This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Epidemiologic data have shown associations between short sleep duration and elevated body mass index. So far, the major evidence in support of a causal mechanism comes from our laboratory studies of healthy young adults submitted to sleep restriction, showing that short sleep results in altered glucose regulation, decreased leptin levels, increased ghrelin levels, and increased hunger and appetite, suggesting an increased risk of weight gain. The majority of the epidemiologic studies did not control for sleep quality. Our preliminary data demonstrates that, in healthy young adults, experimental suppression of deep slow-wave sleep (SWS) without change in total sleep time results in alterations of glucose and appetite regulation, suggesting that reduced sleep quality could also lead to an increased risk of obesity. We therefore propose to obtain causative evidence that link reduced sleep duration and quality to obesity risk. Normal young adults will be studied in laboratory with 4 days with undisturbed sleep (8.5hrs in bed; baseline ), 4 days with short sleep (4.5 hrs in bed; short sleep ) and 4 days of reduced sleep quality (8.5 hrs in bed; SWS suppression ). Both the short sleep and SWS suppression conditions will be followed by 2 nights of undisturbed recovery sleep. The studies will combine brain imaging by PET and fMRI, estimations of sympatho-vagal balance, measurements of orexigenic and anorexigenic factors, cytokines and adipokines, continuous assessment of glucose levels via subcutaneous sensors, in vitro studies of insulin signaling in adipocytes from fat biopsies, and behavioral expression of hunger and food intake.
| Rosenfield, Robert L; Ehrmann, David A (2016) The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev 37:467-520 |
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| Rosenfield, Robert L (2015) The Polycystic Ovary Morphology-Polycystic Ovary Syndrome Spectrum. J Pediatr Adolesc Gynecol 28:412-9 |
| Maitland, Michael L; Xu, Chun-Fang; Cheng, Yu-Ching et al. (2015) Identification of a variant in KDR associated with serum VEGFR2 and pharmacodynamics of Pazopanib. Clin Cancer Res 21:365-72 |
| Bershad, Anya K; Jaffe, Jerome H; Childs, Emma et al. (2015) Opioid partial agonist buprenorphine dampens responses to psychosocial stress in humans. Psychoneuroendocrinology 52:281-8 |
| Refetoff, Samuel; Bassett, J H Duncan; Beck-Peccoz, Paolo et al. (2014) Classification and proposed nomenclature for inherited defects of thyroid hormone action, cell transport, and metabolism. J Clin Endocrinol Metab 99:768-70 |
| Kirkpatrick, Matthew G; Francis, Sunday M; Lee, Royce et al. (2014) Plasma oxytocin concentrations following MDMA or intranasal oxytocin in humans. Psychoneuroendocrinology 46:23-31 |
| Copinschi, Georges; Leproult, Rachel; Spiegel, Karine (2014) The important role of sleep in metabolism. Front Horm Res 42:59-72 |
| Müller, Peter; Quintana, Fernando A; Rosner, Gary L et al. (2014) Bayesian inference for longitudinal data with non-parametric treatment effects. Biostatistics 15:341-52 |
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