90 resultados para chronic alcohol intake
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Chronic alcohol intake decreases adiponectin and sirtuin 1 (SIRT1) expressions, both of which have been implicated in various biological processes including inflammation, apoptosis and metabolism. We have previously shown that moderate consumption of alcohol aggravates liver inflammation and apoptosis in rats with pre-existing nonalcoholic steatohepatitis (NASH). This study investigated whether moderate alcohol intake alters SIRT1 activity, adiponectin/Adiponectin receptor (AdipoR)-related signaling and lipid metabolism in a pre-existing NASH status. Sprague-Dawley rats were fed with a high-fat diet (71% energy from fat) for 6 weeks to induce NASH then subsequently divided into 2 sub-groups: fed either a modified high-fat diet (HFD, 55% energy from fat) or a modified high-fat alcoholic diet (HFA, 55% energy from fat and 16% energy from ethanol) for an additional 4 weeks. We observed in comparison to HFD group, HFA increased hepatic nuclear SIRT1 protein but decreased its deacetylase activity. SREBP-1c protein expression and FAS mRNA levels were significantly upregulated, while DGAT1/2 and CPT-I mRNA levels were downregulated in the livers of HFA compared to HFD. Although hepatic AdipoR1 decreased, HFA did not alter AdipoR2 and their downstream signaling. There were no significant changes in plasma adiponectin and free fatty acids (FFA), as well as adiponectin expression in adipose tissue between the two groups. The present study indicates that suppression in SIRT1 deacetylase activity contributes to alcohol-exacerbated hepatic inflammation and apoptosis in rats with pre-existing NASH. In addition, moderate alcohol intake did not modulate adiponectin/AdipoR signaling axis in this model.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Aquaporins (AQPs), notably AQP-1 and AQP-9, may contribute to reabsorption of fluid and solute across the epididymis. Ethanol is related to be a toxicant affecting directly or indirectly the epididymis and the sperm motility. This study examined the expression of AQP-1 and AQP-9 in adult epididymis of the UChA and UChB 10% (v/v) ethanol-preferring rats, focusing the ethanol-induced hormonal disturbances upon the regulation of these AQPs. Chronic ethanol intake significantly decreased body weight, while UChA and UChB rats displayed a marked loss of epididymal weights. Both ethanol-consuming animals had a severe reduction of testosterone levels, whereas LH and 17β-estradiol were unchanged. Throughout the epididymis, a strong reaction to AQP-1 was observed in myoid and endothelial cells of the UChB ethanol-preferring rats, differently from a moderate intensity in the initial segment of the UChA rats. In addition, AQP-9 showed a strong immunoreaction in the apical membrane of principal cells at initial segment. In cauda epididymis, the level of AQP-9 was reduced along the microvillus projections in both UChA and UChB rats compared to controls. We conclude that chronic ethanol consumption modulates the androgen levels, thereby modifying the expression pattern of AQP-1 and 9 in the epididymis. © 2011 Elsevier Ltd.
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Chronic ethanol intake is associated with sex hormone disturbances, and it is well known that melatonin plays a key role in regulating several reproductive processes. We report the effects of ethanol intake and melatonin treatment (at doses of 100. μg/100. g. BW/day) on sex hormones and steroid receptors in the ovaries, oviducts and uteri of ethanol-preferring rats. After 150 days of treatment, animals were euthanized, and tissue samples were harvested to evaluate androgen, estrogen, progesterone and melatonin receptor subunits (AR, ER-α and ER-β, PRA, PRB and MT1R, respectively). Melatonin decreased estradiol (E2) and increased progesterone (P4) and 6-sulfatoxymelatonin (6-STM), while an ethanol-melatonin combination reduced both P4 and E2. Ovarian AR was not influenced by either treatment, and oviduct AR was reduced after ethanol-melatonin combination. Oviduct ER-α, ER-β and uterine ER-β were down-regulated by either ethanol or melatonin. Conversely, ovarian PRA and PRB were positively regulated by ethanol and ethanol-melatonin combination, whereas PRA was down-regulated in the uterus and oviduct after ethanol consumption. MT1R was increased in ovaries and uteri of melatonin-treated rats. Ethanol and melatonin exert opposite effects on E2 and P4, and they differentially regulate the expression of sex steroid receptors in female reproductive tissues. © 2013 Elsevier Inc.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Progression of chronic hepatitis C is known to be associated with some factors, but influence of HCV genotypes is still controversial. Association between HCV genotypes and other risk factors was examined to determine which factors are associated with progression of infection. One hundred consecutive anti-HCV positive volunteer blood donors were evaluated for several risk factors, examined for HCV genotypes, and submitted to hepatic biopsy and biochemical exams.HCV genotyping were carried out in 89 patients and hepatic biopsy in 78. Transmission routes were found to be illicit intravenous drug use (26%), Gluconergan® use in a non-safe manner (48%) and blood transfusion (15%). HCV genotype was 1 in 45%, 3 in 40%, and it was not associated with the stage of fibrosis or with inflammatory activity. There was no significant association of factors related to infection, chronic alcohol use, or duration of illness, with progression of the lesion. There was a significant association of aminotransferase levels and the fibrosis stage. Univariate analysis showed that the age at contamination, patient's age, GT-gamma, and aminotransferase levels over three times the upper normal limits, were associated with fibrosis stages 2 to 4. Multivariate analysis detected age (odds ratio=1.19), and GT-gamma (odds ratio=2.02) as independent factors.
