The objective of this study was to evaluate the effect of cashew fiber wheter or not associated with low molecular weight compounds on lipid profile, abdominal adiposity, glycemia and insulinemia and serum concentration of ghrelin and leptin hormones from normal mice. We evaluated the cashew fiber in its integral form (IcF) and the cashew fiber after being submitted to the process of extraction of low molecular weight metabolites (cFSM). The two fibers were incorporated into the feed of male Swiss mice for 15 weeks. At the end of the treatment, blood glucose, total cholesterol and fractions, triglycerides, urea, AST, ALT, hormone levels of insulin, leptin and ghrelin were analyzed, as well as GSH and hepatic MDA. The consumption of cFSM diet promoted reduction of glycemia, insulin and ghrelin. Animals fed the IcF diet showed hyperlipidemia, hyperleptinemia and increased abdominal fat. In addition, no changes were observed in the lipid profile of the animals, in the abdominal adiposity and in the leptin hormone in the group that received cFSM diet. We conclude that the removal of small molecules is fundamental to use cashew fiber as a functional food with possible health benefits.
Nonalcoholic fatty liver disease (NAFLD), characterized by hepatosteatosis and steatohepatitis, is intrinsically related to obesity. Our previous study reported on the anti-obese activity of a,b-amyrin (AMY), a pentacyclic triterpene isolated from Protium heptaphyllum. This study investigated its ability to prevent fatty liver and the underlying mechanism using the mouse model of NAFLD. NAFLD was induced in male Swiss mice fed a high fat diet (HFD) for 15 weeks. The controls were fed a normal chow diet (ND). The mice were simultaneously treated with AMY at 10 and 20 mg/kg or fenofibrate at 50 mg/kg. Lipid levels along with metabolic and inflammatory parameters were assessed in liver and serum. The liver sections were histologically examined using H&E staining. RT-qPCR and western blotting assays were performed to analyze signaling mechanisms. Mice fed HFD developed severe hepatic steatosis with elevated triglycerides and lipid droplets compared with ND controls. This was associated with a decrease in AMP-activated protein kinase (AMPK) activity, an increase of mechanistic target of rapamycin complex 1 (mTORC1) signaling, and enhanced sterol regulatory element binding protein 1 (SREBP1) expression, which have roles in lipogenesis, inhibition of lipolysis, and inflammatory response. AMY treatment reversed these signaling activities and decreased the severity of hepatic steatosis and inflammatory response, evidenced by serum and liver parameters as well as histological findings. AMY-induced reduction in hepatic steatosis seemed to involve AMPK-mTORC1-SREBP1 signaling pathways, which supported its beneficial role in the prevention and treatment of NAFLD.
<p><strong>Objetivo:</strong> avaliar a Assistência Farmacêutica no município de Ibiapina-CE. <strong>Métodos: </strong>o estudo é retrospectivo, observacional, transversal e descritivo. A pesquisa foi desenvolvida em Unidades Básicas de Saúde do Sistema Único de Saúde, no Município de Ibiapina, situada no Estado do Ceará, baseando-se na aplicação de um questionário que considerou indicadores de estrutura, processo e resultado<em>. </em><strong>Resultados:</strong> a infraestrutura demostra alguns aspectos com grau crítico, contudo apresenta-se satisfatório quanto ao processo de armazenamento e estocagem. <strong>Conclusão: </strong>partindo de tal premissa, constata-se que a Assistência Farmacêutica na atenção primária em Ibiapina esbarra em dificuldades relacionadas à falta de apoio estrutural para o trabalho.</p>
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.