It has been previously reported that AbMole Citiolone ghrelin system components are regulated by certain metabolic conditions, like obesity, in the stomach, pituitary and hypothalamus. In line with this, the AbMole 12-O-Tiglylphorbol-13-isobutyrate present report is the first to reveal, to the best of our knowledge, that ghrelin system components are also markedly altered under DIO conditions at pancreatic level. However, contrary to that previously reported at the hypothalamic and pituitary level, we observed an up-regulation of ghrelin, In1-ghrelin and GHS-R transcripts at the pancreas of cort+/+ animals under obesity conditions, while GOAT expression level remains unaltered, thus supporting that obesity-induced alterations in the ghrelin-system are tissue-dependent. It is well known that obesity is a chronic inflammation condition that causes a deleterious effect on pancreatic function and, in particular, on beta-cell function. In this sense, the observed increase in pancreatic ghrelin system expression may locally acts as a protective mechanism by promoting beta-cell survival and growth, a function that has been previously described for different ghrelin system components under physiological or pathological conditions. In addition, and similarly to that described for pancreatic ghrelin system profile, In1-ghrelin variant is also predominantly expressed under extreme metabolic conditions. These data again support a relevant role of this ghrelin variant at the pancreatic level that could be, at least in part, responsible for the described actions of ghrelin related peptides on beta-cell survival. In clear contrast to the up-regulation of ghrelin system under HFD conditions in cort +/+ mice described above, we observed a clear shut-down of ghrelin system components in the whole pancreas and islet-enriched culture of obese CORT deficient animals. These findings would support a novel pathophysiological role of CORT in the pancreatic function in individuals under metabolic stress. Conversely, at the endocrine pancreas, In1-ghrelin expression increased in cort2/2 obese animals, throughout a mechanism still unclear that would specifically favor the splicing of ghrelin gene to generate In1-ghrelin variant. These findings suggest that native ghrelin and In-1 ghrelin variant might be differentially regulated in cultured pancreatic islets in a similar manner to that reported in the pituitary, hypothalamus and stomach. Besides ghrelin expression, our data also reveal a significant increase of both insulin 1 and 2 mRNA transcripts in extracts from whole pancreas under obesity conditions. Many mucosal epithelia in humans and animals have evolved to co-exist with a rich and complex microbiota, but have also retained the ability to respond to potential pathogens, and regulate inflammatory responses to avoid tissue damage and disease. All of these mucosal epithelial surfaces are bathed in fluids, and yet little is known about how these fluids influence epithelial regulation of innate defense and inflammation. Like many other tissues surfaces, e.g. airways, gastrointestinal and urogenital tracts, the ocular surface is bathed in a surface liquid, the tear film. We have shown that tear fluid protects ocular surface epithelial cells against bacterial virulence mechanisms in vitro and in vivo, and that in vitro protection can be independent of direct antimicrobial activity.