SLEEP 2014 Final Program - page 98

LateBreakingAbstracts
LBA1
12:40pm – 12:55pm
HomeSleepDuration andGlycemia in Lean
andObeseAdolescents
KorenD
1
, O’SullivanK
1
, Gozal L
2
, BhattacharjeeR
2
, Gozal
D
2
1
Departments of Pediatrics andMedicine, Section ofAdult
andPediatricEndocrinology, Diabetes andMetabolism,
University of Chicago, Chicago, IL, USA,
2
Department of
Pediatrics, Section of PediatricSleepMedicine, University
of Chicago, Chicago, IL, USA
Introduction:
Self-inflictedbehaviorallymediated sleep
restriction is rampant amongadolescents, whomay
sleep as little as 6.4 hours onweeknights. In adults,
chronic sleep restriction increases type 2 diabetes risk
andexperimental sleep restriction causes acute insulin
resistance and glucose intolerance. Pediatric studies have
associated short sleepwith insulin resistance, but have not
examined
home
sleep duration’s influence on post-prandial
glucosemetabolism.We report on apilot study examining
relationships between home sleep anddynamic glucose
and insulin homeostasis in adolescents.
Methods:
10 adolescents (age 13-18 years, Tanner
2-5) underwent oral glucose tolerance test (OGTT),
anthropometrics, overnight polysomnogram, and home
sleep assessment via actigraphy and sleepdiaries.
Continuous variableswere analyzed by correlation
analysis. Linear regressions examined associations
between home sleep duration andmetabolic outcomes,
controlling for weight.
Results:
We found significant negative associations
between home sleep duration (actigraphy) andweight
(r=-0.63, p=0.049) andOGTT90-minute glucose (r=-0.66,
p=0.036). Trends emerged towards associations between
sleep duration andwaist circumference (r=-0.60, p=0.086),
fasting insulin (r=-0.59, p=0.074) and insulin resistance
measures, i.e. homeostasismodel assessment of insulin
resistance (HOMA-IR: r=-0.56, 0.091), andwhole-body
insulin sensitivity index (higher values denote greater
insulin sensitivity: r=+0.56, p=0.091). Linear regression
analysis revealed that sleepdurationwas the primary
predictor of 90-minuteglucose (R
2
change=0.44, p=0.036)
and that bodyweight was not a significant predictor.
Conclusions:
In this pilot study, the first to our knowledge
toexamine potential interrelationships between home sleep
duration anddynamic insulin and glucose homeostasis in
adolescents, significant negative relationships between
home sleep duration and bothweight and post-challenge
glucose levelswere identified, and trends towards negative
associations between home sleep duration andboth central
obesity and insulin resistancewere present. Our early
results point towards an association between sleep and
glucose/insulin homeostasis in adolescents that may be
independent of bodyweight.
Support:
This studywas supported by aCTSAUL1
TR000430 award.
LBA2
12:55pm – 1:10pm
Optogenetic Inhibitionof Basal Forebrain
ParvalbuminGABANeuronsSuppresses
Cortical Activation fromBothGammaBand
AuditoryStimulation andHypercarbia-
inducedArousals fromSleep
ThankachanS, Cordeira JW, KimT, McNally JM, McKenna
JT, Basheer R, Strecker RE, BrownRE, McCarleyRW
VABostonHealthcareSystem&HarvardMedical School,
Brockton, MA, USA
Introduction:
We hypothesized that basal forebrain (BF)
parvalbuminGABA (pvGABA) neurons forma key final
commonpathway for cortical activation from both sensory
and visceral stimuli.We used the40Hz auditory steady
state response (ASSR) as sensory stimuli andmeasured
the resulting activation of cortical gamma bandoscillations
(GBO, ~40Hz). Visceral stimuli were hypercarbia (10%
CO2), tomodel obstructive sleep apnea and its cortical
activation and arousal from sleep.
Methods:
For optogenetic inhibition, we bilaterally injected
a viral vector (AAV-FLEX-ArchT-GFP) with the proton
pumpArchTand a green fluorescent proteinmarker (GFP)
into theBF of parvalbumin (PV)-Cremice (n=12), and
histologically verified transduction. Inhibitionwas induced
by 532 nM bilateral laser illumination preceding andduring
the 500msASSR or 30s hypercarbia stimuli andwas
comparedwith no illumination in the same animal.
Results:
Projections of BF pvGABAneurons to frontal
cortexwas confirmed byGFP-labeled fiber tracing.
AuditoryStimuli: In each of 8 successfully transduced
mice,ArchT inhibition duringwakefulness of BFPV cells
attenuatedASSR-elicitedGBO (binomial p<0.01). Overall,
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