<p>It is widely known that orexin A and B peptides as well as their receptors are expressed in the hypothalamus and distributed throughout the central nervous system, but there have been few studies regarding its presences in other parts of the body. There is now evidence that orexin (ORX) and its receptors (ORXR1/2) are present in the avian liver; however, their regulation under different environmental conditions is still unknown. In the current study, we sought to determine the effects of heat and oxidative stress using hydrogen peroxide (H2O2) and 4-hydroxynonenal (4-HNE) on the hepatic expression of ORX and ORXR1/2 in the avian species. Overall, heat stress significantly down regulated the expression of ORX, and ORXR1/2 mRNA and pro1tein in quail liver and LMH cells. LMH cells treated with H2O2 had decreased ORX protein and increased ORX mRNA levels (P < 0.05). There was a biphasic effect of 4-HNE on the expression of ORX and ORXR1/2 in LMH cells. There was a significant upregulation at low doses (10 and 20 ?M) and significant down-regulation at a high dose (30?M) of 4-HNE. In light of the current data, the hepatic expression of orexin could serve as a molecular signature in the heat and oxidative stress response.

Equine laminitis is a devastating condition that results in the failure of the tissue responsible for suspending the skeleton within the hoof capsule. The digital laminae is composed of two interdigitated layers, the dermal lamellae surrounding the distal pedal bone, and the epidermal lamellae, which interfaces with the hoof wall. During laminitis, these layers separate, allowing for rotation and sinking of the pedal bone. While there are multiple diseases and physiological conditions associated with the development of laminitis, including sepsis, metabolic syndrome, and unequal weight bearing, the exact cause remains elusive. Prior work by our research group identified the metalloprotease ADAMTS-4 as a potential early instigator of disease. The data presented herein catalogs the distribution of the substrates of this enzyme, aggrecan and versican, the ramifications of ADAMTS-4-mediated versican loss in the laminae, and further expands into the repression of the canonical wnt signaling pathway and potential additional metalloprotease (MMP) involvement in disease, utilizing a model of acute, carbohydrate-induced laminitis. Additionally, samples from other models of laminitis induction and clinical samples were screened for differential expression of relevant gene markers, including versican, members of the canonical wnt signaling pathway, and MMP-1 and -13. Together, these data provide a characterization of laminar pathology in the carbohydrate-induced model, as well as highlighting key similarities and differences amongst multiple methods of disease development, and lay important groundwork for developing clinical therapeutic interventions.