Effects of Chronic Insomnia on the Neuroendocrine Regulation of Glucose and Lipid Metabolism
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Effects of Chronic Insomnia on the Neuroendocrine Regulation of Glucose and Lipid Metabolism|
|Study Start Date:||January 2007|
|Estimated Study Completion Date:||December 2008|
Patients with chronic insomnia
age, sex, bmi matched healthy controls
Sleep fragmentation has previously been shown to result in activation of the stress axis as indicated by enhanced cortisol and catecholamine release and a proinflammatory state mirrored by increased concentrations of proinflammatory cytokines such as IL-6 and TNFa. Therefore sleep deprivation is associated with a similar pattern of endocrine and proinflammatory alterations that may promote the insulin resistant state. Thus, it is of paramount interest to clearly define the metabolic alterations in patients with primary insomnia.
Patients with with suspected primary insomnia will be recruited from the sleep clinic at the University Hospital Basel and by newspaper ads. Primary insomnia will be diagnosed by a polysomnographic study and the exclusion of secondary causes such as depression, sleep apnea and restless legs syndrome. Eligible patients will be admitted to the CRC for metabolic studies, including baseline blood samples for the measurement of hormones, cytokines and adipokines, a euglycemic-hyperinsulinemic clamp study for the assessment of glucose turnover and insulin sensitivity and in vivo NMR studies to determine intrahepatic and intramyocellular lipid content.
The data obtained in insomnic patients will be compared to those of a control group matched for age, sex, BMI, menopausal status and physical activity selected from the general population.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00442624
|University Hospital Basel|
|Basel, Switzerland, 4031|
|Principal Investigator:||Stefan Bilz, MD||Cantonal Hospital of St. Gallen|