Madhu N Rao1, Alanna Chau2, Erin Madden3, Sabra Inslicht4, Lisa Talbot4, Anne Richards4, Aoife O'Donovan4, Leslie Ruoff5, Carl Grunfeld6, Thomas C Neylan4. 1. San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA; Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Francisco, CA, USA. Electronic address: Madhu.Rao@usf.edu. 2. Albert Einstein College of Medicine, New York, NY, USA. 3. San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA; Northern California Institute for Research and Education, San Francisco, CA, USA. 4. San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA; Department of Psychiatry, University of California, San Francisco, CA, USA. 5. San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA. 6. San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA; Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Francisco, CA, USA.
Abstract
BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with a 2-4 fold increased risk of developing Type 2 diabetes mellitus. However, detailed assessments of glucose metabolism and insulin secretion in a study designed to minimize confounders are lacking. Furthermore, few studies examine potential mechanisms involved. We analyzed data from a case-control study of medically healthy, medication-free adults to determine whether individuals with PTSD had abnormal glucose or insulin response to oral glucose tolerance test (OGTT) compared to controls. Secondarily, we assessed potential mediators such as sleep, cortisol and adiponectin. METHODS: Data was analyzed from 92 age and gender-matched subjects (44 PTSD, 48 controls). Chronic PTSD was diagnosed using the Structured Clinical Interview for DSM-IV and Clinician Administered PTSD Scale. Subjects underwent 75-g OGTT, actigraphy and sleep diary (to quantify sleep duration), polysomnography (to assess slow wave sleep [SWS] and delta power), and overnight blood sampling (for cortisol and adiponectin). RESULTS: At baseline, individuals with PTSD had mildly increased insulin levels (by 19%, compared to controls, p=0.048) that was mediated primarily by weight. In response to OGTT, the PTSD group had higher levels of insulin at 120 min (by 44%, p=0.03) and insulin AUC (by 43%, p=0.015) compared to controls, after adjusting for confounders. Glucose levels were similar in the two groups. Although self-reported sleep duration, SWS, and delta power differed between PTSD subjects and controls, they did not mediate the effects of PTSD status on insulin response. CONCLUSION: In this case-control study, individuals with PTSD had a hyperinsulinemic response to oral glucose challenge compared to controls, suggestive of insulin resistance. Published by Elsevier Ltd.
BACKGROUND:Posttraumatic stress disorder (PTSD) is associated with a 2-4 fold increased risk of developing Type 2 diabetes mellitus. However, detailed assessments of glucose metabolism and insulin secretion in a study designed to minimize confounders are lacking. Furthermore, few studies examine potential mechanisms involved. We analyzed data from a case-control study of medically healthy, medication-free adults to determine whether individuals with PTSD had abnormal glucose or insulin response to oral glucose tolerance test (OGTT) compared to controls. Secondarily, we assessed potential mediators such as sleep, cortisol and adiponectin. METHODS: Data was analyzed from 92 age and gender-matched subjects (44 PTSD, 48 controls). Chronic PTSD was diagnosed using the Structured Clinical Interview for DSM-IV and Clinician Administered PTSD Scale. Subjects underwent 75-g OGTT, actigraphy and sleep diary (to quantify sleep duration), polysomnography (to assess slow wave sleep [SWS] and delta power), and overnight blood sampling (for cortisol and adiponectin). RESULTS: At baseline, individuals with PTSD had mildly increased insulin levels (by 19%, compared to controls, p=0.048) that was mediated primarily by weight. In response to OGTT, the PTSD group had higher levels of insulin at 120 min (by 44%, p=0.03) and insulin AUC (by 43%, p=0.015) compared to controls, after adjusting for confounders. Glucose levels were similar in the two groups. Although self-reported sleep duration, SWS, and delta power differed between PTSD subjects and controls, they did not mediate the effects of PTSD status on insulin response. CONCLUSION: In this case-control study, individuals with PTSD had a hyperinsulinemic response to oral glucose challenge compared to controls, suggestive of insulin resistance. Published by Elsevier Ltd.
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