This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Obesity has long been recognized as a significant risk factor for the development of type 2 diabetes. There is increasing epidemiologic and laboratory evidence for an association between decreased sleep duration and/or quality and obesity risk. Morbid obesity, even in the absence of sleep apnea, is frequently associated with excessive daytime sleepiness and nocturnal sleep disturbances. Recent studies in healthy adults indicated that short-term partial sleep deprivation is associated with impaired glucose tolerance and a risk of weight gain resulting from reduced leptin levels, increased ghrelin levels, and increased hunger and appetite. Preliminary studies in subjects with impaired glucose tolerance who are short sleepers indicate that sleep extension leads to an improvement of glucose tolerance. Taken together, these studies suggest that chronic sleep loss is a novel, modifibale risk factor for obesity and diabetes. The goal of the proposed project is to test the hypothesis that, in morbidly obese subjects with excessive daytime sleepiness, improvement of sleep duration and quality has beneficial effects on glucose metabolism and appetite regulation. Our preliminary studies have shown that in morbidly obese subjects one inpatient week in the Clinical Research Center with unrestriced bedtimes was associated with decreased sleepiness, improved carbohydrate metabolism, increased leptin levels and decreased appetite and hunger despite severe caloric restriction. We propose to carefully monitor sleep duration during one week of inpatient admission to determine if the improvement in appetite regulation and glucose metabolism is proportional and directly correlated to the amount of sleep extension. Furthermore, we will delineate changes in the hormones regulating appetite (GLP-1, PYY,ghrelin, leptin) and explore the role of cytokines as a link between sleep, glucose metabolism and appetite regulation.
| 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 |
| Garyu, Justin W; Meffre, Eric; Cotsapas, Chris et al. (2016) Progress and challenges for treating Type 1 diabetes. J Autoimmun 71:1-9 |
| 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 |
| Fleming, Gini F; Schumm, Philip; Friberg, Greg et al. (2015) Circadian variation in plasma 5-fluorouracil concentrations during a 24 hour constant-rate infusion. BMC Cancer 15:69 |
| 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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