{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T01:26:56Z","timestamp":1789349216824,"version":"build-2803163510"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,11,23]],"date-time":"2015-11-23T00:00:00Z","timestamp":1448236800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008713","name":"Diabetes Australia Research Trust","doi-asserted-by":"publisher","award":["Y12G BURM"],"award-info":[{"award-number":["Y12G BURM"]}],"id":[{"id":"10.13039\/100008713","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2016,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Postprandial hyperglycaemia is associated with increased arterial stiffness and cardiovascular events. Low\u2010dose prednisolone causes insulin resistance that typically manifests as postprandial hyperglycaemia. We investigated whether prednisolone causes postprandial vascular dysfunction in a cohort of patients with rheumatoid arthritis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design<\/jats:title><jats:p>An open interventional and cross\u2010sectional study was undertaken.<\/jats:p><\/jats:sec><jats:sec><jats:title>Patients and measurements<\/jats:title><jats:p>Eighteen subjects with rheumatoid arthritis who had not taken oral glucocorticoids for \u22656 months were studied before and after prednisolone 6 mg\/day for 7 days to determine the acute effects of prednisolone. Pre\u2010prednisolone data were compared to 18 subjects with rheumatoid arthritis taking long\u2010term (&gt;6 months) prednisolone (6\u00b75 \u00b1 1\u00b78 mg\/day) to assess the chronic effects of prednisolone. Augmentation index (by applanation tonometry) and reactive hyperaemia index (by peripheral artery tonometry) were measured before and after a mixed\u2010meal (10 kcal\/kg, 45% carbohydrate, 15% protein, 40% fat). Insulin sensitivity was estimated by the Matsuda index and sympathetic nervous system activity from urinary noradrenaline excretion.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Matsuda index was lower after acute (2\u00b70 \u00b1 1\u00b70 <jats:italic>vs<\/jats:italic> 3\u00b76 \u00b1 1\u00b71, <jats:italic>P<\/jats:italic> = 0\u00b701) and chronic (1\u00b79 \u00b1 1\u00b70 <jats:italic>vs<\/jats:italic> 3\u00b76 \u00b1 1\u00b71, <jats:italic>P<\/jats:italic> = 0\u00b704) prednisolone. Postprandial augmentation index was lower after acute prednisolone (2551 \u00b1 197 <jats:italic>vs<\/jats:italic> 2690 \u00b1 272%*min, <jats:italic>P<\/jats:italic> \u2264 0\u00b7001), but not chronic prednisolone. There were no significant differences in reactive hyperaemia index with acute or chronic prednisolone. Noradrenaline excretion was lower after acute (54 \u00b1 8 <jats:italic>vs<\/jats:italic> 93 \u00b1 23 nmol\/6 h, <jats:italic>P<\/jats:italic> = 0\u00b702), but not chronic, prednisolone.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Prednisolone\u2010induced insulin resistance is not associated with postprandial vascular dysfunction in patients with rheumatoid arthritis. Reduced sympathetic activity may contribute to the reduction in postprandial arterial stiffness with acute prednisolone.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cen.12966","type":"journal-article","created":{"date-parts":[[2015,10,23]],"date-time":"2015-10-23T06:20:46Z","timestamp":1445581246000},"page":"501-508","source":"Crossref","is-referenced-by-count":18,"title":["Effect of acute and chronic glucocorticoid therapy on insulin sensitivity and postprandial vascular function"],"prefix":"10.1111","volume":"84","author":[{"given":"Anjana","family":"Radhakutty","sequence":"first","affiliation":[{"name":"School of Medicine Flinders University Adelaide Australia"},{"name":"Southern Adelaide Diabetes and Endocrine Services Repatriation General Hospital Adelaide Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brenda L.","family":"Mangelsdorf","sequence":"additional","affiliation":[{"name":"Southern Adelaide Diabetes and Endocrine Services Repatriation General 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Adelaide Adelaide Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malcolm D.","family":"Smith","sequence":"additional","affiliation":[{"name":"School of Medicine Flinders University Adelaide Australia"},{"name":"Department of Rheumatology Repatriation General Hospital Adelaide Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Campbell H.","family":"Thompson","sequence":"additional","affiliation":[{"name":"School of Medicine Flinders University Adelaide Australia"},{"name":"Discipline of Medicine The University of Adelaide Adelaide Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morton G.","family":"Burt","sequence":"additional","affiliation":[{"name":"School of Medicine Flinders University Adelaide Australia"},{"name":"Southern Adelaide Diabetes and Endocrine Services Repatriation General Hospital Adelaide 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