Visfatin induces cholesterol accumulation in macrophages and accelerates the process of atherosclerosis mainly through modulating the expression of SR-A and CD36.”
“Omentin-1, a visceral fat
depot-specific secretory protein, is inversely correlated with obesity and insulin resistance. We investigated, in rats, the effects of chronic omentin-1 administration (8 mu g/kg, intraperitoneally, once daily for 14-days) on feeding behavior and related hypothalamic peptides and neurotransmitters. MCC950 nmr Food intake and body weight were recorded daily throughout the study. We found a significantly increased food intake compared to controls, but only in days 10-14, while body weight significantly increased since day 12 (P< 0.05). Compared with vehicle, omentin-1 treatment led to a significant reduction in both cocaine and amphetamine-regulated transcript (CART) (P< 0.05) and corticotrophin releasing hormone (CRH) (P< 0.05) gene expression, while pro-opiomelanocortin (POMC), agouti-related peptide (AgRP), neuropeptide Y (NPY) and orexin-A gene expression CH5183284 manufacturer were not modified with respect to vehicle-treated rats. We also found an increase in hypothalamic levodopa (L-dopa) (P< 0.05) and norepinephrine (NE) (P< 0.01) synthesis, without any effect on dopamine (DA) and serotonin (5-hydroxytryptamine, 5-HT)
metabolism. Furthermore, in hypothalamic synaptosomes, omentin-1 (10-100 ng/ml) stimulated basal NE release (ANOVA, P< 0.0001; post hoc, P< 0.001 vs.
vehicle), in a dose-dependent manner, leaving unaffected both basal and depolarization-induced DA and 5-HT release. Finally, when synaptosomes were co-perfused with leptin and omentin-1, we observed that leptin was able to reverse omentin-1-induced stimulation of NE. In conclusion, the orexigenic effects of omentin-1 could be related, at least in part, to decreased CART and CRH gene expression and increased NE synthesis and release in the hypothalamus. (C) 2013 Elsevier Inc. All rights reserved.”
“Adhesion of cancer cells to endothelium is considered an essential step in metastasis. However, we have shown in a previous study that when rat colon cancer cells are administered to the vena portae, they get stuck SNX-5422 purchase mechanically in liver sinusoids. Then, endothelial cells retract rapidly and cancer cells bind to hepatocytes. We investigated the molecular nature of these interactions between colon cancer cells and hepatocytes. Cancer cells in coculture with hepatocytes became rapidly activated with distinct morphological changes. Cancer cells formed long cytoplasmic protrusions towards hepatocytes in their close vicinity and these protrusions attached to microvilli of hepatocytes. Then, adhering membrane areas were formed by both cell types. Integrin subunits alpha v, alpha 6 and beta 1 but not alpha L, beta 2, beta 3 and CD44 and CD44v6 were expressed on the cancer cells.