PMID- 26991264 OWN - NLM STAT- MEDLINE DCOM- 20170522 LR - 20211204 IS - 1530-0447 (Electronic) IS - 0031-3998 (Linking) VI - 80 IP - 1 DP - 2016 Jul TI - Effects of neonatal dexamethasone administration on cardiac recovery ability under ischemia-reperfusion in 24-wk-old rats. PG - 128-35 LID - 10.1038/pr.2016.54 [doi] AB - BACKGROUND: Evaluations of stress-induced cardiac functional alterations in adults after neonatal glucocorticoid (GC) treatment have been limited. In the present study, we evaluated adult cardiac functional recovery during postischemic reperfusion and measured cardiac gene expression involved energy metabolism in rats neonatally treated with dexamethasone (DEX). METHOD: Male Wistar rats were injected DEX in first 3 d after birth and controls were received saline (SAL). At 24 wk of age, insulin tolerance tests were performed, plasma lipid levels were measured, and left ventricular function and myocardial infarct size were evaluated. Expressions of genes involved in cardiac energy metabolism were measured by quantitative real-time polymerase chain reaction (PCR) and western blot. RESULTS: In 24-wk-old rats, neonatal DEX administration caused dyslipidemia, impaired cardiac recovery function and increased size of infarction, decreased cardiac expression of glucose transporter 4(GLUT4), peroxisome proliferative-activated receptor gamma coactivator 1alpha (PGC-1alpha) and ratios of phospho-forkhead box O1/forkhead box O1 (p-FoxO1/FoxO1) and phospho AMP-activated protein kinase/AMP-activated protein kinase (p-AMPK/AMPK) but increased pyruvate dehydrogenase kinase isoenzyme 4 (PDK4) expression compared with controls. CONCLUSION: Neonatal DEX administration impairs cardiac functional recovery during reperfusion following ischemia in 24-wk-old rats. Reduced cardiac glucose utilization may contribute to the long-term detrimental effects caused by neonatal DEX treatment. FAU - Jiang, Xinli AU - Jiang X AD - Department of Ophthalmology, the Third Hospital of Hebei Medical University, Shijiazhuang, China. FAU - Ma, Huijie AU - Ma H AD - Department of Physiology, Hebei Medical University, Shijiazhuang, China. FAU - Li, Chunguang AU - Li C AD - Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China. FAU - Cao, Yue AU - Cao Y AD - Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China. FAU - Wang, Yan AU - Wang Y AD - Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China. FAU - Zhang, Yi AU - Zhang Y AD - Department of Physiology, Hebei Medical University, Shijiazhuang, China. FAU - Liu, Yan AU - Liu Y AD - Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20160318 PL - United States TA - Pediatr Res JT - Pediatric research JID - 0100714 RN - 0 (Glucocorticoids) RN - 7S5I7G3JQL (Dexamethasone) RN - EC 2.7.- (Protein Kinases) RN - EC 2.7.11.3 (AMP-Activated Protein Kinase Kinases) RN - IY9XDZ35W2 (Glucose) SB - IM MH - AMP-Activated Protein Kinase Kinases MH - Animals MH - Dexamethasone/*therapeutic use MH - Energy Metabolism/drug effects MH - Glucocorticoids/pharmacology MH - Glucose/metabolism MH - Heart/*drug effects MH - Male MH - Mitochondria/metabolism MH - Myocardial Infarction/physiopathology MH - Myocardial Reperfusion MH - Myocardium/metabolism MH - Protein Kinases/metabolism MH - Rats MH - Rats, Wistar MH - Reperfusion Injury/*drug therapy MH - Time Factors EDAT- 2016/03/19 06:00 MHDA- 2017/05/23 06:00 CRDT- 2016/03/19 06:00 PHST- 2015/09/03 00:00 [received] PHST- 2016/01/08 00:00 [accepted] PHST- 2016/03/19 06:00 [entrez] PHST- 2016/03/19 06:00 [pubmed] PHST- 2017/05/23 06:00 [medline] AID - pr201654 [pii] AID - 10.1038/pr.2016.54 [doi] PST - ppublish SO - Pediatr Res. 2016 Jul;80(1):128-35. doi: 10.1038/pr.2016.54. Epub 2016 Mar 18.