8 research outputs found
Hepcidin expression in colon during trinitrobenzene sulfonic acid-induced colitis in rats
Effects of Yerba maté, a Plant Extract Formulation (“YGD”) and Resveratrol in 3T3-L1 Adipogenesis
We aimed to evaluate the in vitro effects of yerba maté, YGD (a herbal preparation containing yerba maté, guarana and damiana), and resveratrol on adipogenesis. The anti-adipogenic effects of yerba mate, YGD, resveratrol and YGD + resveratrol and yerba mate + resveratrol combinations were evaluated in 3T3-L1 cells by Oil Red staining, cellular triglyceride content, and PCR quantitative array. The results demonstrated that all of the tested compounds inhibited adipogenesis. Yerba maté extract significantly down-regulated the expression of genes that play an important role in regulating adipogenesis, such as Adig, Axin, Cebpa, Fgf10, Lep, Lpl, and Pparγ2. In addition, these genes, YGD also repressed Bmp2, Ccnd1, Fasn, and Srebf1. Resveratrol also modulated the expression of Adig, Bmp2, Ccnd1, C/EBPα, Fasn, Fgf10, Lep, Lpl, and Pparγ2. Moreover, resveratrol repressed Cebpb, Cdk4, Fgf2, and Klf15. The yerba maté extract and YGD up-regulated the expression of genes involved in inhibiting adipogenesis, such as Dlk-1, Klf2, and Ucp1. Resveratrol also induced the expression of Klf2 and Ucp1. In addition resveratrol modulated the Ddit3, Foxo1, Sirt1, and Sirt2. The combined effects of these compounds on gene expression showed similar results observed from individual treatments. Our data indicates that the synergy between the compounds favors the inhibition of adipogenesis
Didox (3,4-dihydroxybenzohydroxamic acid) reduces the vascular inflammation induced by acute intravascular hemolysis
Sem informação81FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP2014/00984-
Caffeinated and decaffeinated instant coffee consumption partially reverses high-fat diet-induced metabolic alterations in mice
Epidemiological data has associated coffee consumption with a lower prevalence of type 2 diabetes, metabolic syndrome and chronic liver disease. However, the mechanisms and coffee substances responsible for these effects remain unclear. In the present study, mice received caffeinated or decaffeinated instant coffee ad libitum during a two week period after inducing obesity by introducing a high-fat diet over a 10 week period. Body weight, glucose homeostasis, and liver and visceral adipose tissue inflammation were assessed. In addition, AKT signaling, the fatty acid profile and liver histopathological analyses were performed. Ingestion of caffeinated or decaffeinated coffee for 2 weeks resulted in reductions in glucose and insulin blood levels, and insulin tolerance was improved without reductions in final body weight or adiposity. Only caffeinated coffee modified the adipokine profile in visceral adipose tissue, resulting in a restoration of adiponectin levels. However, deleterious liver alterations, which manifested as reductions in steatosis, inhibition of iNOS expression and restoration of insulin inducing-AKT phosphorylation, were reversed by the ingestion of both caffeinated and decaffeinated coffee. Serum AST and ALT levels were also improved in mice after coffee ingestion, while the fatty acid profile in the liver and the cytokine profiles in adipose and liver tissues were not altered by coffee ingestion. Thus, instant coffee consumption reverses obesity-induced alterations in mice, and our results corroborate those of epidemiological studies that associated coffee consumption with a lower prevalence of obesity-related pathologies6112012