ORCID Profile
0000-0001-5057-633X
Current Organisation
Pennsylvania State University
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Publisher: Elsevier BV
Date: 04-2018
Publisher: Springer Science and Business Media LLC
Date: 24-08-2019
Publisher: The Endocrine Society
Date: 26-07-2017
Abstract: Sleep abnormalities are associated with low bone mineral density. Underlying mechanisms are unknown. Investigate the impact of sleep restriction with circadian disruption on bone biomarkers. Intervention study. Four bone biomarkers [C-terminal cross-linked telopeptide of type I collagen (CTX) = bone resorption, N-terminal propeptide of type I procollagen (P1NP) = bone formation, sclerostin and fibroblast growth factor 23 = osteocyte function] were measured in bihourly serum s les over 24 hours at baseline and after ∼3 weeks of sleep restriction (5.6 hours sleep/24 hours) with concurrent circadian disruption (recurring 28-hour “day” in dim light) in 10 men (age groups: 20 to 27 years, n = 6 55 to 65 years, n = 4). The effects of sleep/circadian disruption and age on bone biomarker levels were evaluated using maximum likelihood estimation in a mixed model for repeated measures. P1NP levels were lower after intervention compared with baseline (P & 0.001) the decrease in P1NP was greater for younger compared with older men (28.0% vs 18.2%, P & 0.001). There was no change in CTX (Δ = 0.03 ± 0.02 ng/mL, P = 0.10). Sclerostin levels were higher postintervention in the younger men only (Δ = 22.9% or 5.64 ± 1.10 pmol/L, P & 0.001). These data suggest that 3 weeks of circadian disruption with concurrent sleep restriction can lead to an uncoupling of bone turnover wherein bone formation is decreased but bone resorption is unchanged. Circadian disruption and sleep restriction may be most detrimental to bone in early adulthood.
Publisher: Springer Science and Business Media LLC
Date: 29-03-2019
DOI: 10.1038/S41598-019-41712-1
Abstract: The PERIOD2 ( PER2 ) gene is a core molecular component of the circadian clock and plays an important role in the generation and maintenance of daily rhythms. Rs35333999, a missense variant of PER2 common in European populations, has been shown to associate with later chronotype. Chronotype relates to the timing of biological and behavioral activities, including when we sleep, eat, and exercise, and later chronotype is associated with longer intrinsic circadian period (cycle length), a fundamental property of the circadian system. Thus, we tested whether this PER2 variant was associated with circadian period and found significant associations with longer intrinsic circadian period as measured under forced desynchrony protocols, the ‘gold standard’ for intrinsic circadian period assessment. Minor allele (T) carriers exhibited significantly longer circadian periods when determinations were based on either core body temperature or plasma melatonin measurements, as compared to non-carriers (by 12 and 11 min, respectively accounting for ~7% of inter-in idual variance). These findings provide a possible underlying biological mechanism for inter-in idual differences in chronotype, and support the central role of PER2 in the human circadian timing system.
Publisher: Springer Science and Business Media LLC
Date: 26-07-2017
Publisher: The Endocrine Society
Date: 04-05-2020
Abstract: The purpose of this work is to determine whether an uncoupling of bone turnover markers (BTMs) occurs in women exposed to the combination of sleep restriction with circadian disruption (SRCD), as previously reported in men. Four bone biomarkers (N-terminal propeptide of type I procollagen [P1NP] and osteocalcin = bone formation C-telopeptide [CTX] = bone resorption sclerostin = bone formation inhibitor) were measured in bihourly s les over 24 hours at baseline and after approximately 3 weeks of sleep restriction (~5.6 hours of sleep/24 hours) with concurrent circadian disruption (SRCD, recurring 28-hour “day” in dim light). Maximum likelihood estimation in a repeated-measures model was used to assess the effects of SRCD and age on bone biomarkers. Five women were young (22 ± 2.8 years) and four were older (58 ± 1.8 years). Baseline bone biomarker levels did not differ by age (all P ≥ .07). Bone formation markers were lower after SRCD (estimate ± SEE, ΔP1NP = –9.5 ± 2.8 μg/L, P = .01 Δosteocalcin = –2.3 ± 0.9 ng/mL, P = .04). The P1NP decline was greater in young women (ΔP1NP = –12.9 ± 3.7 μg/L, P = .01). After SRCD, CTX was significantly higher in young women (0.182 ± 0.069 ng/mL, P = .04) but did not change in older women. These pilot data are similar to previous findings in men and suggest that SRCD negatively altered bone metabolism in women by decreasing markers of bone formation and, in young women, increasing a marker of bone resorption. If sustained, this pattern of BTM uncoupling may lead to bone loss and lower bone mineral density.
Publisher: American Association for the Advancement of Science (AAAS)
Date: 11-04-2012
DOI: 10.1126/SCITRANSLMED.3003200
Abstract: Sleep deficiency and out-of-synch circadian rhythms impair pancreatic insulin secretion, a possible precursor to metabolic syndrome and diabetes.
Publisher: Informa UK Limited
Date: 18-04-2016
Publisher: Elsevier BV
Date: 06-2022
Publisher: American Diabetes Association
Date: 16-02-2016
DOI: 10.2337/DB15-0999
Abstract: The risk of type 2 diabetes (T2D) is increased by abnormalities in sleep quantity and quality, circadian alignment, and melatonin regulation. A common genetic variant in a receptor for the circadian-regulated hormone melatonin (MTNR1B) is associated with increased fasting blood glucose and risk of T2D, but whether sleep or circadian disruption mediates this risk is unknown. We aimed to test if MTNR1B diabetes risk variant rs10830963 associates with measures of sleep or circadian physiology in intensive in-laboratory protocols (n = 58–96) or cross-sectional studies with sleep quantity and quality and timing measures from self-report (n = 4,307–10,332), actigraphy (n = 1,513), or polysomnography (n = 3,021). In the in-laboratory studies, we found a significant association with a substantially longer duration of elevated melatonin levels (41 min) and delayed circadian phase of dim-light melatonin offset (1.37 h), partially mediated through delayed offset of melatonin synthesis. Furthermore, increased T2D risk in MTNR1B risk allele carriers was more pronounced in early risers versus late risers as determined by 7 days of actigraphy. Our results provide the surprising insight that the MTNR1B risk allele influences dynamics of melatonin secretion, generating a novel hypothesis that the MTNR1B risk allele may extend the duration of endogenous melatonin production later into the morning and that early waking may magnify the diabetes risk conferred by the risk allele.
Location: No location found
Location: United States of America
No related grants have been discovered for Orfeu Buxton.