Macronutrient intake is correlated with dyslipidemia and low-grade inflammation in childhood obesity but mostly in male obese

Condition of hypoxia caused by hypertrophy of adipose cells in obesity triggers macrophages recruitment and production of cytokines. Additionally, high consumption of saturated fatty acids (SFA) and high glycemic index meals may contribute to oxidative stress and chronic low-grade inflammation by increases NF-kB activation. Thus, the aim of the study was to analyze the contribution of the macronutrients intake in the metabolic and inflammatory profile, by levels of lipoproteins, insulin resistance, anti and pro inflammatory cytokines, in obese adolescents according the gender. sample was composed by 37 adolescents, both genders, identified as obese by body mass index (BMI). Body composition was assessed by Dual-energy X-ray absorptiometry (DEXA) and measures of intra-abdominal adiposity (IAAT) and subcutaneous adiposity tissue (SAT) were done by ultrasound. Biochemical analyses were done and the measurement of cytokines; fatty acids and insulin were performed by the technique of immunoassay ELISA. The estimation of macronutrients consumption was made by 3 day food register regarding food intake. Statistical significance was set at p-value < 5% and the statistical software SPSS version 17.0 (SPSS Inc, Chicago, IL) performed all analyses. BMI (p = 0.316), FM (p = 0.416), IAAT (p = 0.505) and SAT (p = 0.935) presented similarities between genders. Cytokines and metabolic variables values were similar between the groups. Only in the male group, metabolic variables and cytokines were significant correlated with the consumption of total lipids or its fractions. Was observed that insulin concentration had significant interaction with MUFA(g) (= -18.4; p = 0.004) and adiponectin with CHO(g) (= -58.2; p = 0.032) in the group male and female, respectively. macronutrients intake is associated with low-grade inflammation in obesity, by production of inflammatory cytokines and alteration of the lipid profile, especially male obese adolescents which seem to be more responsive of this consumption when compared with female obese adolescents.

Hypothalamic energy metabolism is impaired by doxorubicin independently of inflammation in non-tumour-bearing rats

We sought to explore the effects of doxorubicin on inflammatory profiles and energy metabolism in the hypothalamus of rats. To investigate these effects, we formed two groups: a control (C) group and a Doxorubicin (DOXO) group. Sixteen rats were randomly assigned to either the control (C) or DOXO groups. The hypothalamus was collected. The levels of interleukin (IL)-1β, IL-6, IL-10, TNF-α and energy metabolism (malate dehydrogenase, complex I and III activities) were analysed in the hypothalamus. The DOXO group exhibited a decreased body weight (p < 0.01). Hypothalamic malate dehydrogenase activity was reduced when compared with control (p < 0.05). In addition, pro-inflammatory cytokine levels were unchanged. Therefore, our results demonstrate that doxorubicin leads to an impairment of \hypothalamic energy metabolism, but do not affect the inflammatory pathway. Copyright © 2015 John Wiley & Sons, Ltd. Conflict of Interest Significance paragraph The hypothalamus is a central organ that regulates a great number of functions, such as food intake, temperature and energy expenditure, among others. Doxorubicin can lead to deep anorexia and metabolic chaos; thus, we observed the effect of this chemotherapeutic drug on the inflammation and metabolism in rats after the administration of doxorubicin in order to understand the central effect in the hypothalamus. Drug treatment by doxorubicin is used as a cancer therapy; however the use of this drug may cause harmful alterations to the metabolism. Thus, further investigations are needed on the impact of drug therapy over the long term.

Gestational and lactational exposition to Di-N-butyl-phthalate (DBP) increases inflammation and preneoplastic lesions in prostate of wistar rats after carcinogenic N-methyl-N-nitrosourea (MNU) plus testosterone protocol

In the present study, it was evaluated the susceptibility of prostatic lesions in male adult rats exposed to Di-N-butyl-phthalate during fetal and lactational periods and submitted to MNU plus testosterone carcinogenesis protocol. Pregnant females were distributed into four experimental groups: CN (negative control); CMNU (MNU control); TDBP100 (100 mg/kg of DBP); TDBP500 (500 mg/kg of DBP). Females from the TDBP groups received DBP, by gavage, from gestation day 15 (GD15) to postnatal day 21 (DPN21), while C animals received the vehicle (corn oil). CMNU, TDBP100, and TDBP500 groups received a single intraperitoneal injection of MNU (50 mg/kg) on the sixth postnatal week. After that, testosterone cypionate was administered subcutaneously two times a week (2 mg/kg) for 24 weeks. The animals were euthanized on PND220. Distal segment fragments of the ventral (VP) and dorsolateral prostate (DLP) were fixed and processed for histopathological analysis. Protein extracts from ventral prostate were obtained, and western blotting was performed to AR, ERα, MAPK (ERK1/2), and pan-AKT. Stereological analysis showed an increase in the epithelial compartment in TDBP100 and TDBP500 compared to CN. In general, there was increase in the incidence of inflammation and metaplasia/dysplasia in the DBP-treated groups, mainly in DLP, compared to CN and CMNU. Proliferation index was significant higher in TDBP500 and PIN (prostatic intraepithelial neoplasia) was more frequent in this group compared to CMNU. Western blot assays showed an increase in the expressions of AR and MAPK (ERK1/2) in the TDBP100 compared to CN, and ERα and AKT expressions were higher in the TDBP500 group compared do CN. These results showed that different doses of DBP during prostate organogenesis in Wistar rats could increase the incidence of premalignant lesions in initiated rats inducing distinct biological responses in the adulthood. © 2015 Wiley Periodicals, Inc. Environ Toxicol, 2015.

Experimental evidence of heparanase, Hsp70 and NF-κB gene expression on the response of anti-inflammatory drugs in TNBS-induced colonic inflammation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)