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Sleep, Exercise, and Insulin Sensiti...

Porter, Jay W.

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Sleep, Exercise, and Insulin Sensitivity.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Sleep, Exercise, and Insulin Sensitivity./
Author:	Porter, Jay W.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
Description:	145 p.
Notes:	Source: Dissertations Abstracts International, Volume: 82-08, Section: B.
Contained By:	Dissertations Abstracts International82-08B.
Subject:	Physiology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27994080
ISBN:	9798569970131

Sleep, Exercise, and Insulin Sensitivity.
Porter, Jay W.

Sleep, Exercise, and Insulin Sensitivity. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 145 p.

Source: Dissertations Abstracts International, Volume: 82-08, Section: B.

Thesis (Ph.D.)--University of Missouri - Columbia, 2020.

This item must not be sold to any third party vendors.

Accumulating evidence supports short sleep duration as a novel risk factor for obesity and diabetes, but little work has been done outside of healthy men or with consideration to changes in physical activity. Thirteen overweight and obese adults were sleep restricted for five nights with a six-hour sleep opportunity each night, followed by a two-day recovery period. Sleep restriction had no impact on glucose tolerance in response to a mixed meal test despite an increased peak glucose response (+7.3 mg/dL) and elevated non-esterified free fatty acid concentration (NEFA, +0.1 mmol/L). Sleep restriction did not modify step counts or physical activity intensities. Recovery period restored glucose responses, NEFA concentrations, and improved homeostatic model assessment of insulin resistance (HOMA-IR), despite increased sedentary time and reduced step counts. Daily exercise increased step counts (+4,700 steps/day, p<0.001), decreased sedentary time (-2.6%, p=0.02), and increased moderate-vigorous physical activity (+3.7%, p<0.001). Exercise reduced the insulin response to a meal but was not effective at preventing the increased peak glucose response or elevated NEFA. Adipose tissue samples, obtained after baseline, sleep restriction, and exercise (N=8), showed no increase in lipolytic capacity following sleep restriction. Protein content of fatty acid synthase tended to increase following sleep restriction (p=0.07), but not following exercise. Sleep restriction did not adversely affect glucose tolerance, but increased circulating NEFA are seen with no changes in adipose tissue lipolytic capacity. Recovery sleep showed a powerful effect of sleep on glucose metabolism.

ISBN: 9798569970131Subjects--Topical Terms:

518431
Physiology.
Subjects--Index Terms:

Sleep duration

Sleep, Exercise, and Insulin Sensitivity.
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300 $a 145 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-08, Section: B.
500 $a Advisor: Kanaley, Jill A.
502 $a Thesis (Ph.D.)--University of Missouri - Columbia, 2020.
506 $a This item must not be sold to any third party vendors.
520 $a Accumulating evidence supports short sleep duration as a novel risk factor for obesity and diabetes, but little work has been done outside of healthy men or with consideration to changes in physical activity. Thirteen overweight and obese adults were sleep restricted for five nights with a six-hour sleep opportunity each night, followed by a two-day recovery period. Sleep restriction had no impact on glucose tolerance in response to a mixed meal test despite an increased peak glucose response (+7.3 mg/dL) and elevated non-esterified free fatty acid concentration (NEFA, +0.1 mmol/L). Sleep restriction did not modify step counts or physical activity intensities. Recovery period restored glucose responses, NEFA concentrations, and improved homeostatic model assessment of insulin resistance (HOMA-IR), despite increased sedentary time and reduced step counts. Daily exercise increased step counts (+4,700 steps/day, p<0.001), decreased sedentary time (-2.6%, p=0.02), and increased moderate-vigorous physical activity (+3.7%, p<0.001). Exercise reduced the insulin response to a meal but was not effective at preventing the increased peak glucose response or elevated NEFA. Adipose tissue samples, obtained after baseline, sleep restriction, and exercise (N=8), showed no increase in lipolytic capacity following sleep restriction. Protein content of fatty acid synthase tended to increase following sleep restriction (p=0.07), but not following exercise. Sleep restriction did not adversely affect glucose tolerance, but increased circulating NEFA are seen with no changes in adipose tissue lipolytic capacity. Recovery sleep showed a powerful effect of sleep on glucose metabolism.
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