{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T10:26:37Z","timestamp":1789986397734,"version":"4.0.1"},"reference-count":44,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2010,1,5]],"date-time":"2010-01-05T00:00:00Z","timestamp":1262649600000},"content-version":"vor","delay-in-days":2105,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["beva.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Equine Veterinary Journal"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Reasons for performing study<\/jats:italic>\n                    : The mechanisms underlying the increased risk of laminitis in horses with equine Cushing's disease (ECD) are poorly understood.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Hypothesis<\/jats:italic>\n                    : That abnormalities in glucose homeostasis, similar to those which cause microvascular dysfunction in human diabetics, contribute to development of laminitis in horses with ECD.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Methods<\/jats:italic>\n                    : Thirty\u2010one aged horses were divided into 3 groups based on clinical signs and dexamethasone suppression testing (DST).\n                    <jats:italic>Group 1<\/jats:italic>\n                    (n = 12) had clinical ECD as evidenced by hirsutism.\n                    <jats:italic>Group 2<\/jats:italic>\n                    (n = 10) had a positive DST but no hirsutism.\n                    <jats:italic>Group 3<\/jats:italic>\n                    (n = 9) were controls without ECD, with a negative DST and no clinical evidence of ECD. Biochemical indices of glucose metabolism, vascular function and oxidative stress were determined in single morning blood samples.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Results<\/jats:italic>\n                    : Group 1 had abnormalities in glucose homeostasis, including increased levels of glucose and insulin, compared to\n                    <jats:italic>Groups 2<\/jats:italic>\n                    and\n                    <jats:italic>3. Groups 1<\/jats:italic>\n                    and\n                    <jats:italic>2<\/jats:italic>\n                    had significantly lower plasma thiol (PSH) levels and nonsignificantly lower albumin\u2010corrected PSH levels than Group 3, consistent with oxidative stress.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Conclusions and potential relevance<\/jats:italic>\n                    : The observed abnormalities in glucose metabolism and oxidative stress could potentially contribute to development of laminitis in horses with ECD, by similar mechanisms to those that cause microvascular dysfunction in human diabetics. The absence of inter\u2010group differences in the biochemical indices of vascular function precludes their use as preclinical diagnostic indicators of vascular dysfunction. The study also highlighted limitations in the premortem diagnosis of ECD.\n                  <\/jats:p>","DOI":"10.2746\/0425164044877215","type":"journal-article","created":{"date-parts":[[2007,4,12]],"date-time":"2007-04-12T19:03:27Z","timestamp":1176404607000},"page":"226-229","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Biochemical indices of vascular function, glucose metabolism and oxidative stress in horses with equine Cushing's disease"],"prefix":"10.1111","volume":"36","author":[{"given":"J. A.","family":"Keen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Mclaren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. J.","family":"Chandler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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