AGE Advanced glycation endproducts BW Black walnut ECD Equine Cushing’s disease GC Glucocorticoid IR Insulin resistance NEFA Nonesterified fatty acid PPID Pituitary pars intermedia dysfunction ROS Reactive oxygen species

significantly fewer publications have addressed the association between laminitis and pathological conditions of the horse’s endocrinological system (Schott 2002). This difference in research emphasis can be partly explained by the availability of useful and predictable models for the purposes of studying experimentally-induced laminitis that involve administration of either starch or a soluble extract of BW via nasogastric tube (Adair et al. 2000). In contrast, the exogenous administration of GCs to horses rarely and unpredictably results in laminitis (Johnson et al. 2002). Paradoxically, using starch/BW models, results of recent research show clearly that activation of inflammatory mediators occurs during the early stages of laminitis, suggesting that GCs (anti-inflammatory agents) should theoretically protect against the development of laminitis (Fontaine et al. 2001). Therefore, an alternative explanation for development of laminitis in the face of increased GC action should be sought. Although a satisfactory explanation for the association between GCs and laminitis is lacking, several hypothetical explanations have been suggested (Johnson et al. 2002). Specifically, GCs might act directly to cause laminitis by: affecting vascular smooth muscle in such a manner as to enhance vasospasticity and reduce blood flow; weakening have given financial support for the publication of this issue, namely Dodson & Horrell, RIRDC and BEVA Trust, have provided a valuable stepping stone in the aim towards improving the welfare of horses. I am very grateful to the Guest Editors, Professor Leo Jeffcott and Dr Celia Marr, for the substantial amount of work that they have contributed to this Laminitis Special Issue.