High-fat diet (HFD) often causes obesity and it has detrimental effects on the sensory system. In particular, sensory-mediated responses are crucial for maintaining energy balance, as they are involved in a metabolic regulation; however, there is still no clear explanation about the relationship between HFD-induced stress and sensory system. To gain insight on how HFD-induced stress affects olfactory sensitivity and behavioral responses, we have used a Drosophila melanogaster model for olfactory and nutrient-related signaling and accessed physiological, behavioral, and transcriptional changes. We demonstrated that lifespan and climbing ability in HFD-treated flies decreased and that olfactory sensitivity and behavioral responses to odorants were changed. Olfactory sensitivity to eight of ten odorants after 14 days on HFD treatment were reduced, while behavioral attraction was increased to benzaldehyde in flies that were treated with HFD. This behavioral and physiological modification in HFD-treated flies for 14 days was accompanied by a significant decrease in DmOrco gene expression in a peripheral olfactory organ, suggesting that is could be involved in the action of metabolic and sensory signal. Gene expression profiles of antennae showed significant differences on the olfactory receptors, odorant-binding proteins, and insulin signaling. Our results suggested that olfactory sensitivity and behavioral responses to HFD-induced stress are mediated through olfactory and nutrient-related signaling pathways.

The present study aimed to determine whether circulating serum concentrations of 25-hydroxyvitamin D [25-(OH) D] differed between healthy dogs and dogs with acute pancreatitis (AP). Twenty-two healthy dogs and twenty client-owned dogs with AP were enrolled in the study. Serum concentrations of 25-(OH) D, blood ionized calcium (iCa), and serum C-reactive protein (CRP) were measured. Concentrations of serum 25-(OH) D and blood iCa in dogs with AP were significantly lower than those of healthy dogs, and serum concentrations of CRP in dogs with AP were significantly higher than those of healthy dogs. A significant difference in 25-(OH) D serum concentrations was observed between survivor and non-survivor dogs with AP. After resolution of clinical signs, concentrations of serum 25-(OH) D, blood iCa, and serum CRP did not differ compared to those before treatment. This study shows that dogs with AP exhibit decreased 25-(OH) D levels, which might be associated with calcium imbalances and mortality rate in canine AP.

The activation of PPARg by ligands, including conjugated linoleic acid (CLA) isomers, plays an important role in the immune response. Among CLA isomers, trans-10, cis-12 (t10c12)-CLA is known to participate in the modulation of pro-inflammatory cytokine secretion. The aim of the present study was to assess the effect of t10c12-CLA on PPARg activation, NF-kB activation and TNF-a expression in lipopolysaccharide (LPS)-naive and LPS-stimulated porcine peripheral blood mononuclear cells (PBMC). In addition, the effect of PPARg inhibition on NF-kB activation and TNF-a expression in porcine PBMC was examined. t10c12-CLA was found to increase TNF-a expression and NF-kB activity in LPS-naive porcine PBMC. In contrast, t10c12-CLA decreased TNF-a expression and NF-kB activity in LPS-stimulated porcine PBMC. t10c12-CLA up-regulated PPARg activity and mRNA expression in both LPS-naive and LPS-stimulated porcine PBMC. GW9662, a PPARg antagonist, completely negated the modulating effects of t10c12-CLA on TNF-a expression and NF-kB activity in both LPS-naive and LPS-stimulated porcine PBMC. These results suggest that t10c12-CLA can modulate TNF-a production and NF-kB activation by a PPARg-dependent pathway in porcine PBMC.

No abstract

No abstract