Literature DB >> 23063043

Autonomic markers of impaired glucose metabolism: effects of sleep-disordered breathing.

Wenli Wang1, Susan Redline, Michael C K Khoo.   

Abstract

BACKGROUND: The association between diabetes and abnormalities in autonomic function is well-known, but it is not clear if this association can be extended to subjects with prediabetic impaired glucose metabolism (IGM). Sleep-disordered breathing (SDB), which commonly occurs in this population, is often overlooked. We sought to determine how autonomic function, monitored in an overnight sleep study setting, may be impaired in subjects with IGM and/or SDB.
METHODS: Polysomnograms (PSGs) selected from the Cleveland Family Study database were categorized into four groups: normal, SDB (respiratory disturbance index > 5/h), IGM, and both SDB and IGM. Impaired glucose metabolism was defined as an oral glucose tolerance test (OGTT) level > 140 mg/dl. Time-domain and frequency-domain indices of heart rate variability were used to quantify autonomic impairment. Baroreflex sensitivity determined using pulse transit time (BRS(PTT)), an indirect measure of baroreflex sensitivity based on spontaneous pulse transit time fluctuations, was used as a surrogate measure of baroreflex sensitivity.
RESULTS: Based on 31 PSGs from subjects (16 males, 15 females) ages 20.8-61.2 years, both SDNN and BRS(PTT) were found to be 20-25% lower in SDB and ~40% lower in IGM and SDB + IGM as compared to subjects without either condition. In analyses of continuous measures, mean standard deviation of 5 min R-R intervals (SDNN) and BRS(PTT) were found to be negatively correlated with OGTT following adjustment for age and body mass index. Oral glucose tolerance test and age were the two most significant factors for predicting SDNN and BRS(PTT).
CONCLUSIONS: Our analyses suggest that cardiac autonomic control is impaired in IGM, regardless of whether SDB is present. The abnormal autonomic function involves degradation of baroreflex regulation.
© 2012 Diabetes Technology Society.

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Year:  2012        PMID: 23063043      PMCID: PMC3570851          DOI: 10.1177/193229681200600521

Source DB:  PubMed          Journal:  J Diabetes Sci Technol        ISSN: 1932-2968


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