作者: Madhu N. Rao , Alanna Chau , Erin Madden , Sabra Inslicht , Lisa Talbot
DOI: 10.1016/J.PSYNEUEN.2014.07.006
关键词:
摘要: Author(s): Rao, Madhu N; Chau, Alanna; Madden, Erin; Inslicht, Sabra; Talbot, Lisa; Richards, Anne; O'Donovan, Aoife; Ruoff, Leslie; Grunfeld, Carl; Neylan, Thomas C | Abstract: Posttraumatic stress disorder (PTSD) is associated with a 2–4 fold increased risk of developing Type 2 diabetes mellitus. However, detailed assessments glucose metabolism and insulin secretion in study designed to minimize confounders are lacking. Furthermore, few studies examine potential mechanisms involved. We analyzed data from case–control medically healthy, medication-free adults determine whether individuals PTSD had abnormal or response oral tolerance test (OGTT) compared controls. Secondarily, we assessed mediators such as sleep, cortisol adiponectin. Data was 92 age gender-matched subjects (44 PTSD, 48 controls). Chronic diagnosed using the Structured Clinical Interview for DSM-IV Clinician Administered Scale. Subjects underwent 75-g OGTT, actigraphy sleep diary (to quantify duration), polysomnography assess slow wave [SWS] delta power), overnight blood sampling (for adiponectin). At baseline, mildly levels (by 19%, controls, p = 0.048) that mediated primarily by weight. In group higher at 120 min 44%, 0.03) AUC 43%, 0.015) after adjusting confounders. Glucose were similar two groups. Although self-reported duration, SWS, power differed between they did not mediate effects status on response.Posttraumatic response.In this study, hyperinsulinemic challenge suggestive resistance.