Brown algae and its carotenoids have been shown to have a positive influence on obesity and its comorbidities. This study evaluated the effect of Undaria pinnatifida and fucoxanthin on biochemical, physiological and inflammation markers related to obesity and on the expression of genes engaged on white adipose tissue lipid metabolism in a murine model of diet-induced obesity. The treatments improved energy expenditure, β-oxidation and adipogenesis by upregulating PPARα, PGC1α, PPARγ and UCP-1. Adipogenesis was also confirmed by image analysis of the retroperitoneal adipose tissue, by measuring cell area, perimeter and cellular density. Additionally, the treatments, ameliorated adipose tissue accumulation, insulin resistance, blood pressure, cholesterol and triglycerides concentration in serum, and reduced lipogenesis and inflammation by downregulating acetyl-CoA carboxylase (ACC) gene expression, increasing serum concentration and expression of adiponectin as well as downregulating IL-6 expression. Both fucoxanthin and Undaria pinnatifida may be considered for treating obesity and other diseases related.

Background: Legg–Calvé–Perthes Disease (LCPD) is a necrosis of the femoral head which affects the range of motion of the hips. Its incidence is variable, ranging from 0.4/100,000 to 29.0/ 100,000 children. Although LCPD was first described in the beginning of the past century, limited is known about its etiology. Our objective is to describe the main areas of interest in Legg–Calve–Perthes disease. Methods: A review of the literature regarding LCPD etiology was performed, considering the following inclusion criteria: Studies reporting clinical or preclinical results. The research group carried out a filtered search on the PubMed and Science Direct databases. To maximize the suitability of the search results, we combined the terms ‘‘Perthes disease” OR “LCPD” OR “children avascular femoral head necrosis” with “diagnostic” OR “treatment” OR “etiology” as either key words or MeSH terms. Results: In this article been described some areas of interest in LCPD, we include topics such as: history, incidence, pathogenesis, diagnosis, treatment and possible etiology, since LCPD has an unknown etiology. Conclusions: This review suggests that LCPD has a multifactorial etiology where environmental, metabolic and genetic agents could be involved.

Hepcidin regulates iron metabolism. Its synthesis increases in infection and decreases in iron deficiency. The aim of this study was to evaluate the relationship between H. pylori infection and iron deficiency by levels of hepcidin in children. A total of 350 school-age children participated in this cross-sectional study. Determinations of serum ferritin, hemoglobin, hepcidin, C-reactive protein, and α-1-acid-glycoprotein were done. Active H. pylori infection was performed with a ¹³C-urea breath test. In schoolchildren without H. pylori infection, hepcidin was lower in those with iron deficiency compared to children with normal iron status (5.5 ng/mL vs. 8.2 ng/mL, p = 0.017); while in schoolchildren with H. pylori infection the levels of hepcidin tended to be higher, regardless of the iron nutritional status. Using multivariate analysis, the association between H. pylori infection and iron deficiency was different by hepcidin levels. The association between H. pylori and iron deficiency was not significant for lower values of hepcidin (Odds Ratio = 0.17; 95% Confidence Interval [CI] 0.02–1.44), while the same association was significant for higher values of hepcidin (OR = 2.84; CI 95% 1.32–6.09). This joint effect is reflected in the adjusted probabilities for iron deficiency: Individuals with H. pylori infection and higher levels of hepcidin had a probability of 0.24 (CI 95% 0.14–0.34) for iron deficiency, and this probability was 0.24 (CI 95% 0.14–0.33) in children without H. pylori infection and lower levels of hepcidin. In children with H. pylori infection and iron deficiency, the hepcidin synthesis is upregulated. The stimulus to the synthesis of hepcidin due to H. pylori infection is greater than the iron deficiency stimulus.

Background. Little is known about the effects of cocoa and its main flavanols on the prothrombotic state associated with the development of hypertension in diet-induced obesity models. Purpose. To evaluate the effects of cocoa powder, cocoa extract and their main flavanols on plasma biomarkers related to impaired coagulation and fibrinolysis and its association with hypertension and obesity-related metabolic disorders in rats fed a hypercaloric diet. Methods. Male Wistar rats were randomly assigned to 7 treatment groups (n = 7): normal diet (ND); hypercaloric diet control group (HCD); HCD + cocoa powder (CO); HCD + cocoa extract (CO-EX); HCD + (−)-epicatechin (EPI); HCD + (+)-catechin (CAT); and HCD + procyanidin B2 (PB2). Blood pressure was measured using the tail-cuff method (week 7). At the end of the experimental period (week 8), rats were sacrificed and blood samples were collected immediately for coagulation and biochemical analyses. Results. Oral administration of CO, CO-EX and their main flavanols significantly decreased plasma biomarkers related to impaired coagulation and fibrinolysis (vWF, FVIII, fibrinogen and PAI-1) in rats fed a hypercaloric diet. These effects were associated with decreased systolic and diastolic blood pressure, aortic oxidative stress (MDA levels) and improvement of dyslipidemia, insulin resistance and circulating markers of inflammation (TNF-α, IL-6 and CRP) compared to the HCD group. Conclusion. Our results showed that cocoa and its main flavanols may improve endothelial dysfunction and exert their antihypertensive effects by decreasing the prothrombotic state in rats fed a hypercaloric diet. Moreover, improvement of obesity-related metabolic disorders may also contribute to their BP-lowering effect.