 %) and apo B-100/apo A-I ratio (11·5 and 11·6 %), respectively. In patients following the healthy diet, (b-carotene concentration rose by 26·9 %, whereas the b-carotene and lycopene levels dropped by 21·0 and 22·8 % in the group receiving the free diet þ PS, respectively. No change was observed in carotenoid levels in healthy diet þ PS group. In conclusion, the efficacy of PS in relation to lipoprotein profile is not influenced by saturated fat or dietary cholesterol intake, which confirms the positive effect of healthy diet therapy in improving the negative effects that PS exert on carotenoid levels.