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The effects of chronic alcohol ingestion on the secretory epithelium of the seminal vesicle were studied in rats (Rattus norvegicus). Male adult albino Wistar rats were divided into two groups: alcoholic and control. Tips of the seminal vesicle were removed and prepared for light and electron microscopy. Ultrastructural observations on the epithelial cells of the seminal vesicle showed reduced epithelial cell size, decreased apical secretory vacuoles, irregularly shaped nuclei with deep infoldings, increased lipid droplets and dense bodies, a small number of microvilli covering the cell surface, and signs of degeneration. In addition to the hormonal effects, alcohol may act on the secretory epithelium of the seminal vesicle.
Morphological alterations on the prostate of Calomys callosus submitted to chronic ethanol ingestion
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The objective of the present study was to assess the possible toxic effects of chronic alcohol ingestion on the ultrastructure of the glandular epithelium of the prostate of the rodent Calomys callosus, in order to contribute to the understanding of the consequences of alcohol abuse for the morphology of the male reproductive apparatus. Sixteen adult animals aged three months were divided into two experimental groups. The control group received a solid diet and tap water, and the alcoholic group received the same solid diet and ethanol P.A. diluted 20% in water (v/v). After 120 days of treatment, all animals were anesthetized, weighed and sacrificed. At the end of treatment, mean body weight did not differ between control and alcoholic animals. The prostate epithelial cells of the alcoholic group showed intense atrophy and ultrastructural alterations such as the presence of lipid droplets, altered nuclei, ruptured mitochondrial cristae, and intense dilatation of the cisterns of the granular endoplasmic reticulum. It was concluded that 20% ethanol provokes marked lesions on the epithelium of the prostate probably interfering on the glandular secretion.
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BACKGROUND AND OBJECTIVES: Gross motor (GM) deficits are often reported in children with prenatal alcohol exposure (PAE), but their prevalence and the domains affected are not clear. The objective of this review was to characterize GM impairment in children with a diagnosis of fetal alcohol spectrum disorder (FASD) or moderate to heavy maternal alcohol intake.METHODS: A systematic review with meta-analysis was conducted. Medline, Embase, Allied and Complementary Medicine Database, Cumulative Index to Nursing and Allied Health Literature, PsycINFO, PEDro, and Google Scholar databases were searched. Published observational studies including children aged 0 to <= 18 years with (1) an FASD diagnosis or moderate to heavy PAE, or a mother with confirmed alcohol dependency or binge drinking during pregnancy, and (2) GM outcomes obtained by using a standardized assessment tool. Data were extracted regarding participants, exposure, diagnosis, and outcomes by using a standardized protocol. Methodological quality was evaluated by using Strengthening the Reporting of Observational Studies in Epidemiology guidelines.RESULTS: The search recovered 2881 articles of which 14 met the systematic review inclusion criteria. The subjects' mean age ranged from 3 days to 13 years. Study limitations included failure to report cutoffs for impairment, nonstandardized reporting of PAE, and small sample sizes. The meta-analysis pooled results (n = 10) revealed a significant association between a diagnosis of FASD or moderate to heavy PAE and GM impairment (odds ratio: 2.9; 95% confidence interval: 2.1-4.0). GM deficits were found in balance, coordination, and ball skills. There was insufficient data to determine prevalence.CONCLUSIONS: The significant results suggest evaluation of GM proficiency should be a standard component of multidisciplinary FASD diagnostic services.